Between 2000 and 2010, Mé decins Sans Frontiè res diagnosed and treated 4,831 patients with visceral leishmaniasis (VL) in the Pokot region straddling the border between Uganda and Kenya. A retrospective analysis of routinely collected clinical data showed no marked seasonal or annual fluctuations. Males between 5 and 14 years of age were the most affected group. Marked splenomegaly and anemia were striking features. An rK39 antigen-based rapid diagnostic test was evaluated and found sufficiently accurate to replace the direct agglutination test and spleen aspiration as the first-line diagnostic procedure. The case-fatality rate with sodium stibogluconate as first-line treatment was low. The VL relapses were rare and often diagnosed more than 6 months post-treatment. Post-kala-azar dermal leishmaniasis was rare but likely to be underdiagnosed. The epidemiological and clinical features of VL in the Pokot area differed markedly from VL in Sudan, the main endemic focus in Africa.
The simultaneous occurrence of acromegaly, hyperthyroidism and hyperparathyroidism is extremely rare and even that of acromegaly and hyperparathyroidism very unusual. Chromophobe adenomata producing either acromegaly, Cushing's syndrome or hyperthyroidism have been described in a limited number of cases.
A unique case of a patient with acromegaly, hyperthyroidism and hyperparathyroidism and a chromophobe pituitary adenoma was studied. In the blood an unusually high level of thyrotrophin (TSH) was found (about 2 mU/ml) but no »long-acting thyroid stimulator« (LATS). The TSH activity remained unaffected by thyroidectomy and by treatment with triiodothyronine but was not found in the blood after surgical hypophysectomy. The pituitary tumour contained TSH only about 20 mU/209 mg weight of tissue, i. e. less than is found in normal human pituitary glands. There was evidence of inadequate secretion of corticotrophin and gonadotrophins. The evidence suggests that both the acromegaly and the hyperthyroidism were caused by increased production of growth hormone (STH) and TSH by the pituitary tumour. The hyperparathyroidism was due to a parathyroid adenoma.
In four other acromegalic but euthyroid patients no TSH or LATS activity could be detected in the blood. In these patients the protein-bound iodine (PBI), free thyroxine and triiodothyronine-Sephadex uptake tests were normal. In addition in one of these patients, hyperparathyroidisni due to a parathyroid adenoma was observed. The occurrence of a parathyroid adenoma in acromegaly may be one facet of the multiple endocrine adenoma syndrome.
In all 5 subjects the hydroxyproline in serum and urine was increased.
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