Aylwin IV DD- 1081 - History

Aylwin IV DD- 1081 - History

Aylwin IV

(DE-1081: dp. 3,963; 1. 438'; b. 47'; dr. 25'; s. 27 k.; cpl. 245;
a. 15", 4 12.75" tt., ASROC, Sea Sparrow; cl. Knox)

The fourth Aylwin (DE-1081) was laid down on 13 November 1969 at Westwego, La., by the Avondale Shipyard Inc.; launched on 29 August 1970; sponsored by Mrs. Charles K. Duncan; and commissioned on 18 September 1971 at the Boston Naval Shipyard, Comdr. Dan E. ;Penn in command. Early in December, the destroyer escort sailed for her home and arrived there on 10 December. After in port, Aylwin headed for Guantanamo down training. While en roue, Aylwin stopped at Andros Island, Bahamas, for weapons testing. Arriving at Guantanamo Bay on 24 January 1972, the ship began four weeks of intensive training. She visited Santo Domingo for a liberty call before returning to Norfolk for post-shakedown availability. Late in October, the vessel participated in LANTREDEX 2-72 and then made final preparations for her first overseas deployment. On 1 December, Aylwin departed Norfolk to join the 6th Fleet in the Mediterranean. Her first stop was at El Ferrol, Spain. Departing that port on 13 December, she transited the Strait of Gibraltar and proceeded to Athens, Greece, where she spent the holiday season.

On 6 January 1973, Aylwin got underway for antisubmarine warfare (ASW) operations to be held in the eastern Mediterranean in conjunction with Task Force (TF) 60. The ship pulled in to Golfe Juan, France, on 17 January, then continued on to Gibraltar. Next came ASW operations in the eastern Mediterranean followed by a visit to Naples, Italy, for a two-week tender availability. The destroyer escort then visited Dubrovnik, Yugoslavia. On 17 February, she participated in NATO Exercise "National Week," held in conjunction with British, Italian, and Turkish warships. She arrived at Alanya, Turkey, on 28 February and then stopped at Athens; La Maddalena, Italy; Alicante, Barcelona, and Valencia, Spain; Tunis, Tunisia; Villefranche, Cannes, and Toulon, France; and Gibraltar. On 20 June, Aylwin got underway once more for the United States. She paused at the Naval Weapons Station, Yorktown, Va., on 27 June, to unload her weapons and returned to Norfolk the next day ending an absence of seven months. The ship was drydocked from 19 July to 20 August. She received the light air multi-purpose system (LAMPS) modification during a yard period lasting through 26 October. A tender availability came in November, and December found the ship in a standdown period.

The destroyer escort sailed on 19 February 1974 for refresher training at Guantanamo Bay. While there, she took part in ASW exercises in addition to testing her new LAMPS equipment. She returned to Norfolk on 27 April to make final preparations for her second overseas deployment. On 17 June, Aylwin set sail for the Mideast and the Indian Ocean. Her first stop was Roosevelt

Early in December port, Norfolk, Va., spending the holidays Bay, Cuba, for shake Roads, Puerto Rico, where she held gunnery exercises. She then proceeded to Trinidad for a refueling stop. Aylwin next put in to Recife, Brazil for a brief liberty period.

She got underway again on the 28th to cross the Atlantic and arrived at Freetown, Sierra Leone, on 2 July. Aylwin's next stop was Luanda, Angola. Her visit there was curtailed by an outbreak of violence associated with that country's bid for independence from Portugal. The vessel weighed anchor on 13 July, sailed around the Cape of Good Hope, and entered the Indian occurred, the ship only righted herself to 60 degrees. For the next 20 minutes, the typhoon lashed at Aylwin with her full fury,often pushing the ship over to rolls that varied between 30 an 0 degrees.

As the sea continued its destructive work, tearing loose the whaleboat and its davits, Aylwin continued to struggle for survival. At 1245, Machinists Mate 1st Class Sarenski was swept overboard; followed 10 minutes later by the chief engineer, Lt. E. R. Rendahl, USNR. Neither was rescued.

At 1330, the engine-room ventilators failed. Now denied fresh air, the engine room became an oven as its temperature shot up to 180 degrees, forcing its abandonment. For the next six hours, Aylwin doggedly hung on, fighting the raging sea for her life. As if the fury of the storm without were not enough, a leak in the engine room at 1930 drew all pumps into action. Eventually the inrush of water was brought under control just as it crept up above the floorplates. The sloshing of this water further reduced the ship's already "tender" stability.

Each man in Aylwin fought the fear that the ship would turn turtle-each roll could be deeper; each might be the last. Every sailor hoped and prayed to be delivered from the typhoon; and providentially, Aylwin did survive Neptune's onslaught.

However, other ships had not fared so well. The storm claimed Hull, Monaghan, and Spence (DD-512), each with heavy loss of life. Seventeen other ships suffered varying degrees of damage in the storm.

Her flooding under control, Aylwin arrived at Ulithi three days before Christmas. There, she received repairs alongside Markab (AD-21) that lasted into January 1945. While at Ulithi, Aylwin conducted a brief patrol of the harbor after an explosion in Mazama (AE-12)- believed to have been cause by a submarine torpedo-but found no evidence of submarine activity.

The destroyer continued her operations as screen for replenishment groups into February of 1945. As part of the screen of TG 50.8, she-together with Crowley (DE-303), Weaver (DE741), Suamico (AO-49), Shasta (AE-6), and Wrangell (AE12) reached Iwo Jima on 21 February. She then began protecting the transports. On 23 February, Aylwin was assigned to TF 54, the fire support group, and relieved Tuscaloosa (CA-37) in fire support sector 1.

By that time, marines had occupied the southern section of Iwo Jima and were advancing to the north against stiff enemy opposition. On 23 and 24 February, Aylwin fired close support, expending 330 rounds of 5-inch, neutralizing enemy-held positions on call, before she left Iwo Jima on the 25th for a fueling rendezvous en route back to Ufithi where she arrived on the 28th.

Dunn the first phase of the invasion of Okinawa, Aylwin operated between Kerama Retto and Ulithi. In early April, she endured her second typhoon on 5 June 1945. Although much less destructive than the first, this storm caused Lt. Comdr. Rogers to report: " with the present sea-keeping and characteristics, the Farragut-class destroyers are unable to adequately cope with severe typhoon conditions."

Aylwin rendezvoused with the storm-damaged Pittsburgh (CA-72) which had lost her bow in this tempest, joining that cruiser late in the afternoon. She subsequently searched unsuccessfully for the damaged warship's severed bow before putting into Apra Harbor, Guam, on 10 June for repairs lasting until 6 July.

On that day she got underway to return to the Carolines and reached Ulithi on the next. She sortied on the 10th as an escort for Convoy UOK-39 and safely saw her 41 charges to Okinawa.

After returning to Ulithi with another convoy, Aylwin began steaming off the anchorage on picket station B-6 at 1640 on 3 August. The next morning at 0306, while on station, she received orders to proceed to latitude 11'451 north, longitude 133 35' east, to search for survivors of the torpedoed Indianapolis. Aylwin accordingly broke off her patrol, raced to the scene of the disaster, and searched her assigned area. However, by that time, the sea had claimed many of the survivors. The destroyer located and examined three bodies, removing all identification materials and fingerprinting them before burying them at sea. She also found and brought on board two aircraft-type rubber rafts and an empty floater net. At 0525 on 6 August, she headed back to Ulithi.

Underway again on 13 August, Aylwin escorted a convoy of troopships to the Marianas, reaching Apra Harbor on 14 August. When Japan capitulated the following day, Aylwin was at Apra Harbor.

Three days later, the destroyers got underway for the Hawaiian Islands, in company with MacDonough and Rudyerd Bay (CVE-81), and reached Pearl Harbor soon thereafter. On 27 August, Aylwin embarked four officers and 50 enlisted men at that port for passage to the west coast and, the following. day, sailed for the California coast. The veteran destroyer disembarked her passengers at San Diego and, after tarrying there lie east from 3 to 11 September, got underway for Panama and the coast of the United States.

Transiting the canal for the last time on 20 September, Aylwin reached New York City on 25 September. Decommissioned at the New York Navy Yard on 16 October 1945, Aylwin was struck from the Navy list on 1 November 1945. Stripped for disposal, her hulk was sold and delivered to George N. Nutman, Inc., of Brooklyn, N.Y.. on 20 December 1946 and cut up for scrap by 2 September 1948.

Aylwin (DD-355) received 13 battle stars for her World War I I service.


Constantinople

Constantinople ( / ˌ k ɒ n s t æ n t ɪ ˈ n oʊ p əl / [5] Greek: Κωνσταντινούπολις Kōnstantinoupolis Latin: Constantinopolis Ottoman Turkish: قسطنطينيه‎ ‎, romanized: Ḳosṭanṭīnīye) was the capital city of the Roman Empire (330–395), the Byzantine Empire (395–1204 and 1261–1453), the brief Crusader state known as the Latin Empire (1204–1261), and the Ottoman Empire (1453–1922).

  • 330 AD: Founding of Constantinople
  • c. 404/05-413 AD: Construction of the Theodosian Walls
  • 474 AD: Great Fire of Constantinople [1]
  • 532 AD: Nika Riots and Fire of Constantinople
  • 537 AD: Completion of the Hagia Sophia by Justinian I[2][3][4]
  • 626 AD: First Siege of Constantinople
  • 674–678 AD: First Arab Siege of Constantinople
  • 717–718 AD: Great Siege of Constantinople/Second Arab Siege of Constantinople
  • 1204 AD: Sack of Constantinople
  • 1261 AD: Liberation of Constantinople
  • 1422 AD: First Ottoman Siege of Constantinople
  • 1453 AD: Fall of Constantinople

In 324, the ancient city of Byzantium was renamed “New Rome” and declared the new capital of the Roman Empire by Emperor Constantine the Great, after whom it was renamed, and dedicated on 11 May 330. [6] From the mid-5th century to the early 13th century, Constantinople was the largest and wealthiest city in Europe. [7] The city became famous for its architectural masterpieces, such as Hagia Sophia, the cathedral of the Eastern Orthodox Church, which served as the seat of the Ecumenical Patriarchate, the sacred Imperial Palace where the Emperors lived, the Galata Tower, the Hippodrome, the Golden Gate of the Land Walls, and opulent aristocratic palaces. The University of Constantinople was founded in the fifth century and contained artistic and literary treasures before it was sacked in 1204 and 1453, [8] including its vast Imperial Library which contained the remnants of the Library of Alexandria and had 100,000 volumes. [9] The city was the home of the Ecumenical Patriarch of Constantinople and guardian of Christendom's holiest relics such as the Crown of thorns and the True Cross.

Constantinople was famed for its massive and complex defenses. The Theodosian Walls consisted of a double wall lying about 2 kilometres (1.2 mi) to the west of the first wall and a moat with palisades in front. [10] This formidable complex of defences was one of the most sophisticated of Antiquity. The city was built intentionally to rival Rome, and it was claimed that several elevations within its walls matched the 'seven hills' of Rome. Because it was located between the Golden Horn and the Sea of Marmara the land area that needed defensive walls were reduced, and this helped it to present an impregnable fortress enclosing magnificent palaces, domes, and towers, the result of the prosperity it achieved from being the gateway between two continents (Europe and Asia) and two seas (the Mediterranean and the Black Sea). Although besieged on numerous occasions by various armies, the defenses of Constantinople proved impregnable for nearly nine hundred years.

In 1204, however, the armies of the Fourth Crusade took and devastated the city and, for several decades, its inhabitants resided under Latin occupation in a dwindling and depopulated city. In 1261 the Byzantine Emperor Michael VIII Palaiologos liberated the city, and after the restoration under the Palaiologos dynasty, enjoyed a partial recovery. With the advent of the Ottoman Empire in 1299, the Byzantine Empire began to lose territories and the city began to lose population. By the early 15th century, the Byzantine Empire was reduced to just Constantinople and its environs, along with Morea in Greece, making it an enclave inside the Ottoman Empire after a 53-day siege the city eventually fell to the Ottomans, led by Sultan Mehmed II, on 29 May 1453, [11] whereafter it replaced Edirne (Adrianople) as the new capital of the Ottoman Empire. [12]


Gruffydd ap Cynan

Please see Darrell Wolcott: The Royal Family of Gwynedd - The Children of Gruffudd, Nephew of Iago http://www.ancientwalesstudies.org/id80.html, for a detailed look at the trees for BOTH Gruffudd(s) ap Cynan(Steven Ferry, March 30, 2017.)

