Immunoglobulin levels and electron microscopy in eosinophilic pneumonia.
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Biomedical subjects
Publications and source records attributed to R L Edwards.
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An LH-RH test was performed before and 44 and 92 h after treatment with 2.5 mg oestradiol benzoate in 17 patients with a diagnosis of polycystic ovarian (PCO) disease. The responses were compared with the same tests performed on ten normal subjects during the early follicular phase of their menstrual cycles (days 4--6). Patients were divided into two groups on the basis of their LH responses to LH-RH. In Group A (seven patients) the response at 92 h was greater than at 44 h as in the normal subjects, but in Group B (ten patients) the response at 44 h was greater than at 92 h. Basal serum hormone values were similar in the two groups except for androgens and oestrone, which were significantly (P less than 0.01) higher in Group B patients. There was a negative correlation between the basal androgen and oestrone concentrations and the LH and FSH amplifications at 92 h in all PCO patients. The ratios of the basal concentrations of LH to FSH and the ratios of the highest levels of each achieved during the basal LH-RH test, were significantly higher in the two groups of patients when compared to controls (P less than 0.01). The test is of value in predicting the subsequent responsiveness to clomiphene. All patients in Group A showed evidence of ovulation following treatment with 100 mg clomiphene for 5 days, but only one of Group B responded in this way.
Premature ovarian failure was studied in ten women under the age of 30; eight had an ovarian biopsy and five of these showed primordial follicles. Plasma levels of oestradiol and progesterone were similar to the follicular phase of a normal menstrual cycle, but in eight patients cervical smears showed a cornification index of less than one per cent. Levels of both androgens and of sex hormone binding globulin capacity were generally normal. Administration of LH-RH caused a release of FSH which was similar to post menopausal women and higher than both. Two patients were treated with exogenous gonadotrophins without effect.
A male forestry worker presented with chest pain followed by severe continuing haemoptysis and an extensive bilateral nodular pulmonary infiltrate. A needle biopsy of lung demonstrated micronodular deposits of malignant tissue. The patient died from respiratory failure. Necropsy showed a disseminated haemangiosarcoma arising in the right atrium. Haemoglobin and serum iron levels were normal. Electron microscopy of the lung biopsy showed a close relationship between tumour cells and basement membrane and suggested that haemorrhage occurred directly from the tumour nodules. The ultrastructure of alveoli adjacent to tumour deposits was normal. This case provides further indirect evidence that the clinical and histological features of idiopathic pulmonary haemosiderosis cannot be explained by the mere occurrence of alveolar haemorrhage.
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Basal prolactin concentrations were measured in 77 patients presenting with amenorrhoea; 17 per cent were found to have hyperprolactinaemia. The release of prolactin in response to a standard dose of thyrotrophin releasing hormone for amenorrhoeic subjects with normal basal levels of prolactin was within the normal range. However, patients with hyperprolactinaemic amenorrhoea and no evidence of pituitary tumour were found to have a blunted response.
Intravascular lysis of leucocytes was an early event in the process of tissue injury in a patient with limited Wegener's granulomatosis. This lysis, with consequent liberation of free organelles into the circulation, was followed by platelet aggregation and fibrin deposition in vessels with intact endothelial cells. Necrosis of endothelial cells also occurred early in the tissue injury. Complete obstruction of vessel lumina, with necrosis of their walls and of alveolar pneumocytes, followed. The alveolar spaces filled with fibrin and cell debris, and macrophages and fibroblasts migrated into these areas. The ultrastructural findings offer a rationale for current therapy. Cyclophosphamide therapy led to improvement in the clinical state, pulmonary function and histological changes.
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Fourteen patients with amenorrhoea and hyperprolactin-anemia but no evidence of pituitary tumours were each given an intramuscular injection of 1 mg oestradiol benzoate. Thirteen patients failed to release luteinizing hormone in response to the oestrogen. This hypothalamic abnormality may help to explain the menstrual disturbances in subjects with hyperprolactinaemia.
An ultrastructural study of lung distinguised between lesions of the alveolar capillary basement membrane in a case of Good pasture's syndrome and in three cases of idiopathic pulmonary hemosiderosis. In Goodpasture's syndrome, diffuse vascular injury with wide endothelial gaps, diffusely fragmented basement membranes and an electron dense layer on the basement membrane was found. In idiopathic pulmonary hemosiderosis, focal ruptures of the basement membrane were associated with hydropic changes in pneumocytes and, although fibroblasts were not seen, collagen deposition occurred within the basement membrane. immunofluorescent studies failed to show deposition of immunoglobulins G (IgG), A (IgA), M (IgM) or C3 in the lung in either disease. The ultrastructural lesions appear to separate these clinically similar entities.
Injection of oestradiol benzoate was found to elicit a surge of luteinizing hormone (LH) in 15 of 19 patients with polycystic ovary (PCO) syndrome; follicle stimulating hormone (FSH) was also released, in conjunction with the LH surge, in eight patients. It is concluded that the oestrogen feedback mechanisms controlling mid-cycle gonadotrophin release are functioning normally in the majority of patients with PCO syndrome. Ovulation was subsequently induced by clomiphene alone in those patients who had an LH surge, and by a combination of clomiphene and human chorionic gonadotrophin (HCG) in those who had not shown any LH release.
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