Ascites in agnogenic myeloid metaplasia. Association with peritoneal implant of myeloid tissue and therapy
β Scribed by Nalin M. Patel; E. Stephen Kurtides
- Publisher
- John Wiley and Sons
- Year
- 1982
- Tongue
- English
- Weight
- 220 KB
- Volume
- 50
- Category
- Article
- ISSN
- 0008-543X
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β¦ Synopsis
The case of a patient with agnogenic myeloid metaplasia and myelofibrosis engrafted upon a longstanding treated case of polycythemia rubra Vera and presenting with ascites due to peritoneal implants of myeloid tissue is presented. Comments on the differential diagnosis of ascites in general, and especially in myelofibrosis, are entered. The specific simple methodology for the confirmation of this diagnosis through microscopic examination of the sediment of the ascitic fluid for the detection of megakaryocytes and erythroblasts is presented. Radiotherapy in moderate amounts offers a very effective and long-lasting form of this entity.
Comer 501189-1190, 1982.
BDoMiNAL ENLARGEMENT is very common in ag-
A nogenic myeloid metaplasia. This is usually a reflection of massive hepato-and especially splenomegaly. At times, however, it is due to massive ascites. This may be the result of portal hypertension or the occurrence of ectopic myelometaplastic foci in the peritoneum.'** We report a patient with massive ascites and agnogenic myeloid metaplasia in whom the ascites were thought to be the result of peritoneal myeloid metaplastic implants. The ascites was treated successfully with irradiation. Clues to diagnosis are also presented.
Case Report
A 70-year-old white man professional painter entered the hospital because of increasing abdominal girth, discomfort, and anorexia. He denied pain, nausea, vomiting, melena, fever, but did report a 4.5 kg weight gain over the preceding six weeks. There was no angina, dyspnea or cardiopulmonary symptoms.
Some 35 years earlier he was found to have polycythemia rubra Vera. He experienced lengthy remissions which, however, diminished in duration over the subsequent 20 years, following four sequential courses of P-32 orally.
Seventeen years prior to the present admission, he was splenectomized at Evanston Hospital while under our care following a traumatic rupture of his spleen in a car accident. About 2000 cc of blood was evacuated from the abdominal cavity. Postoperatively, he developed an acute upper gastrointestinal
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