Please see Darrell Wolcott: Edwin of Tegeingl and His Family - Was Owain ap Edwin Really a Traitor http://www.ancientwalesstudies.org/id87.html. (Steven Ferry, April 17, 2017.)

  1. ID: I4341
  2. Name: Gruffudd ap Cyan
  3. Given Name: Gruffudd ap
  4. Surname: Cyan
  5. Suffix: King Of Gwynedd 1 2
  6. Sex: M
  7. Birth: 1055 in Dublin, Ireland 3
  8. Death: 1137 in Bangor, England 1 2
  9. Burial: Bangor Cathedral, Is Gwyrfai, Caernarvonshire, Wales
  10. Change Date: 21 Sep 2005 at 15:23

Painting: Gruffydd ap Cynan escapes from Chester, Illustration by T. Prytherch in 1900.

Father: Ragnhildir (Ranult) ingen Olaf Of Dublin b: Abt 1030

Marriage 1 Angharat verch Owain b: Abt 1065 in Tegeingl, Flintshire, Wales

Gruffydd ap Cynan (standard Welsh: Gruffydd ap Cynan) (c. 1055 – 1137) was a King of Gwynedd. In the course of a long and eventful life, he became a key figure in Welsh resistance to Norman rule, and was remembered as King of all Wales. As a descendant of Rhodri Mawr, Gruffydd ap Cynan was a senior member of the princely house of Aberffraw. Through his mother Gruffydd had close family connections with the Danish settlement around Dublin and he frequently used Ireland as a refuge and as a source of troops. He three times gained the throne of Gwynedd and then lost it again before regaining it once more in 1099 and this time keeping power until his death. Gruffydd laid the foundations which were built upon by his son Owain Gwynedd and his great-grandson Llywelyn the Great.

The history of Gruffydd ap Cynan

Unusually for a Welsh king or prince, a near-contemporary biography of Gruffydd, The history of Gruffydd ap Cynan, has survived. Much of our knowledge of Gruffydd comes from this source, though allowance has to be made for the fact that it appears to have been written as dynastic propaganda for one of Gruffydd's descendants. The traditional view among scholars was that it was written during the third quarter of the 12th century during the reign of Gruffydd's son, Owain Gwynedd, but it has recently been suggested that it may date to the early reign of Llywelyn the Great, around 1200. The name of the author is not known. Most of the existing manuscripts of the history are in Welsh but these are clearly translations of a Latin original. It is usually considered that the original Latin version has been lost, and that existing Latin versions are re-translations from the Welsh. However Russell (2006) has suggested that the Latin version in Peniarth MS 434E incorporates the original Latin version, later emended to bring it into line with the Welsh text. [edit]Genealogy

According to the Life of Gruffydd ap Cynan, Gruffydd was born in Dublin and reared near Swords, County Dublin in Ireland. He was the son of a Welsh Prince, Cynan ap Iago, who was a claimant to the Kingship of Gwynedd but was probably never king of Gwynedd, though his father, Gruffydd's grandfather, Iago ab Idwal ap Meurig had ruled Gwynedd from 1023 to 1039. When Gruffydd first appeared on the scene in Wales the Welsh annals several times refer to him as "grandson of Iago" rather than the more usual "son of Cynan", indicating that his father was little known in Wales. Cynan ap Iago seems to have died while Gruffydd was still young, since the History describes his mother telling him who his father was. Gruffydd's mother, Ragnaillt, was the daughter of Olaf of Dublin, son of King Sigtrygg Silkbeard and a member of the Hiberno-Norse dynasty. Through his mother, who appears in the list of the fair women of Ireland in the Book of Leinster, Gruffydd claimed relationships with many of the leading septs in Ireland, including those of the Ua Briain. During his many struggles to gain the kingship of Gwynedd, Gruffydd received considerable aid from Ireland, both from the Hiberno-Norse at Dublin, but also those at Wexford, and also from Muircheartach Ua Briain. [edit]First bid for the throne

Gruffydd made his first attempt to take over the rule of Gwynedd in 1075, following the death of Bleddyn ap Cynfyn. Trahaearn ap Caradog had seized control of Gwynedd but had not yet firmly established himself. Gruffydd landed on Anglesey with an Irish force, and with the assistance of troops provided by the Norman Robert of Rhuddlan first defeated and killed Cynwrig ap Rhiwallon, an ally of Trahaearn who held Llŷn, then defeated Trahaearn himself in the battle of Gwaed Erw in Meirionnydd and gained control of Gwynedd. Gruffydd then led his forces eastwards to reclaim territories taken over by the Normans, and despite the assistance previously given by Robert of Rhuddlan attacked and destroyed Rhuddlan castle. However tension between Gruffydd's Danish-Irish bodyguard and the local Welsh led to a rebellion in Llŷn and Trahaearn took the opportunity to counter attack, defeating Gruffydd at the battle of Bron yr Erw above Clynnog Fawr the same year. [edit]Second bid for the throne and capture by the Normans

Gryffydd ap Cynan's Coat of Arms Gruffydd fled to Ireland but in 1081 returned and made an alliance with Rhys ap Tewdwr prince of Deheubarth. Rhys had been attacked by Caradog ap Gruffydd of Gwent and Morgannwg, and had been forced to flee to the St David's Cathedral. Gruffydd this time embarked from Waterford with a force composed of Danes and Irish and landed near St David's, presumably by prior arrangement with Rhys. He was joined here by a force of his supporters from Gwynedd, and he and Rhys marched north to seek Trahaearn ap Caradog and Caradog ap Gruffydd who had themselves made an alliance and been joined by Meilyr ap Rhiwallon of Powys. The armies of the two confederacies met at the Battle of Mynydd Carn, with Gruffydd and Rhys victorious and Trahaearn, Caradog and Meilyr all being killed. Gruffydd was thus able to seize power in Gwynedd for the second time. He was soon faced with a new enemy, as the Normans were now encroaching on Gwynedd. Gruffydd had not been king very long when he was enticed to a meeting with Hugh Earl of Chester and Hugh Earl of Shrewsbury at Rug, near Corwen. At the meeting Gruffydd was seized and taken prisoner. According to his biographer this was by the treachery of one of his own men, Meirion Goch. Gruffydd was imprisoned in Earl Hugh's castle at Chester for many years while Earl Hugh and Robert of Rhuddlan went on to take possession of Gwynedd, building castles at Bangor, Caernarfon and Aberlleiniog. [edit]Escape from captivity and third reign

Gruffydd reappeared on the scene years later, having escaped from captivity. According to his biography he was in fetters in the market-place at Chester when Cynwrig the Tall on a visit to the city saw his opportunity when the burgesses were at dinner. He picked Gruffydd up, fetters and all, and carried him out of the city on his shoulders. There is debate among historians as to the year of Gruffydd's escape. Ordericus Vitalis mentions a "Grifridus" attacking the Normans in 1088. The History in one place states that Gruffydd was imprisoned for twelve years, in another that he was imprisoned for sixteen years. Since he was captured in 1081, that would date his release to 1093 or 1097. J.E. Lloyd favours 1093, considering that Gruffydd was involved at the beginning of the Welsh uprising in 1094. K.L. Maund on the other hand favours 1097, pointing out that there is no reference to Gruffydd in the contemporary annals until 1098. D. Simon Evans inclines to the view that Ordericus Vitalis' date of 1088 could be correct, suggesting that an argument based on the silence of the annals is unsafe. Gruffydd again took refuge in Ireland but returned to Gwynedd to lead the assaults on Norman castles such as Aber Lleiniog. The Welsh revolt had begun in 1094 and by late 1095 had spread to many parts of Wales. This induced William II of England (William Rufus) to intervene, invading northern Wales in 1095. However his army was unable to the Welsh to battle and returned to Chester without having achieved very much. King Willam mounted a second invasion in 1097, but again without much success. The History only mentions one invasion by Rufus, which could indicate that Gruffydd did not feature in the resistance to the first invasion. At this time Cadwgan ap Bleddyn of Powys led the Welsh resistance. In the summer of 1098 Earl Hugh of Chester joined with Earl Hugh of Shrewsbury in another attempt to recover his losses in Gwynedd. Gruffydd and his ally Cadwgan ap Bleddyn retreated to Anglesey, but then were forced to flee to Ireland in a skiff when a fleet he had hired from the Danish settlement in Ireland accepted a better offer from the Normans and changed sides. [edit]King for the fourth time and consolidation

The situation was changed by the arrival of a Norwegian fleet under the command of King Magnus III of Norway, also known as Magnus Barefoot, who attacked the Norman forces near the eastern end of the Menai Straits. Earl Hugh of Shrewsbury was killed by an arrow said to have been shot by Magnus himself. The Normans were obliged to evacuate Anglesey, and the following year Gruffydd returned from Ireland to take possession again, having apparently come to an agreement with Earl Hugh of Chester. With the death of Hugh of Chester in 1101 Gruffydd was able to consolidate his position in Gwynedd, as much by diplomacy as by force. He met King Henry I of England who granted him the rule of Llŷn, Eifionydd, Ardudwy and Arllechwedd, considerably extending his kingdom. By 1114 he had gained enough power to induce King Henry to invade Gwynedd in a three-pronged attack, one detachment led by King Alexander I of Scotland. Faced by overwhelming force, Gruffydd was obliged to pay homage to Henry and to pay a heavy fine, but lost no territory. By about 1118 Gruffydd's advancing years meant that most of the fighting which pushed Gwynedd's borders eastward and southwards was done by his three sons by his wife Angharad, daughter of Owain ab Edwin: Cadwallon, Owain Gwynedd and later Cadwaladr. The cantrefs of Rhos and Rhufoniog were annexed in 1118, Meirionnydd captured from Powys in 1123 and Dyffryn Clwyd in 1124. Another invasion by the king of England in 1121 was a military failure. The king had to come to terms with Gruffydd and made no further attempt to invade Gwynedd during Gruffydd's reign. The death of Cadwallon in a battle against the forces of Powys near Llangollen in 1132 checked further expansion for the time being. Gruffydd was now powerful enough to ensure that his nominee, David the Scot was consecrated as Bishop of Bangor in 1120. The see had been effectively vacant since Bishop Hervey le Breton had been forced to flee by the Welsh almost twenty years before, since Gruffydd and King Henry could not agree on a candidate. David went on to rebuild Bangor Cathedral with a large financial contribution from Gruffydd. Owain and Cadwaladr in alliance with Gruffydd ap Rhys of Deheubarth gained a crushing victory over the Normans at Crug Mawr near Cardigan in 1136 and took possession of Ceredigion. The latter part of Guffydd's reign was considered to be a "Golden Age" according to the Life of Gruffydd ap Cynan Gwynedd was "bespangled with lime-washed churches like the stars in the firmament". [edit]Death and succession

Gruffydd was buried in Bangor Cathedral Gruffydd died in his bed, old and blind, in 1137 and was mourned by the annalist of Brut y Tywysogion as the head and king and defender and pacifier of all Wales. He was buried by the high altar in Bangor Cathedral which he had been involved in rebuilding. He also made bequests to many other churches, including one to Christ Church Cathedral, Dublin where he had worshipped as a boy. He was succeeded as king of Gwynedd by his son Owain Gwynedd. His daughter, Gwenllian, who married Gruffydd ap Rhys of Deheubarth, son of his old ally Rhys ap Tewdwr, is also notable for her resistance to English rule. [edit]Children

Cadwallon ap Gruffydd (killed 1132) Owain Gwynedd (Owain ap Gruffydd), married (1) Gwladus (Gladys) ferch Llywarch, daughter of Llywarch ap Trahaearn (2) Cristin ferch Goronwy, daughter of Goronwy ab Owain Cadwaladr ap Gruffydd, married Alice de Clare, daughter of Richard Fitz Gilbert de Clare Susanna, married Madog ap Maredudd, prince of Powys Gwenllian ferch Gruffydd, married Gruffydd ap Rhys, prince of Deheubarth [edit]References

Gruffydd ap Cynan From Wikipedia, the free encyclopedia

Gruffydd ap Cynan (also spelled Gryffydd ap Cynan) (c. 1055 – 1137) was a King of Gwynedd. In the course of a long and eventful life, he became a key figure in Welsh resistance to Norman rule, and was remembered as King of all Wales. As a descendant of Rhodri Mawr, Gruffydd ap Cynan was a senior member of the princely house of Aberffraw.

