The development of a testosterone stimulation test in the Virginia opossum (Didelphis virginiana) and its use in evaluating deslorelin contraception.

The aims of the present study were to examine the variability of testosterone secretion in the Virginia Opossum over a 24 h period and to develop a testosterone stimulation test that would provide an index of the prevailing testosterone biosynthetic capacity of the testes; the latter was used to clinically evaluate the efficacy of a gonadotrophin-releasing hormone agonist contraceptive. Sexually-mature captive opossums (n = 12) located in Africam Safari (Mexico) sampled every 12 h over 24 h consistently showed basal (<0.21 ng mL(-1)) blood testosterone concentrations. Intra-muscular injection of buserelin (2 microg mL(-1)) and human chorionic gonadotrophin (hCG; 1000 IU) resulted in an increase (P < 0.05) of plasma testosterone concentrations with maximal concentrations (3.9 ng mL(-1) and 5.8 ng mL(-1) respectively) occurring 120 min after injection. Plasma testosterone declined relatively rapidly to basal concentrations after 240 min with hCG but remained elevated after the same period of time with buserelin. Male opossums treated with (n = 6) and without (n = 6) a controlled-release deslorelin implant (Suprelorin; 4.7 mg deslorelin) were evaluated over a 10-week period for changes in testosterone secretion (hCG stimulation test) and sperm production (spermatorrhea). At the end of this period, the animals were hemi-castrated and their relative testicular quantitative histology compared. Testosterone concentration decreased over the course of the study in both treated and control animals (P < 0.0001) but there was no apparent effect of deslorelin on testosterone secretion, testicular histology (relative proportions of testicular cell types and seminiferous tubule diameter), or sperm production (presence of sperm in the cauda epididymis or urine).

Iron deficiency anaemia: are the British Society of Gastroenterology guidelines being adhered to?

BACKGROUND: The British Society of Gastroenterology (BSG) issued guidelines on the investigation of iron deficiency anaemia (IDA) ensuring standardised and comprehensive gastrointestinal investigation in all patients. It was apparent that not all patients in the authors' hospital were investigated according to these guidelines. OBJECTIVE: To determine whether patients who were referred for upper gastrointestinal endoscopy for investigation of IDA were confirmed to be iron deficient, and whether the BSG guidelines were being fully implemented. METHODS: All patients referred for upper gastrointestinal endoscopy over an 18 month period on a computer database (Endoscribe) were reviewed. Haematology, biochemistry, and radiology results were obtained and the frequency of the various diagnoses recorded. RESULTS: A total of 320 patients (133 male; mean age 71.5 years) were initially referred for upper gastrointestinal endoscopy for investigation of IDA, of whom 95 were iron deficient. Of these, 44 (46%) had duodenal biopsies performed, three (7%) of whom were diagnosed with coeliac disease. Five patients were diagnosed with upper gastrointestinal carcinoma (one oesophageal, four gastric). Of the remaining 87 patients, 65 (75%) underwent lower gastrointestinal investigations with four having colorectal carcinoma, four colonic polyps, and one angiodysplasia. CONCLUSIONS: Duodenal biopsies were performed in less than half of the patients. In those not diagnosed with coeliac disease or upper gastrointestinal carcinoma, only three quarters underwent lower gastrointestinal assessment. Approximately 10% were diagnosed with gastrointestinal malignancy as a cause for their anaemia and in 66% of patients no gastrointestinal cause was found. All physicians need to be made fully aware of the BSG guidelines for investigation of IDA.

Fatal pneumococcal septicaemia in a coeliac patient.

A 78-year-old lady initially presented with painful hips, low back pain, lethargy and weight loss. She had a past history of osteomalacia. Investigations revealed evidence of malabsorption and jejunal biopsy revealed sub-total villous atrophy in keeping with coeliac disease. Peripheral blood film was within normal limits. She responded well clinically to a gluten-free diet and calcium and vitamin D supplementation. Four years after the initial diagnosis she presented acutely with vomiting, pleuritic chest pain, pyrexia and bronchospasm. Blood cultures confirmed the presence of Streptococcus pneumoniae and she was treated appropriately with ampicillin. Despite this she died shortly after admission. It is recognized that blood film examination alone cannot exclude hyposplenism complicating coeliac disease and it is presumed that this was the reason for the development of fatal pneumococcal septicaemia in this patient. Prophylactic vaccination may be appropriate in hyposplenism secondary to coeliac disease.

Humoral hypercalcemia of malignancy in canine lymphosarcoma.

Studies on the pathogenesis of hypercalcemia in canine lymphosarcoma have led to conflicting results. The biochemical and bone histomorphometric findings in canine lymphosarcoma were examined in 19 hypercalcemic and 17 nonhypercalcemic dogs with lymphosarcoma. Compared to the nonhypercalcemic group, the hypercalcemic dogs demonstrated an increase in fasting and 24-h calcium excretion, an increase in fractional phosphorus excretion, and a significant increase in nephrogenous AMP excretion. Plasma 1,25-dihydroxyvitamin D and immunoreactive PTH levels were equivalent in the two groups. Quantitative bone histomorphometry performed on iliac crest biopsies revealed increased parameters of bone resorption in those hypercalcemic dogs with no evidence of tumor at the biopsy site, without a compensatory increase in bone formation. Acid-urea tumor tissue extracts from eight hypercalcemic and six nonhypercalcemic dogs were examined for adenylate cyclase-stimulating activity (ACSA). All tumors from hypercalcemic dogs contained ACSA, whereas none of the tumors from nonhypercalcemic dogs had ACSA. Further purification of one tumor extract yielded an adenylate cyclase-stimulating protein which appeared to interact specifically with the PTH receptor. We conclude that in some cases, hypercalcemia in canine lymphosarcoma is mediated by a tumor-derived circulating bone-resorbing factor which is distinct from PTH. ACSA detected in tumor tissue appears to be a reliable marker for the syndrome in vivo. The role of this activity in the pathogenesis of the syndrome remains to be determined.