We report a patient with aneurysmal (angiomatoid) fibrous histiocytoma manifested clinically as a single firm subcutaneous nodule, diagnosed as an epithelial cyst. Histologically, the growth showed massive histiocytic proliferation and areas with a vascular component. The lesion was histologically mistaken for Kaposi's sarcoma.
A 49-year-old woman with metastatic colon and primary infiltrating ductal breast carcinoma presented with a 10-day history of multiple facial ulcerations after having received two courses of chemotherapy with cisplatin and fluorouracil and 30 Gy of total brain irradiation. These lesions initially appeared 3 days following her second course of chemotherapy as erythematous plaques that developed bullae and subsequently opened and drained. When the patient presented to her physician 1 week prior to admission, she was afebrile and had mucositis, the facial lesions mentioned above, and a white blood cell count of 0.9 X 109/L. She was treated with nystatin for her mucositis and cefadroxil for her facial ulcerations. She also continued to receive dexamethasone for cerebral edema secondary to brain metastases. Over the next week, her facial lesions continued to enlarge, and she developed a new bulla on her abdomen.On admission to the hospital, the patient was afebrile and had stable vital signs. Examination of her skin revealed five deeply ulcerating tumors on her right cheek, right and left chin, right forehead, and right medial canthus. They had erythematous rolled borders and a black central eschar (Fig 1). She also had a 3-cm nodule with white central necrotic tissue and bullae on her left lower abdomen (Fig 2).Laboratory studies included a complete blood cell count, which revealed a white blood cell count of 26X10VL, with a differential cell count of 0.42 segmented neutrophils, 0.21 lymphocytes, 0.19 band cell forms, 0.07 metamyelocytes, 0.06 myelocytes, and 0.04 promyelocytes. A skin biopsy specimen was taken from one of these ulcérations (Fig 3).
on pulse or blood pressure were seen. Two patients showed a transient fall in systolic and diastolic pressures of about 10 mmHg after the first injection, but this returned to the resting level and was not repeated on subsequent instillations. Temperature remained within normal limits throughout and no cases of infection occurred. DiscussionWith the intrauterine route of adniinistration termination of pregnancy was effected in 14 out of 15 cases. In this small series no obvious differences were seen between patients in the first and those in the second trimester of pregnancy. There was a wide range of 71 to 34 hours in the inductionabortion interval in the successful cases, with a mean time of 18 hours. The total dose in patients receiving PGE2 varied from 350 to 2,500 ,ug, with a mean dose of 1,177 ,Ig. This is considerably less than the total dose required by intravenous infusion, which in our own series was from 270 to 6,750 ,ug, with an average of 3,500 ,ug.We have not found the side effects of vomiting and diarrhoea a serious problem with intravenous infusions of PGE2. Vomiting may occur with the higher doses but is rarely persistent and diarrhoea is practically never seen. It might be expected that these subjective symptoms would be less with intrauterine instillation but in fact most patients in this study vomited on one or two occasions. In contrast, diarrhoea and vomiting commonly accompany infusions of high concentrations of PGF2a intravenously. Karim and Filshie (1970b) reported diarrhoea in 50% of patients receiving 50 ,ug of PGF2a a minute. With intrauterine administration of PGF2a these symptoms are probably much reduced (Wiqvist and Bygdeman, 1970) and the two patients in this study receiving PGF2a were symptom-free.The only data with which we can compare the results of this study are those reported by Wiqvist and Bygdeman (1970). They recorded complete or "partial" abortion in 12 out of 13 patients given prostaglandins. All their patients, however, were in the first trimester, while most of ours were in the second, and only three were given PGE2 (in amounts up to 1,050 ,ug) the rest receiving PGF2a (maximum total dose 5,400,ug Medical_Journal, 1971, 1, 590-591 Gaucher's disease is a rare familial disorder of sphingolipid metabolism characterized by abnormal storage of cerebroside in reticuloendothelial cells. It is caused by a deficiency of the enzyme glucocerebrosidase. The commoner childhood form usually runs an acute course. In the adult it is protracted with progressive splenomegaly, hepatomegaly, skeletal lesions, pigmentation, and often evidence of hypersplenism (Medoff
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