Through his mother Gruffydd had close family connections with the Danish settlement around Dublin and he frequently used Ireland as a refuge and as a source of troops. He three times gained the throne of Gwynedd and then lost it again before regaining it once more in 1099 and this time keeping power until his death. Gruffydd laid the foundations which were built upon by his son Owain Gwynedd and his great-grandson Llywelyn the Great.

The history of Gruffydd ap Cynan

Unusually for a Welsh king or prince, a near-contemporary biography of Gruffydd, "The history of Gruffydd ap Cynan", has survived. Much of our knowledge of Gruffydd comes from this source, though allowance has to be made for the fact that it appears to have been written as dynastic propaganda for one of Gruffydd's descendants. The traditional view among scholars was that it was written during the third quarter of the 12th century during the reign of Gruffydd's son, Owain Gwynedd, but it has recently been suggested that it may date to the early reign of Llywelyn the Great, around 1200. The name of the author is not known.

Most of the existing manuscripts of the history are in Welsh but these are clearly translations of a Latin original. It is usually considered that the original Latin version has been lost, and that existing Latin versions are re-translations from the Welsh. However Russell (2006) has suggested that the Latin version in Peniarth MS 434E incorporates the original Latin version, later emended to bring it into line with the Welsh text.

According to the Life of Gruffydd ap Cynan, Gruffydd was born in Dublin and reared near Swords, County Dublin in Ireland. He was the son of a Welsh Prince, Cynan ap Iago, who was a claimant to the Kingship of Gwynedd but was probably never king of Gwynedd, though his father, Gruffydd's grandfather, Iago ab Idwal ap Meurig had ruled Gwynedd from 1023 to 1039. When Gruffydd first appeared on the scene in Wales the Welsh annals several times refer to him as "grandson of Iago" rather than the more usual "son of Cynan", indicating that his father was little known in Wales. Cynan ap Iago seems to have died while Gruffydd was still young, since the History describes his mother telling him who his father was.

Gruffydd's mother, Ragnaillt, was the daughter of Olaf of Dublin, son of King Sigtrygg Silkbeard and a member of the Hiberno-Norse dynasty. Through his mother, who appears in the list of the fair women of Ireland in the Book of Leinster, Gruffydd claimed relationships with many of the leading septs in Ireland, including those of the Ua Briain.

During his many struggles to gain the kingship of Gwynedd, Gruffydd received considerable aid from Ireland, both from the Hiberno-Norse at Dublin, but also those at Wexford, and also from Muircheartach Ua Briain.

Gruffydd made his first attempt to take over the rule of Gwynedd in 1075, following the death of Bleddyn ap Cynfyn. Trahaearn ap Caradog had seized control of Gwynedd but had not yet firmly established himself. Gruffydd landed on Anglesey with an Irish force, and with the assistance of troops provided by the Norman Robert of Rhuddlan first defeated and killed Cynwrig ap Rhiwallon, an ally of Trahaearn who held Llŷn, then defeated Trahaearn himself in the battle of Gwaed Erw in Meirionnydd and gained control of Gwynedd.

Gruffydd then led his forces eastwards to reclaim territories taken over by the Normans, and despite the assistance previously given by Robert of Rhuddlan attacked and destroyed Rhuddlan castle. However tension between Gruffydd's Danish-Irish bodyguard and the local Welsh led to a rebellion in Llŷn and Trahaearn took the opportunity to counter attack, defeating Gruffydd at the battle of Bron yr Erw above Clynnog Fawr the same year.

Second bid for the throne and capture by the Normans

Gruffydd fled to Ireland but in 1081 returned and made an alliance with Rhys ap Tewdwr prince of Deheubarth. Rhys had been attacked by Caradog ap Gruffydd of Gwent and Morgannwg, and had been forced to flee to the St David's Cathedral. Gruffydd this time embarked from Waterford with a force composed of Danes and Irish and landed near St David's, presumably by prior arrangement with Rhys. He was joined here by a force of his supporters from Gwynedd, and he and Rhys marched north to seek Trahaearn ap Caradog and Caradog ap Gruffydd who had themselves made an alliance and been joined by Meilyr ap Rhiwallon of Powys. The armies of the two confederacies met at the Battle of Mynydd Carn, with Gruffydd and Rhys victorious and Trahaearn, Caradog and Meilyr all being killed. Gruffydd was thus able to seize power in Gwynedd for the second time.

He was soon faced with a new enemy, as the Normans were now encroaching on Gwynedd. Gruffydd had not been king very long when he was enticed to a meeting with Hugh Earl of Chester and Hugh Earl of Shrewsbury at Rug, near Corwen. At the meeting Gruffydd was seized and taken prisoner. According to his biographer this was by the treachery of one of his own men, Meirion Goch. Gruffydd was imprisoned in Earl Hugh's castle at Chester for many years while Earl Hugh and Robert of Rhuddlan went on to take possession of Gwynedd, building castles at Bangor, Caernarfon and Aberlleiniog.

Escape from captivity and third reign

Gruffydd reappeared on the scene years later, having escaped from captivity. According to his biography he was in fetters in the market-place at Chester when Cynwrig the Tall on a visit to the city saw his opportunity when the burgesses were at dinner. He picked Gruffydd up, fetters and all, and carried him out of the city on his shoulders. There is debate among historians as to the year of Gruffydd's escape. Ordericus Vitalis mentions a "Grifridus" attacking the Normans in 1088. The History in one place states that Gruffydd was imprisoned for twelve years, in another that he was imprisoned for sixteen years. Since he was captured in 1081, that would date his release to 1093 or 1097. J.E. Lloyd favours 1093, considering that Gruffydd was involved at the beginning of the Welsh uprising in 1094. K.L. Maund on the other hand favours 1097, pointing out that there is no reference to Gruffydd in the contemporary annals until 1098. D. Simon Evans inclines to the view that Ordericus Vitalis' date of 1088 could be correct, suggesting that an argument based on the silence of the annals is unsafe.

Gruffydd again took refuge in Ireland but returned to Gwynedd to lead the assaults on Norman castles such as Aber Lleiniog. The Welsh revolt had begun in 1094 and by late 1095 had spread to many parts of Wales. This induced William II of England (William Rufus) to intervene, invading northern Wales in 1095. However his army was unable to the Welsh to battle and returned to Chester without having achieved very much. King Willam mounted a second invasion in 1097, but again without much success. The History only mentions one invasion by Rufus, which could indicate that Gruffydd did not feature in the resistance to the first invasion. At this time Cadwgan ap Bleddyn of Powys led the Welsh resistance.

In the summer of 1098 Earl Hugh of Chester joined with Earl Hugh of Shrewsbury in another attempt to recover his losses in Gwynedd. Gruffydd and his ally Cadwgan ap Bleddyn retreated to Anglesey, but then were forced to flee to Ireland in a skiff when a fleet he had hired from the Danish settlement in Ireland accepted a better offer from the Normans and changed sides.

King for the fourth time and consolidation

The situation was changed by the arrival of a Norwegian fleet under the command of King Magnus III of Norway, also known as Magnus Barefoot, who attacked the Norman forces near the eastern end of the Menai Straits. Earl Hugh of Shrewsbury was killed by an arrow said to have been shot by Magnus himself. The Normans were obliged to evacuate Anglesey, and the following year Gruffydd returned from Ireland to take possession again, having apparently come to an agreement with Earl Hugh of Chester.

With the death of Hugh of Chester in 1101 Gruffydd was able to consolidate his position in Gwynedd, as much by diplomacy as by force. He met King Henry I of England who granted him the rule of Llŷn, Eifionydd, Ardudwy and Arllechwedd, considerably extending his kingdom. By 1114 he had gained enough power to induce King Henry to invade Gwynedd in a three-pronged attack, one detachment led by King Alexander I of Scotland. Faced by overwhelming force, Gruffydd was obliged to pay homage to Henry and to pay a heavy fine, but lost no territory. By about 1118 Gruffydd's advancing years meant that most of the fighting which pushed Gwynedd's borders eastward and southwards was done by his three sons by his wife Angharad, daughter of Owain ab Edwin: Cadwallon, Owain Gwynedd and later Cadwaladr. The cantrefs of Rhos and Rhufoniog were annexed in 1118, Meirionnydd captured from Powys in 1123 and Dyffryn Clwyd in 1124. Another invasion by the king of England in 1121 was a military failure. The king had to come to terms with Gruffydd and made no further attempt to invade Gwynedd during Gruffydd's reign. The death of Cadwallon in a battle against the forces of Powys near Llangollen in 1132 checked further expansion for the time being.

Gruffydd was now powerful enough to ensure that his nominee, David the Scot was consecrated as Bishop of Bangor in 1120. The see had been effectively vacant since Bishop Hervey had been forced to flee by the Welsh almost twenty years before, since Gruffydd and King Henry could not agree on a candidate. David went on to rebuild Bangor Cathedral with a large financial contribution from Gruffydd.

Owain and Cadwaladr in alliance with Gruffydd ap Rhys of Deheubarth gained a crushing victory over the Normans at Crug Mawr near Cardigan in 1136 and took possession of Ceredigion. The latter part of Guffydd's reign was considered to be a "Golden Age" according to the Life of Gruffydd ap Cynan Gwynedd was "bespangled with lime-washed churches like the stars in the firmament".

Gruffydd was buried in Bangor Cathedral

Gruffydd died in his bed, old and blind, in 1137 and was mourned by the annalist of Brut y Tywysogion as the head and king and defender and pacifier of all Wales. He was buried by the high altar in Bangor Cathedral which he had been involved in rebuilding. He also made bequests to many other churches, including one to Christ Church Cathedral, Dublin where he had worshipped as a boy. He was succeeded as king of Gwynedd by his son Owain Gwynedd. His daughter, Gwenllian, who married Gruffydd ap Rhys of Deheubarth, son of his old ally Rhys ap Tewdwr, is also notable for her resistance to English rule.

Children Cadwallon ap Gruffydd (killed 1132) Owain Gwynedd, married (1) Gwladus (Gladys) ferch Llywarch, daughter of Llywarch ap Trahaearn (2) Cristin ferch Goronwy, daughter of Goronwy ab Owain Cadwaladr ap Gruffydd, married Alice de Clare, daughter of Richard Fitz Gilbert de Clare Susanna, married Madog ap Maredudd, prince of Powys Gwenllian, married Gruffydd ap Rhys, prince of Deheubarth

References R.R. Davies (1991). The age of conquest: Wales 1063-1415. O.U.P. ISBN 0-19-820198-2. Simon Evans (1990). A Mediaeval Prince of Wales: the Life of Gruffudd Ap Cynan. Llanerch Enterprises. ISBN 0-947992-58-8. Arthur Jones (1910). The history of Gruffydd ap Cynan: the Welsh text with translation, introduction and notes. Manchester University Press. . Translation online at The Celtic Literature Collective K.L. Maund (ed) (1996). Gruffudd ap Cynan : a collaborative biography. Boydell Press. ISBN 0-85115-389-5. Kari Maund (ed) (2006). The Welsh kings:warriors, warlords and princes. Tempus. ISBN 0-7524-2973-6. Paul Russell (ed) (2006). Vita Griffini Filii Conani: The Medieval Latin Life of Gruffudd Ap Cynan. University of Wales Press. ISBN 0-7083-1893-2. Ancestral Roots of Certain American Colonists Who Came to America Before 1700 by Frederick Lewis Weis, Lines: 176B-26, 239-5 Historical Event: William took seven months to prepare his invasion force, using some 600 transport ships to carry around 7,000 men (including 2,000-3,000 cavalry) across the Channel. On 28 September 1066, with a favourable wind, William landed unopposed at Pevensey and, within a few days, raised fortifications at Hastings. Having defeated an earlier invasion by the King of Norway at the Battle of Stamford Bridge near York in late September, Harold undertook a forced march south, covering 250 miles in some nine days to meet the new threat, gathering inexperienced reinforcements to replenish his exhausted veterans as he marched.

At the Battle of Senlac (near Hastings) on 14 October, Harold's weary and under-strength army faced William's cavalry (part of the forces brought across the Channel) supported by archers. Despite their exhaustion, Harold's troops were equal in number (they included the best infantry in Europe equipped with their terrible two-handled battle axes) and they had the battlefield advantage of being based on a ridge above the Norman positions.

The first uphill assaults by the Normans failed and a rumour spread that William had been killed William rode among the ranks raising his helmet to show he was still alive. The battle was close-fought: a chronicler described the Norman counter-attacks and the Saxon defence as 'one side attacking with all mobility, the other withstanding as though rooted to the soil'. Three of William's horses were killed under him.

William skilfully co-ordinated his archers and cavalry, both of which the English forces lacked. During a Norman assault, Harold was killed - hit by an arrow and then mowed down by the sword of a mounted knight. Two of his brothers were also killed. The demoralised English forces fled.

The Histort of Gruffudd ap Cynan (ed. Arthur Jones), 1910 Hist. W., gw. mynegai Trans. Cymm., 1913-4, 244 B.B.C.S., v, 25. T.P. .

It was part of the traditional lore of the Welsh bards that Gruffudd ap Cynan had made certain regulations to govern their craft, and his name was used to give authority to the 'statute' drawn up in connection with the Caerwys eisteddfod of 1523. There is nothing to substantiate this tradition, but it is not unreasonable to suggest that Gruffudd may nave brought bards and musicians with him from Ireland and that these may have had some influence on the craft of poetry and music in Cymru. He may also have made some formal changes in the bardic organization. It is clear that a genuine and persistant tradition to this effect existed in the 16th cent. It is perhaps worth noting that the 'History' mentions the death in battle of Gellan, Gruffudd's harpist, in 1094.

Gruffudd ap Cynan is the only mediaeval Welsh prince whose biography, in the form of pure eulogy, has survived. Linguistic characteristics prove it to have been a translation of a Latin original now lost. It was probably written by a cleric towards the end of the 12th cent. [Dictionary of Welsh Biography pp310-311]

GRUFFUDD AP CYNAN the most successful king of Gwynedd during the twenty years which followed Gruffudd ap Llywelyn was Bleddyn ap Cynfyn, who was related to the royal family through his mother, Angharad, the widow of Llywelyn ap Seisyll and the mother of Gruffudd Bleddyn was a half-brother to 1067 Gruffudd. He and his brother Rhiwallon attacked Hereford in 1067, and in the following year succeeded in meeting the challenge of two of the sons of Gruffudd.

He suffered at the hands of Robert of Rhuddlan and the Normans in 1073, and met his end in a battle against Rhys ap Owain and the nobles of Ystrad Tywi in 1075. Bleddyn was one of the few kings who reformed the Law of Hywel, and according to the Brut kept in Llanbadarn Fawr, he proved during his twelve year reign, to be the 'most civilised and merciful of the kings, gentle towards his enemy, kind and genial, generous to the poor and defenceless, and having respect for the rights of the Church."

He was succeeded on the throne by Trahaearn ap Caradog, the king of Arwystli, who ruled for six years. With the death of Bleddyn, Gruffudd ap Cynan, of the ancient lineage of Gwynedd, returned from Ireland to claim the throne. Quite a lot is known about this man from the biography which was written shortly after his death. He was born in Dublin about 1054, the son of Cynan ap lago, who was an exile in Ireland, and Rhagnall, of the royal family of Dublin Scandinavians. He landed in Abermenai, received help from Robert of Rhuddlan, attacked Cynwrig of Llyn and defeated him. Moving down to Meirionnydd, he met Talhaearn on the field of Gwaeterw in the Glyngin valley, and defeated him also. He did not feel under any obligation to Robert of Rhuddlan who was endangering the independence of Gwynedd he attacked him successfully in 1075 but failed to take him prisoner. Unfortunately the Irish members of ap Cynan's retinue were making him unpopular in Llyn a number of them were killed by the natives. Trahaearn saw his opportunity, and with help from Powys he overcame ap Cynan, who again fled to Ireland, thereby losing and winning a kingdom in the same year.

He returned in 1081 when he fought beside Rhys ap Tewdwr on Mynydd Cam, where Trahaearn was killed. 1081 Shortly after reoccupying his heritage, there came another quick turn in his career: through treachery he was taken prisoner by the Normans near Corwen, and kept in prison in Chester for some years. In 1088 he attacked Robert of Rhuddlan near Llandudno, and killed him. About the same time, with a troop of Scandinavians from the Orkneys, he sailed up the Severn, pitched camp on Barri Island and attacked Gwynllwg (Wentloog). A little later he again enlisted the help of the Danes to defeat the Normans in Anglesey.

Before coming to the next milestone in his career attention must be drawn to the great and sudden success of the Normans in other parts of Cymru. When Rhys ap Tewdwr was killed in 1093 the bulwark which stood in the way of their advance was holed. No sooner was he dead than they occupied Brycheiniog and Buallt. Fitzhamon razed the plain of Morgannwg between Taf and Tawe, and rebuilt the Roman castle in Cardiff which is today the college of music and drama.

Roger, the Earl of Shrewsbury, occupied Ceredigion. He built a castle in Aberteifi (Cardigan) before building in Pembroke the only western castle which proved capable of withstanding every Welsh attack. Dyfed was overcome, the fourth of the old Welsh kingdoms to disappear finally into the Norman maw. The royal family of Dyfed had been founded by Eochaid Allmuir, an Irishman of the third century, when the Romans were strong in the land of the blue stones of Cor y Cewri. The old kingdom had vanished in the age of the Mabinogion and with it a host of memories. In the middle of the twentieth century they are recalled by Waldo Williams, the greatest poet to be reared in Dyfed in the course of her long history:

Un funud fach cyn elo'r haul o'r wybren, Un funud fwyn cyn delo'r hwyr i'w hynt, I gofio am y pethau anghofiedig Ar goll yn awr yn Dwell yr amser gynt.

Pel ewyn ton a dyr ar draethell unig, Pel can y gwynt lie nid oes glust a glyw, Mi wn eu bod yn galw'n ofer arnom- Hen bethau anghofiedig dynol ryw.

Camp a chelfyddyd y cenhedloedd cynnar, Anheddau bychain a neuaddau mawr, Y chwedlau cain a chwalwyd ers canrifoedd Y duwiau na wyr neb amdanynt 'nawr.

A geiriau bach hen ieithoedd diflanedig, Hoyw yng ngenau dynicn oeddynt hwy, A thlws i'r clust ym mharabl plant bychain, Ond tafod neb ni eilw arnynt mwy.

O, genedlaethau dirifedi daear, A'u breuddwyd dwyfol a'u dwyfoldeb brau, A erys ond tawelwch i'r calonnau


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The family's stronghold was the Kingdom of Gwent, and Caradog appears to have been able to add Morgannwg during his early career. He first appears in the historical record in 1065. Harold Godwinson, after defeating Gruffydd ap Llywelyn in 1063 had begun to build a hunting lodge in Portskewet. Caradog attacked and destroyed it, going on to ravage the district with his forces.

Caradog now set out to emulate his father and grandfather by adding Deheubarth to his realm. In 1072 he defeated and killed the ruler of Deheubarth, Maredudd ab Owain, in a battle by the Rhymney River. In 1078 he won another victory over Rhys ab Owain who had succeeded Maredudd as prince of Deheubarth, killing him too. By 1081 he had forced the new prince of Deheubarth, Rhys ap Tewdwr to flee to the St David's Cathedral.


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Background and sources

Nearly all evidence for Solomon’s life and reign comes from the Bible (especially the first 11 chapters of the First Book of Kings and the first nine chapters of the Second Book of Chronicles). According to those sources, his father was David (flourished c. 1000 bce ), the poet and king who, against great odds, founded the Judaean dynasty and united all the tribes of Israel under one monarch. Solomon’s mother was Bathsheba, formerly the wife of David’s Hittite general, Uriah. She proved to be adept at court intrigue, and through her efforts, in concert with the prophet Nathan, Solomon was anointed king while David was still alive, despite the fact that he was younger than his brothers.

Material evidence for Solomon’s reign, as for that of his father, is scant. Although some scholars claim to have discovered artifacts that corroborate the biblical account of his reign in the early 10th century bce , others claim that the archaeological record strongly suggests that the fortified cities and even the Temple of Jerusalem actually emerged more than a century later. In the latter view, the kingdom of Solomon was far from the vast empire that the biblical narrative describes.


Aylwin IV DD- 1081 - History

OBJECTIVE. Breast density is documented to reduce sensitivity and specificity of mammography. However, little is known regarding the effect of normal background parenchymal enhancement on accuracy of breast MRI. The purpose of this study was to evaluate the effect of background parenchymal enhancement on MRI diagnostic performance.

MATERIALS AND METHODS. A review of our established MRI data identified all women undergoing breast MRI from March 1, 2006, through June 30, 2007. Prospectively reported background parenchymal enhancement categories of minimal, mild, moderate, or marked (anticipated BI-RADS MRI lexicon definitions) and assessments were extracted from the database for each patient. Outcomes were determined by pathologic analysis, imaging, and linkage with the regional tumor registry with a minimum of 24 months of follow-up. Patients were dichotomized into categories of minimal or mild versus moderate or marked background parenchymal enhancement. Associations with patient age, abnormal interpretation rate, positive biopsy rate, cancer yield, sensitivity, and specificity were compared using chi-square and z score tests.

RESULTS. The study cohort included 736 women. Moderate or marked background parenchymal enhancement was significantly more frequent among patients younger than 50 years compared with those 50 years old and older (39.7% vs 18.9% p < 0.0001). Moderate or marked background parenchymal enhancement was also associated with a higher abnormal interpretation rate compared with minimal or mild background parenchymal enhancement (30.5% vs 23.3% p = 0.046). Positive biopsy rate, cancer yield, sensitivity, and specificity were not significantly different according to background parenchymal enhancement category.

CONCLUSION. Increased background parenchymal enhancement on breast MRI is associated with younger patient age and higher abnormal interpretation rate. However, it is not related to significant differences in positive biopsy rate, cancer yield, sensitivity, or specificity of MRI.

MRI is a very valuable tool for the detection and characterization of breast carcinoma. The identification of breast cancer using MRI is largely dependent on the enhancement of malignant lesions after IV administration of contrast agent, resulting in visible areas with both morphologic and kinetic features. However, enhancement on MRI is not limited to malignancies or discrete benign lesions of the breast. It has been recognized that normal breast parenchyma enhances after IV administration of contrast agent, a phenomenon now termed “background parenchymal enhancement.” Such physiologic background parenchymal enhancement has been described in premenopausal women, in whom it can fluctuate with the menstrual cycle [1, 2], and has been found to increase in postmenopausal women undergoing hormone replacement therapy [3, 4]. Some researchers have hypothesized that background parenchymal enhancement may decrease the sensitivity of breast MRI by obscuring enhancing malignancies or may diminish the specificity of this tool by causing enhancement patterns that overlap with the appearance of cancers. Recognizing background parenchymal enhancement and distinguishing it from suspicious findings are potentially important in reducing false-positive assessments of breast MRI examinations while maintaining high sensitivity. As such, the American College of Radiology (ACR) BI-RADS MRI Committee plans to incorporate the assessment of background parenchymal enhancement into the next version of the published lexicon (Morris E, written communication, 2010).

To date, studies of background parenchymal enhancement have largely been limited to describing its occurrence and imaging patterns. There have been few investigations of the impact on MRI diagnostic performance for this potentially important imaging entity. Thus, the purpose of this study was to determine whether background parenchymal enhancement affects key measures of breast MRI performance. In particular, we sought to evaluate whether the extent of background parenchymal enhancement, when characterized using anticipated BI-RADS categories, effects breast MRI diagnostic outcomes.

This study was approved by our institutional review board and was HIPAA compliant. A review of our prospectively populated MRI data was performed to identify all women 18 years old or older undergoing breast MRI examinations at our institution between March 1, 2006, and June 30, 2007. None of the patients in this group were excluded from the study. For women with multiple examinations in the study interval, only the most recent MRI examination was included in the analysis set. Thus, each patient contributed a single MRI examination to the study.

For the study cohort, breast MRI examination and patient outcomes data were obtained from the Consortium Oncology Data Integration project (IR no. 5586, protocol 1833E). Consortium Oncology Data Integration is a solid tumor clinical research database developed and maintained by the Fred Hutchinson Cancer Research Center in collaboration with the University of Washington. Data in Consortium Oncology Data Integration have been obtained in accordance with applicable human subjects laws and regulations, including any requiring informed consent. There are many sources of data for Consortium Oncology Data Integration, including our prospectively recorded breast MRI data forms, our institutional pathology database, and the Cancer Surveillance System regional tumor registry. The Cancer Surveillance System is a part of the National Cancer Institute’s Surveillance, Epidemiology, and End Results program and collects population-based data on the incidence, treatment, and follow-up on all newly diagnosed cancers (except nonmelanoma skin cancers) occurring in residents of the Puget Sound region. This registry has achieved case ascertainment of 95% or higher completeness according to the North American Association of Central Cancer Registries [5].

A, 63-year-old woman with family history of breast cancer. Contrast-enhanced axial bilateral breast maximum-intensity-projection (MIP) MRI performed as high-risk screening shows minimal background parenchymal enhancement.

B, 42-year-old woman with history of multiple biopsies. Contrast-enhanced axial bilateral breast MIP MRI performed as high-risk screening shows atypical ductal hyperplasia and mild background parenchymal enhancement.

C, 27-year-old woman with strong family history of breast and ovarian cancer. Contrast-enhanced axial bilateral breast MIP MRI performed for high-risk screening shows moderate background parenchymal enhancement.

D, 26-year-old woman with history of chest radiation for cancer. Contrast-enhanced axial bilateral breast MIP MRI performed for high-risk screening shows marked background parenchymal enhancement.

At the time of clinical interpretation, all breast MRI examinations were assessed by one of four fellowship-trained breast imagers who had from 1 to 10 years of breast MRI experience. For each MRI examination, background parenchymal enhancement was prospectively assigned one of four categories in accordance with the anticipated BI-RADS MRI lexicon classification system: minimal (≤ 25% enhancement of glandular tissue) ( Fig. 1A ), mild (25–50% enhancement of glandular tissue) ( Fig. 1B ), moderate (50–75% enhancement of glandular tissue) ( Fig. 1C ), or marked (> 75% enhancement of glandular tissue) ( Fig. 1D ). A combination of the unenhanced, initial contrast-enhanced, subtraction, and maximum-intensity-projection images was typically used to determine background parenchymal enhancement. BI-RADS MRI lesion features, assessments, and recommendations in accordance with the current BI-RADS MRI lexicon [6] were also prospectively recorded at the time of clinical interpretation, and all MRI variables were subsequently entered into our Consortium Oncology Data Integration database. These imaging variables, as well as patient age and clinical indication for undergoing breast MRI, were extracted from the electronic database for this study.

Fig. 2 38-year-old woman with strong family history of breast cancer. Image is example of false-positive finding with moderate background parenchymal enhancement. Bilateral maximum-intensity-projection breast MRI shows enhancing 5-mm oval mass (arrow) in left breast at 9 o’clock position. Pathology results indicated benign fibroadenoma.

Fig. 3 52-year-old woman with family history of ovarian cancer and recent biopsy revealing lobular carcinoma in situ, atypical ductal hyperplasia, and radial scar in left breast. Image is example of false-positive finding with marked background parenchymal enhancement. Bilateral breast maximum-intensity-projection MRI shows 9-mm lobular mass (arrow) in right breast at 12 o’clock position. Pathology results indicated fibroadenoma. Note two oval masses (circle) in right posterolateral breast and axilla, which were shown on ultrasound to be lymph nodes.

Fig. 4 62-year-old woman with newly diagnosed invasive ductal carcinoma (dashed arrow) in right breast. Image is example of true-positive and false-positive findings with marked background parenchymal enhancement. Bilateral breast maximum-intensity-projection MRI shows lobular masses in left breast at 11 o’clock (solid arrow) and 5 o’clock (circle) positions. Biopsy of left 11 o’clock position mass yielded intraductal carcinoma, whereas biopsy of left 5 o’clock position mass showed fibroadenoma.

A, Example of false-negative finding with mild background parenchymal enhancement. Bilateral breast maximum-intensity-projection MRI shows known newly diagnosed right breast cancer (arrow) at 1 o’clock position. Left breast was determined to be negative and assessed as BI-RADS category 1.

B, Two days later, mammogram was performed, for which patient was overdue. Mammograms in craniocaudal (B) and mediolateral oblique (C) spot views revealed spiculated mass in right breast (data not shown), corresponding to known biopsy-proven cancer, and grouped amorphous calcifications (oval) in left breast at 1 o’clock position. These calcifications were biopsied, and pathologic results indicated ductal carcinoma in situ.

C, Two days later, mammogram was performed, for which patient was overdue. Mammograms in craniocaudal (B) and mediolateral oblique (C) spot views revealed spiculated mass in right breast (data not shown), corresponding to known biopsy-proven cancer, and grouped amorphous calcifications (oval) in left breast at 1 o’clock position. These calcifications were biopsied, and pathologic results indicated ductal carcinoma in situ.

Benign versus malignant outcomes were determined by biopsy, imaging surveillance, and data from Consortium Oncology Data Integration with a minimum of 24 months of follow-up. Final histopathologic outcomes for high-risk lesions at core needle biopsy (i.e., atypical ductal or lobular hyperplasia, lobular carcinoma in situ, radial scar, or phyllodes tumor) were based on subsequent benign (no upgrade to malignancy) or malignant (upgrade to malignancy) surgical biopsy results. Any invasive carcinoma or ductal carcinoma in situ histology was categorized as malignant. Follow-up or pathologic findings were confirmed in all study patients using clinical and tumor registry databases.

A, Example of false-negative finding in patient with marked background parenchymal enhancement. Maximum-intensity-projection (MIP) image is shown. Bilateral breast MRI was performed for screening. No suspicious enhancing abnormalities were detected. Right breast was given BI-RADS category 2 assessment for benign changes of prior lumpectomy, and left breast was given BI-RADS category 1 (negative).

B, Eight months after screening MRI, scheduled mammogram (craniocaudal spot magnification view shown) revealed fine linear and pleomorphic calcifications (oval) in right breast. Biopsy of these calcifications indicated invasive ductal carcinoma.

C, Follow-up breast MRI was performed 7 days after mammogram to evaluate for extent of disease (approximately 8 months after original screening MRI). MIP (C) and axial (D) subtraction images show significant change compared with screening MRI obtained previously, with new heterogeneous nonmasslike enhancement involving majority of right breast, as above, corresponding to biopsy-proven malignancy.

D, Follow-up breast MRI was performed 7 days after mammogram to evaluate for extent of disease (approximately 8 months after original screening MRI). MIP (C) and axial (D) subtraction images show significant change compared with screening MRI obtained previously, with new heterogeneous nonmasslike enhancement involving majority of right breast, as above, corresponding to biopsy-proven malignancy.

All statistical outcome definitions were derived from the fourth edition of the ACR BI-RADS Atlas Follow-Up and Outcome Monitoring section [6]. Abnormal interpretation rate was defined as the percentage of all study examinations receiving initial BI-RADS category 0, 3, 4, or 5 assessments. BI-RADS categories 0 and 3 were included as abnormal interpretations because, from the index examination, each resulted in a recommendation for additional immediate (BI-RADS category 0) or short-term follow-up (BI-RADS category 3) imaging. This reflects the fact that breast MRI serves as an amalgam of study types, acting as both a screening and a diagnostic study. A negative (nonactionable) MRI examination was defined as one with a final BI-RADS category 1, 2, 3, or 6 assessment. A positive (actionable) MRI examination was defined as one with a final BI-RADS category 4 or 5 assessment. True-positive results were defined as positive MRI examinations with tissue diagnoses of malignancy during the follow-up interval. False-positive results were defined as positive MRI examinations with no tissue diagnoses of malignancy during the follow-up interval (Figs. 2 , 3 , and 4 ). True-negative results were defined as negative MRI examinations with no tissue diagnoses of malignancy during the follow-up interval. False-negative results were defined as negative MRI examinations with tissue diagnoses of malignancy during the follow-up interval (Figs. 5A , 5B , 5C , 6A , 6B , 6C , and 6D ). Positive biopsy rate was defined as the percentage of biopsies performed that resulted in a tissue diagnosis of cancer. Cancer yield was defined as the percentage of biopsy-proven cancers resulting from a positive MRI examination. Because each patient contributed one examination to the study, results at patient and examination levels are equivalent.

Our study was not an evaluation of the diagnostic performance of breast MRI for detecting known biopsy-proven BI-RADS category 6 lesions. We assessed the diagnostic performance of this tool for identifying and excluding malignancy not known or suspected before breast MRI. An examination was assigned the highest-order actionable BI-RADS category according to a hierarchy (i.e., BI-RADS category 5 > 4 > 0 > 3 > 6 > 2 > 1). Thus, an examination with BI-RADS category 6 as the highest-order assessment had no suspicious finding in addition to the known malignancy.

Fig. 7 Flowchart of study patients by background parenchymal enhancement category with initial and final BI-RADS assessments and malignant outcomes, according to Standards of Reporting of Diagnostic Accuracy recommendations. In group with minimal or mild background parenchymal enhancement, initial assessment was BI-RADS category 0 in 12 patients. After additional imaging, final assessment was BI-RADS category 2 in one patient, category 3 in three patients, and category 4 in eight patients. In group with moderate or marked background parenchymal enhancement, initial assessment was BI-RADS category 0 in 12 patients. After additional imaging, final assessment was BI-RADS category 3 in four patients and category 4 in eight patients. Two malignancies occurring in patients with BI-RADS category 6 assessments were not biopsy-proven BI-RADS category 6 lesions known before breast MRI but were separate additional malignancies.

Patients were dichotomized into categories of minimal or mild versus moderate or marked background parenchymal enhancement for data analyses. For patients in the minimal or mild versus moderate or marked groups, associations with age younger than 50 years versus 50 years old or older were determined and compared using chi-square analyses. Menopausal status was not available for the study cohort at the time of our analyses. Thus, age 50 years old or older served as a surrogate for postmenopausal status. Abnormal interpretation rate, positive predictive value, and cancer yield were calculated and compared across groups using a chi-square test. Sensitivity and specificity were determined and compared across groups using the z score statistic.

With the exception of MRI examinations for newly diagnosed breast cancers, we attempt to perform breast MRI in premenopausal women on days 7–14 of their menstrual cycle, although we do not currently have data regarding the frequency with which this timing is achieved. All breast MRI examinations, including those for implant evaluation, were performed with contrast agent at our institution. MRI examinations were performed with the patient prone in a 1.5-T commercially available system (LX 1.5T scanner, GE Healthcare) using a dedicated breast coil (GE HD 8-channel Breast Array coil, GE Healthcare). During the study period, two scanning protocols were used as clinical practice and technology evolved. All protocols were consistent with the guidelines established by the International Breast MRI Consortium and by the ACR Imaging Network MRI trials. Imaging sequences included unenhanced and at least two contrast-enhanced T1-weighted fat-suppressed 3D fast spoiled gradient recalled series. From March 2006 through June 2006, scans were performed in the axial plane with the following parameters: TR/TE, 6.2/3 flip angle, 10° FOV, 32–38 cm slice thickness, 2.2 mm and matrix size 350 × 350. From July 2006, scans were performed in the axial plane with the following parameters: TR/TE, 5.5/2.7 flip angle, 10° FOV, 32–38 cm slice thickness, 1.6 mm and matrix size, 420 × 420. For all protocols, initial contrast-enhanced acquisitions were centered at 1.5 minutes after contrast agent administration. Delayed acquisitions were centered between 4.5 and 7.5 minutes after contrast agent administration, depending on the protocol. Gadodiamide (Omniscan, Mallinckrodt) contrast agent was used (0.1 mmol/kg dose power-injected at 2 mL/s) followed by a 10-mL saline flush.

All MRI examinations were processed using a commercially available computer-aided evaluation system (CADstream, Confirma) and were reviewed on high-resolution PACS monitors.

A total of 736 women 18 years old or older (mean age, 52 years range, 18–86 years) underwent breast MRI from March 1, 2006, to June 30, 2007, and they comprise the study population. None of the 736 patients was excluded. Clinical indications for breast MRI were high-risk screening (368/736 [50.0%]), evaluation of the extent of disease in patients with a recent diagnosis of breast cancer (279/736 [37.9%]), problem solving (32/736 [4.3%]), short-term follow-up (26/736 [3.5%]), evaluation of response to neoadjuvant treatment (23/736 [3.2%]), evaluation of silicone breast implants (5/736 [0.7%]) and other (3/736 [0.4%]).

Figure 7 is a flowchart of the study patients categorized into minimal or mild versus moderate or marked enhancement groups, with initial and final BI-RADS assessments and malignant outcomes, according to the Standards of Reporting of Diagnostic Accuracy recommendations. Outcomes were malignant for 68 (9%) and benign for 668 (91%) of the 736 patients. The 68 malignancies were 27 invasive ductal carcinomas, six invasive lobular carcinomas, three cases of mixed invasive ductal carcinoma and invasive lobular carcinoma, 29 cases of ductal carcinoma in situ, and three miscellaneous other breast cancers. Four of the malignancies were false-negative MRI cases and are described later in this article.

The overall frequencies of background parenchymal enhancement categories were 64.3% for minimal (n = 473), 8.6% for mild (n = 63), 20.0% for moderate (n = 147), and 7.2% for marked (n = 53) enhancement. The extent of background parenchymal enhancement varied significantly by age (Table 1). Moderate or marked background parenchymal enhancement was significantly more frequent among women younger than 50 years (116/292 [39.7%]) than among women 50 years old or older (84/444 [18.9%]) (p < 0.0001).

The abnormal interpretation rate for women in the moderate or marked background parenchymal enhancement category (30.5% [61/200]) was significantly higher than that for women in the minimal or mild category (23.3% [125/536]) (Table 2 p = 0.046). Positive biopsy rates were not affected by background parenchymal enhancement, with a proportion of cancer at biopsy of 44.4% (20/45) in the moderate or marked background parenchymal enhancement category compared with 47.3% (44/93) in the minimal or mild background parenchymal enhancement category (p = 0.75). There was also no significant difference in cancer yield according to background parenchymal enhancement, with a 10.0% (20/200) yield among women in the moderate or marked category compared with 8.2% (44/536) in the minimal or mild group (p = 0.44).

TABLE 1: Background Parenchymal Enhancement and Association With Age

TABLE 2: Breast MRI Performance Measures as a Function of Background Parenchymal Enhancement

Sensitivity was not significantly different across background parenchymal enhancement categories, with results of 90.9% (20/22) in the moderate or marked group and 95.7% (44/46) in the minimal or mild background parenchymal enhancement group (p = 0.82). Four breast cancers occurred during the 2-year follow-up after negative breast MRI examinations and were false-negative cases. In three cases (two in the minimal or mild enhancement group and one in the moderate or marked enhancement group), biopsy of suspicious calcifications seen at mammography revealed ductal carcinoma in situ in two patients (Figs. 5A , 5B , and 5C ) and invasive ductal carcinoma in one (Figs. 6A , 6B , 6C , and 6D ) patient. In the last case (moderate or marked enhancement group), skin punch biopsy based on physical examination findings revealed Paget disease of the nipple. Specificity was slightly lower in women with moderate or marked background parenchymal enhancement (82.6% [147/178]) than in women with minimal or mild background parenchymal enhancement (88.4% [433/490]), but the difference was not statistically significant (p = 0.07).

Akin to mammographic breast density, background parenchymal enhancement on MRI is a tissue characteristic that varies widely among patients. Importantly, although fibroglandular tissue volume on breast MRI has been linked to mammographic density and is not dependent on contrast agent administration [7], background parenchymal enhancement is an imaging characteristic of normal breast parenchyma defined by the amount of fibroglandular breast tissue that enhances. Normal background parenchymal enhancement has been described to have the appearance of diffuse or nodular enhancement patterns, which can vary depending on the phase of menstrual cycle [1], has been shown to be increased in women undergoing hormone replacement therapy [3, 4], and also has been found to be increased in the lactating breast [8]. The amount of background parenchymal enhancement that occurs is thought to be associated with endogenous hormone levels. The underlying tissue cause of background parenchymal enhancement has yet to be fully characterized but may be related to the increased vascular permeability associated with estrogen and the elevated metabolic activity associated with progesterone [9].

Multiple studies have revealed the negative effect of increased mammographic breast density on the sensitivity and specificity of breast cancer detection [10–19]. Thus, although breast density and background parenchymal enhancement are not clearly linked, many have wondered whether the tissue characteristic of background parenchymal enhancement might have a similar important effect on the diagnostic accuracy of breast MRI. In particular, it has been hypothesized that background parenchymal enhancement could cause false-negatives by obscuring malignancies, or could result in false-positive results by mimicking the appearance of breast cancer. As such, recognizing background parenchymal enhancement and categorizing it as minimal, mild, moderate, or marked in extent is anticipated to be a component of the updated BI-RADS breast MRI lexicon. However, there are currently sparse data regarding background parenchymal enhancement and its impact on breast MRI performance. Two studies have very recently investigated the impact of background parenchymal enhancement on diagnostic performance [20, 21]. Hambly et al. [20] evaluated the effect of background parenchymal enhancement on short-term follow-up and cancer detection rates in 250 baseline high-risk screening MRI examinations. Uematsu and colleagues [21] assessed the impact of background parenchymal enhancement on accuracy for determining extent of malignancy in 146 MRI examinations performed for newly diagnosed breast cancer. These important preliminary studies are augmented by our investigation. Our study of 736 MRI examinations is the largest to date, to our knowledge, and includes a spectrum of indications for breast MRI such that our results should be more generalizable to broad clinical practice. Furthermore, we have performed linkage to a regional tumor registry to accurately determine true- and false-positive and -negative results with a minimum of 24 months of follow-up.

We found that background parenchymal enhancement was influenced by age, with women younger than 50 years having more extensive background parenchymal enhancement compared with older women. A similar inverse correlation of age with breast density has been well established in mammography [22]. Although we were not able to evaluate the relationship between background parenchymal enhancement and mammographic breast density in our study, it is important to note that background parenchymal enhancement and amount of fibroglandular tissue are not necessarily associated. Indeed, two recent studies by Ko et al. [19] and Cubuk et al. [23] specifically found no correlation between background parenchymal enhancement and mammographic density.

We found that increased background parenchymal enhancement was associated with a significantly higher abnormal interpretation rate for MRI, with women in the moderate or marked category more likely to be given initial assessments leading to additional imaging or biopsy (BI-RADS category 0, 3, 4, or 5). This is in keeping with the results of Hambly et al. [20] regarding the significantly greater frequency of abnormal interpretations in their study, measured in particular by BI-RADS category 3 assessments, in women with greater than minimal background parenchymal enhancement. In our study, although a higher number of women in the moderate or marked background parenchymal enhancement group were initially assessed as having abnormal findings, our measures of final outcome of positive biopsy rate, cancer yield, sensitivity, and specificity were not significantly different between the background parenchymal enhancement groups. This is also similar to the results of Hambly and colleagues [20], who found no difference in the positive biopsy rate or cancer yield based on background parenchymal enhancement in their study. Their study included only patients who underwent biopsy, and sensitivity and specificity were not assessed.

Our study has limitations. It is a single-institution investigation in the academic setting, with fellowship-trained breast imagers experienced in breast MRI interpretation. Our results may not be generalizable to less-established practices. In addition, there may be a selection bias in including only the most recent MRI examinations in the study interval for patients with more than one MRI examination. Background parenchymal enhancement may change over time, such as by decreasing in women with breast cancer treated with neoadjuvant or adjuvant systemic therapy. Furthermore, we were not able to evaluate the relationships between background parenchymal enhancement and other variables such as mammographic breast density, menopausal status, or timing relative to the menstrual cycle in premenopausal women. Other than MRI performed for newly diagnosed breast cancers, we attempt to perform MRI examinations in premenopausal women on days 7–14 of their menstrual cycle, but we do not currently have data regarding the frequency with which this timing is achieved. These are important topics that warrant further investigation.

In summary, our study shows that moderate or marked background parenchymal enhancement resulted in more assessments, leading to additional imaging or biopsy, but that these initial findings did not impact final diagnostic performance outcomes when compared with women with minimal or mild background parenchymal enhancement. These results are encouraging and suggest that breast MRI maintains its utility as a diagnostic tool even in the presence of more extensive background parenchymal enhancement. In studies to date, background parenchymal enhancement does not appear to have the impact on MRI diagnostic accuracy that breast density has on mammographic performance. Further studies of this key breast MRI tissue characteristic across institutions and clinical indications are warranted.


Isolated Diffuse Ground-Glass Opacity in Thoracic CT: Causes and Clinical Presentations

Ground-glass opacity (GGO) is defined as increased attenuation of the lung parenchyma without obscuration of the pulmonary vascular markings on CT images. This was originally described with reference to thin-section (high-resolution) CT with collimations of approximately 1 mm. However, GGO also may be evident on thicker-section images and will have a similar meaning. GGO may be the result of a wide variety of interstitial and alveolar diseases and frequently represents a nonspecific finding [1, 2]. GGOs often will be present in the company of other interstitial or alveolar findings on CT. As an alveolar finding, GGO represents partially filled alveoli and often is found at the margins of the consolidated lung. With interstitial diseases, it has been associated with active inflammation in some cases [3–8]. In other situations, GGO adjacent to interstitial abnormalities represents fine fibrosis, below the resolution of CT images. Therefore, if all causes of GGOs are grouped together, there is an impossibly broad differential generated, which includes a large number of interstitial diseases and a large array of alveolar diseases. However, the number of diseases that cause diffuse GGOs in isolation or as the predominant finding, is relatively small and easily can be prioritized with simple clinical information. By isolated, we mean patients who show only GGOs without other interstitial or alveolar findings. By diffuse, we mean patients with GGO that involves the majority of both lungs.

We have chosen to emphasize clinical information as the best means of narrowing the differential diagnosis of patients with isolated diffuse GGO (ID-GGO) because there is sub-stantial overlap in the appearance of ID-GGO among the various etiologies. Thus, in our experience, the various subtypes of GGO—for example, centrilobular nodules and mosaic attenuation—are not able to be discriminated among the causes of ID-GGO [9].

Four large categories of diseases may produce ID-GGO: diffuse pneumonias, primarily opportunistic infections some chronic interstitial diseases acute alveolar diseases and a group of unusual miscellaneous disorders [9]. Table 1 lists the most common causes of ID-GGO.

There are five clinical scenarios in which ID-GGO is most often encountered: patients who are immunocompromised, patients who are receiving bone marrow–suppressing medications, outpatients who have slowly progressive dyspnea, inpatients and outpatients who have acutely developing dyspnea, and inpatients who are acutely ill. We will review these clinical scenarios and the etiologies most commonly encountered with each scenario.

In scenario one, an immunocompromised patient presents with dyspnea and often fever. Patients included in this category are HIV-positive individuals, patients who have undergone organ transplantation, and patients who have received high-dose corticosteroids. In this scenario, the opportunistic infections that cause ID-GGO form the primary differential diagnosis.

Diffuse infections, particularly Pneumocystis carinii pneumonia (PCP), are among the most common causes of ID-GGOs. In a series of pathologically proven causes of ID-GGO, the most common causes were a variety of diffuse pneumonias, which accounted for 38% (12 of 32) of cases [9]. Most of these infections are opportunistic and should be among the first entities to consider when ID-GGO is the dominant finding on a CT scan of an immunocompromised host.

Pneumocystis carinii pneumonia.—PCP is a globally distributed saprophytic fungus [10]. Patients with AIDS and other causes of immunosuppression, such as organ transplant recipients, patients with lymphoproliferative disorders, and patients on high-dose corticosteroids are predisposed to this opportunistic infection [11, 12]. Despite dramatic declines in the incidence of PCP in HIV-infected patients as a result of highly active antiretroviral therapy (HAART) and PCP prophylaxis, PCP remains the most common opportunistic infection in this population [11, 13, 14]. PCP most commonly occurs in the 4th to 6th month following transplantation and may have up to a 47% mortality rate [15, 16]. A history of high-dose corticosteroid administration, cancer chemotherapy, or a hematologic malignancy also may predispose a patient to PCP infection [11, 14].

Patients characteristically will present with fever, nonproductive cough, and dyspnea [17]. Marked hypoxemia also is characteristic of PCP. In those patients who have received corticosteroids, a characteristic presentation of PCP is the occurrence of fever, dyspnea, and ID-GGO toward the end of the steroid taper. Survival with modern therapy has improved dramatically in patients with HIV and now approaches 90%. However, PCP continues to have an ominous prognosis in other patients, with a 30–60% mortality rate [11].

ID-GGOs, either uniformly distributed or in a mosaic pattern, are the most common manifestations of PCP on CT scans [18] ( Fig. 1 ). In HIV-positive patients, this appearance is so characteristic of PCP that some physicians argue that it is pathognomonic of PCP and no further testing is necessary. With more severe disease, GGO may progress to consolidation. The CT appearance of PCP rarely may take a variety of more unusual patterns including upper-lobe-predominant disease, focal areas of consolidation, nodules, and thin-walled cavities [18–22].

Cytomegalovirus pneumonia.—Cytomegalovirus (CMV) is a DNA virus of the herpes group and like other herpes viruses, it can remain dormant within a host cell for years and be reactivated when host immune defenses are depressed. CMV may be an important pathogen in immunocompromised patients such as HIV-positive patients and in patients who have undergone organ transplantation [12]. The majority of adults have been exposed to CMV and, as a result, CMV infection usually is a reactivation of dormant foci. In patients receiving organ transplants, the timing of immunosuppression is well defined, corresponding to the date of transplantation. Thus, the timing of CMV reactivation also is well defined and most often occurs 1 to 6 months following transplantation [23]. CMV infection in HIV-positive individuals has declined dramatically with the institution of HAART [24]. However, the occurrence of CMV disease in patients with AIDS is associated with greater levels of immunosuppression and greater mortality rates than in the general HIV-positive population [25].

Many patients in whom CMV can be detected in blood, urine, and respiratory secretions clinically will be asymptomatic. In patients with clinical symptoms, fever, cough, dyspnea, tachypnea, and an increased alveolar-arterial gradient (Aa gradient) most often will be the presenting symptoms [26].

Many patients with CMV viremia will have normal imaging studies. However, in those with imaging findings, CMV pneumonia usually will appear as ID-GGO on CT scans [23, 26, 27] ( Fig. 2 ). In some cases, small (< 5 mm) nodules may be detected and in more severe cases, diffuse consolidation may be present.

P. carinii and CMV pneumonias affect similar populations, often have similar imaging characteristics, and often cannot be distinguished on the basis of imaging. In general, PCP is more common however, in certain select settings or situations, such as during the first months after organ transplantation, CMV is a frequent cause of ID-GGO [23, 26, 27].

Herpes simplex virus.—Herpes viruses are a type of DNA virus, which may remain dormant within host cells and reactivate at times of reduced host immunity. A large percentage of the adult population is infected with herpes simplex virus (HSV), which in most cases produces no clinical symptoms [28]. HSV pneumonia is a rare event and most commonly is seen in immunocompromised patients such as organ transplant recipients, patients with AIDS, patients with severe burns, and patients with malignancies [29–32].

Because it represents a reactivation infection, herpes simplex pneumonia characteristically will occur in the first few months following organ transplantation [33, 34]. Patients usually will have oral or genital ulcers before the onset of pulmonary symptoms. Dyspnea, cough, and fever herald the onset of pneumonia.

Herpes pneumonias may appear as ID-GGO, widespread consolidation, or a combination of both on chest radiographs and CT scans [35, 36]. Rarely, only GGO will be present [35]. Associated small pleural effusions commonly are found both by CT and chest radiographs [35].

Respiratory syncytial virus.—Respiratory syncytial virus (RSV) is a common cause of bronchiolitis and pneumonia in children and adults. Infection is most likely to occur in the late winter and early spring and commonly causes fever, cough, dyspnea, and otalgia with clinical signs of rales, rhonchi, or wheezes. In immunocompetent adults, the course usually is self-limited and is treated on an outpatient basis. However, in immunocompromised adults, RSV infection may result in a clinically significant pneumonia [37, 38].

The majority of patients with RSV pulmonary infection will have normal radiographic findings [39]. CT scans in 10 patients with RSV infection following lung transplantation revealed diffuse GGOs in seven patients, pulmonary consolidation in five patients, and tree-in-bud opacities in four patients [40] ( Fig. 3 ).

Other viruses.—Many other viruses commonly produce upper–respiratory tract illnesses and occasionally may produce a limited pneumonia. It is likely that many of these will appear as widespread or small focal regions of GGO, which are self-limited and radiographically resolve spontaneously. Because few of these patients are definitively diagnosed, it is unknown how often ID-GGO is a manifestation of community-acquired viral pneumonias.

In scenario two, a patient receiving bone marrow–suppressing chemotherapy, usually for metastatic carcinoma, presents with respiratory symptoms in the setting of thrombocytopenia and neutropenia. These patients are a special subset of immunocompromised individuals who are at risk for opportunistic infections as a result of neutropenia but who also are at risk for other causes of ID-GGO. These patients frequently are thrombocytopenic and are therefore at increased risk for diffuse aveolar hemorrhage, DAH. They also may develop drug toxicity as a result of the systemic chemotherapies they have received. This leads to the differential of and drug toxicity. In our experience, drug toxicity is the most difficult entity to diagnose and the most common cause of ID-GGO in this population.

In our study of the causes of ID-GGO, drug toxicity accounted for 4% of all pathology-proven cases and therefore represents an important cause of ID-GGO [9]. Because of the wide variety of pharmacologic agents that can result in ID-GGO, there are several histopathologic patterns of drug-related damage to the pulmonary parenchyma. These include noncardiogenic pulmonary edema, diffuse alveolar damage (DAD), nonspecific interstitial pneumonia (NSIP), DAH, bronchiolitis obliterans with organizing pneumonia (BOOP), hyper-sensitivity pneumonitis (HP), eosinophilic pneumonia, bronchiolitis obliterans, and venoocclusive disease [41]. Note that the first six patterns of damage listed here often will appear as ID-GGO on CT scans. Drugs, which can cause permeability edema, include cytosine arabinoside (ara-C), gemcitabine, interleukin-2, tumor necrosis factor, and all-transretinoic acid (ATRA). Other chemotherapy medications that have been shown to cause ID-GGO include daunorubicin, bleomycin, vincristine, carmustine, methotrexate, topotecan, carboplatin, and vinorelbine [41] (Figs. 4 and 5 ). There likely are many more. In a study of drug toxicity in patients with autologous bone marrow transplantation, 65% of cases of drug toxicity manifested as GGO [42].

In this third scenario, an otherwise healthy outpatient will complain of mild chronic dyspnea. Findings of the chest radiograph most often will appear normal or may show a faint haze, which may be interpreted as diffuse GGO. In this situation, ID-GGO most often will indicate one of the following chronic interstitial diseases: HP, desquamative interstitial pneumonia (DIP), respiratory bronchiolitis interstitial lung disease (RBILD), NSIP, acute interstitial pneumonia (AIP), BOOP, and sarcoidosis. Rarely, these patients will have some of the unusual unclassified causes of ID-GGO such as pulmonary alveolar proteinosis (PAP) or bronchoalveolar carcinoma (BAC). A history of smoking may be an important additional factor in this population. DIP and RBILD are seen almost exclusively among smokers and therefore would be unlikely diagnoses in patients who do not smoke.

An outpatient with chronic respiratory symptoms but without other clinically relevant medical conditions who presents with ID-GGO often will have a chronic interstitial lung disease. In our study of causes of ID-GGO, chronic diffuse interstitial lung diseases accounted for 31% (10/32) of pathology-proven cases [9]. Those interstitial diseases that most likely will present as ID-GGO include HP, DIP, RBILD, and NSIP. Other interstitial diseases that rarely may present as ID-GGO include sarcoidosis and BOOP.

Hypersensitivity pneumonitis.—Inhalation of organic or inorganic particles by sensitized individuals may result in the allergic phenomenon known as HP. In most cases, the allergens are a variety of microorganisms that may reside in decaying vegetable matter such as thermophilic actinomycetes, the Penicillium species, the Aspergillus species, and the Mycobacterium avium-intracellulare complex [43]. A notable exception to this general rule is bird fancier's disease in which the allergens are proteins contained in bird feathers, serum, or guano. Acute HP causes a capillary leak pulmonary edema secondary to an overwhelming allergic response. With lower-dose, chronic exposures, a granulomatous fibrosis develops in the interstitial spaces of the lungs [44].

There are many of causes of HP, including farmer's lung, cotton worker's lung (byssinosis), sugar cane worker's lung (bagassosis), and mushroom worker's diseases [43]. Urban populations can be exposed via contaminated ventilation systems, especially humidifiers and air conditioners. Hobbies such as raising pigeons or parakeets can result in a form of HP called bird fancier's disease.

CT examinations of HP result in a wide spectrum of findings including diffuse alveolar consolidation in acute HP, diffuse nodular interstitial lung disease in subacute and chronic HP, and irregular bands of fibrosis with distortion of the hila in chronic HP [45–49]. However, ID-GGO is among the more common manifestations of subacute HP and, other than pulmonary edema, HP is probably the most common cause of ID-GGOs in normal hosts [45, 47, 49] ( Fig. 6 ). These ID-GGOs often will appear as a mosaic pattern.

Desquamative interstitial pneumonia.— DIP is characterized pathologically by infiltration of alveoli by macrophages associated with mild interstitial fibrosis. In the past, many individuals believed that DIP was an early phase of usual interstitial pneumonia (UIP). Currently, DIP is believed to be a direct result of smoking-related lung toxicity. Patients with DIP typically are between ages of 30 to 50 years and present with chronic progressive dyspnea, with or without fevers [50]. Most patients will improve clinically and radiographically with corticosteroid therapy or smoking cessation [6, 51].

CT scans show ID-GGO in many patients with DIP. Some studies have found that the GGOs predominantly are distributed in the periphery of the lung [52–54]. However, in many other cases, GGOs also may show a diffuse or random distribution ( Fig. 7 ). A pattern of subpleural reticulation may be seen in a minority of patients.

Respiratory bronchiolitis interstitial lung disease.—The histology of RBILD reveals extensive infiltration of alveoli by macrophages associated with mild interstitial fibrosis in a peribronchiolar distribution [55]. Thus, it is histologically identical to DIP with the additional criterion that it be most severe in the centrilobular regions of the secondary pulmonary lobule. This similarity has led some authors to suggest that DIP and RBILD are two manifestations of the same disease [55, 56]. On CT, RBILD often will appear as ID-GGO. Very fine, often centrilobular, nodules also may be apparent on chest CT [56].

Nonspecific interstitial pneumonia.—NSIP represents an interstitial pneumonia that does not meet criteria for UIP, DIP, AIP, or BOOP and thus has a variable histologic and radiologic appearance [57, 58]. It has been associated with collagen vascular disorders, chronic passive congestion, and drug toxicity but is most often an idiopathic disorder. When idiopathic, NSIP most often affects patients in their 40s, 50s, and 60s and presents with an insidious onset of cough and dyspnea [55].

ID-GGOs are the most common radiographic findings in NSIP and are found in nearly 100% of cases. GGO often is found in a subpleural distribution but may also show a random or diffuse distribution [56, 57, 59, 60] ( Fig. 8 ). Reticulation, either randomly or in a subpleural distribution, also is a common finding in one half to four fifths of cases [56, 57, 60, 61]. Irregular linear opacities and traction bronchiectasis also may be seen [56, 59, 60].

Acute interstitial pneumonia.—AIP is a rapidly progressive interstitial fibrosis that resembles the organizing stage of DAD. It usually will present with progressive dyspnea leading to respiratory failure over several weeks or months, and occasionally with an antecedent viral-like prodrome [55]. Chest CT may show alveolar consolidation, GGOs, or both, often with associated traction bronchiectasis [55, 62].

Lymphocytic interstitial pneumonia.— Lymphocytic interstitial pneumonia (LIP) is an idiopathic interstitial abnormality characterized by diffuse lymphocytic infiltration of the interstitium of the lung [63]. It usually is associated with Sjögren's syndrome in adults and HIV infection in children. Some reports have suggested that LIP may represent a precursor to lymphoma or a low-grade lymphoma however, others suggest that LIP represents a variant of lymphoid hyperplasia and is not a premalignant condition [64–66]. Diffuse GGO appears to be the most common CT finding in LIP and is present in nearly all patients [66–71]. Bronchovascular and septal thickening also have been reported [70, 71]. Thin-walled cysts also may be present in some cases. Serial CT examinations show reversibility of all findings except cysts [70].

Cryptogenic organizing pneumonia and bronchiolitis obliterans with organizing pneumonia.—BOOP is a histologic pattern of lung injury. This often is due to a variety of pulmonary insults such as infectious pneumonia, connective tissue disorders, and bone marrow transplantation. However, in some cases it may have no recognizable cause. The American Thoracic Society/European Respiratory Society International Multidisciplinary Consensus Classification Conference has identified cryptogenic organizing pneumonia (COP) as the preferred term for idiopathic BOOP [66]. COP is a rare inflammatory condition presenting with progressive dyspnea and often with fever and constitutional symptoms that are unresponsive to standard pneumonia therapies. It is persistent and can lead to serious illness if not treated with corticosteroids, a therapy that in most cases will result in a complete cure of the disease. BOOP, regardless of cause, most often will appear as multifocal alveolar opacities scattered throughout the lungs [72]. Rarely, BOOP may appear as ID-GGO.

Sarcoidosis.—Sarcoidosis is an idiopathic granulomatous disorder with multisystemic ramifications including changes in the meninges, bone, eyes, heart, and skin. Racial predilections include African American and Puerto Rican residents of the United States and West Indians in the United Kingdom. It characteristically presents in patients between the ages of 20 and 40 years but may be encountered at nearly any age.

There are a wide variety of CT manifestations of sarcoidosis. Hilar and mediastinal adenopathy is present in the early and middle stages of the disease. The interstitial lung disease most commonly appears as many small nodules, usually along the bronchovascular bundles but occasionally as randomly distributed interstitial nodules [73–75]. Irregular linear bands of fibrosis, traction bronchiectasis, and coarse cystic spaces may develop in stage IV sarcoidosis. GGOs are among the least common presentations of sarcoidosis ( Fig. 9 ). When GGOs do occur in patients with sarcoidosis, careful inspection of the CT image often will reveal a fine stippled appearance to the GGO, as if it were composed of innumerable, tiny, 1- to 2-mm, ill-defined nodules. Sarcoidosis, HP, and RBILD are the causes of GGO most likely to give this fine stippled appearance. Rarely, sarcoidosis may appear as multiple large ground-glass masses. This pattern is known as alveolar sarcoid. This appearance is virtually pathognomonic of sarcoidosis.

PAP.—Other disorders that present as ID-GGO include PAP and BAC. PAP is a rare, idiopathic disorder of middle-aged adults. Accumulation of protein and lipid-rich material within the lung alveoli results in the subacute onset of slowly progressive and often incapacitating dyspnea [76–78]. This accumulation appears to be a result of an abnormality of surfactant production, metabolism, or clearance. Occasionally PAP may be associated with exposure to a variety of inorganic dusts, most commonly silica, such as is seen in sandblasters [79]. When found in association with silica or other exposures, PAP typically will present with an acute onset of symptoms. Leukemia and lymphoma also may predispose patients to PAP [80, 81]. PAP was fatal in approximately one third of patients before the availability of therapy involving high-volume bronchoalveolar lavage since the introduction of this therapy, many patients can be cured of the disorder and others may be treated successfully with repeated episodes of bronchoalveolar lavage [82].

Thin-section CT characteristically will show GGOs in association with thickening of the interlobular septa of the secondary pulmonary lobules [83–85] ( Fig. 10 ). This combination of findings has been termed the “crazy paving appearance” and, when present, is quite suggestive of PAP. However, occasionally PAP will present as ID-GGO.

Bronchoalveolar carcinoma.—A form of well-differentiated pulmonary adenocarcinoma, BAC, has a wide variety of radiographic appearances including solitary pulmonary nodules, focal alveolar opacities resembling pneumonia, ground-glass nodules, diffuse alveolar consolidation, and ID-GGOs. Most diffuse BACs will have a dominant mass, nodule, or area of consolidation with associated ID-GGO. Rarely, there will be no such sentinel patch and only ID-GGOs will be present [86].

In scenario four, the interstitial causes of ID-GGO usually will have a prolonged clinical presentation, and chest radiographs most often will be normal in appearance or show nonspecific interstitial abnormalities. The alveolar causes of ID-GGO usually will present acutely and chest radiographs often will show diffuse alveolar consolidation. ID-GGO in this setting most often will be secondary to one of the acute alveolar causes of ID-GGO: cardiogenic pulmonary edema, acute respiratory distress syndrome (ARDS), other causes of permeability edema, or DAH.

In our study of the causes of ID-GGO, acute alveolar diseases such as DAH, cardiogenic edema, and noncardiogenic pulmonary edema accounted for 19% (6/32) of pathology-proven causes of ID-GGO [9]. Because of the need for pathologic proof, pulmonary edema as a cause of ID-GGO is probably underrepresented in this series and pulmonary edema likely represents the single most common cause of ID-GGO. Thus, an acute clinical presentation of respiratory symptoms in a patient with ID-GGO should raise the possibility of hydrostatic and capillary leak pulmonary edema and DAH.

Pulmonary edema is a result of imbalances in the Starling forces, which govern the transport of fluids between the vascular and interstitial spaces of the lung. During homeostasis, there is a near balance between these forces, and the small net transfer of fluid into the interstitium is removed via the pulmonary lymphatics. However, a disturbance of this equilibrium will lead to excessive transport of water and solutes into the interstitial space. If the process continues, the interstitial lymphatics become overwhelmed and fluid overflows into the alveoli, leading to alveolar edema [87].

Typically, pulmonary edema is subdivided into two major etiologic subcategories: hydrostatic pulmonary edema and increased permeability pulmonary edema. In hydrostatic edema, there is increased intravascular hydrostatic pressure, which results in a net force driving water and solutes into the interstitial and, subsequently, alveolar spaces of the lung. Hydrostatic edema most often is a manifestation of left-sided heart failure. Increased permeability edema usually is a result of disruption of the capillary epithelial membrane, which allows plasma proteins to pass into the interstitial space. These proteins exert an osmotic force drawing water into the interstitial space, and if of sufficient volume, they spill into the alveolar spaces [87]. Permeability edema most often is a result of ARDS but has a number of other causes.

Cardiogenic pulmonary edema.—Left-sided heart failure is by far the most common cause of hydrostatic edema and thus commonly is known as cardiogenic pulmonary edema. On thin-section CT, the most common manifestation of cardiogenic pulmonary edema is ID-GGO ( Fig. 11 ). CT also may show thickening of the interlobular septa. The GGOs associated with hydrostatic edema often will have a central, perihilar distribution and be associated with enlarged pulmonary vessels and an enlarged heart.

Adult respiratory distress syndrome.— ARDS is the most common cause of noncardiogenic pulmonary edema and is a common physiologic response to a wide variety of insults including sepsis, aspiration of gastric contents, overwhelming pneumonia, severe trauma, multiple fractures, major burns, pancreatitis, prolonged hypotension, disseminated intravascular coagulation, drug overdose, and thoracic surgery [88, 89].

CT scans of ARDS most often will show bilateral GGO, pulmonary consolidation, or a combination of both [90, 91]. ID-GGO is most often a manifestation of the earlier exudative phase of disease [90, 91]. Pulmonary opacities often will be most severe in the more gravity-dependent regions of the lung. Unlike chest radiographs, which characteristically show uniform consolidation across the lung parenchyma, 75% of the time CT scan opacification will appear inhomogeneous or patchy.

Other noncardiogenic pulmonary edema.— It is likely that all causes of pulmonary edema can occasionally result in ID-GGO ( Fig. 4 ). ID-GGO has been reported in cases of near drowning [92] and fat emboli syndrome [93].

Alveolar hemorrhage may result from a large number of disorders however, when the process is diffuse, the differential diagnosis is moderately limited. The most common causes of DAH in outpatients are the group of entities often referred to as the pulmonary–renal syndromes [19]. Goodpasture's syndrome, Wegener's granulomatosis, and systemic lupus erythematosus are prime examples. Although these disorders may have other pulmonary manifestations, DAH is among the most common radiographically identifiable abnormality. Vasculitises other than Wegener's granulomatosis, such as Churg-Strauss vasculitis and microscopic polyangiitis, also are less common causes of DAH. Patients with lymphoma and leukemia also are inclined to DAH as a result of platelet deficiency or platelet malfunction. DAH is a feared complication of bone marrow transplantation because of its high mortality in this population [94]. Bleeding disorders such as antiphospholipid-antibody syndrome and use of anticoagulatory drugs also may predispose patients to DAH.

CT scans of DAHs may reveal frank consolidation with obliteration of the pulmonary vascular markings, but often they will appear as ID-GGOs ( Fig. 12 ). On thin-section CT images, ID-GGO may be spread uniformly throughout the lung, be randomly distributed, appear as centrilobular opacities, or have a mosaic pattern.

In scenario five, it is quite common for generally debilitated hospitalized patients to undergo CT scanning for a wide variety of clinical indications unrelated to dyspnea or hypoxia. For example, chest CT scans often will be obtained on ICU patients to search for causes of a persistent fever. These patients represent a subset of scenario four: patients with the acute development of dyspnea. ID-GGO in these patients most often will signify mild interstitial pulmonary edema due to congestive heart failure, volume overload, or ARDS. It is rare for these patients to have predisposing conditions for DAH or the more unusual causes of pulmonary edema, and therefore, the differential diagnosis is further limited in this patient population in comparison with those of the more general scenario four.

Unlike GGOs, in the company of other imaging findings ID-GGOs are caused by a relatively limited group of diseases. These can be grouped into four large categories of disease: diffuse pneumonias, some chronic interstitial diseases, acute alveolar diseases, and a group of unusual miscellaneous disorders. Furthermore, the presentation of ID-GGO often falls into one of five clinical scenarios: patients who are immunocompromised, patients who are receiving bone marrow–suppressing medications, outpatients who have slowly progressive dyspnea, inpatients and outpatients who have acutely developing dyspnea, and inpatients who are acutely ill. These clinical scenarios engender limited differential diagnoses in most cases, as outlined in Table 2.


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