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WM Drake, F Miraki, A Siddiqi, M Yateman, NC Barnes, C Camacho-Hubner and JP Monson

Mesenchymal tumours are a well recognised cause of spontaneous hypoglycaemia. The mechanism is thought to relate to hypersecretion by tumour cells of high molecular mass insulin-like growth factor-II (pro-IGF-II), with consequent suppression of growth hormone (GH) secretion. The use of recombinant human (rh)GH has been reported to alleviate hypoglycaemia in non-islet cell tumour hypoglycaemia, and the mechanism is thought to relate to GH-mediated increments in serum levels of IGF-binding protein-3 (IGFBP-3), thereby reducing the bioavailability of IGF-II. We report the effect of increasing doses of rhGH on the clinical condition and serum IGF-I and IGFBP-3 levels in two patients with solitary pleural fibrous tumours causing severe hypoglycaemia. Hypoglycaemia was successfully alleviated in each patient although, despite using large doses of rhGH, the observed increments in IGFBP-3 were only modest. We postulate that the beneficial effects of rhGH in this situation are likely to be multifactorial and not simply related to increments in serum IGFBP-3 levels.

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CW le Roux, PJ Jenkins, SL Chew, C Camacho-Hubner, AB Grossman, GM Besser and JP Monson

OBJECTIVE: Epidemiological studies have shown an increased risk for prostate carcinoma in men with serum IGF-I in the upper part of the age-related reference range. Recombinant human GH (rhGH) is widely used in patients with GH deficiency, usually raising the serum IGF-I levels into the normal range: safety surveillance is therefore mandatory, with particular regard to neoplasia. The aim was to examine whether rhGH replacement in hypopituitary adults is associated with changes in serum prostate-specific antigen (PSA) as a surrogate marker of changes in prostatic growth. DESIGN AND METHODS: A prospective longitudinal study was used with a median follow-up of 22 (range 2.5-32) months, in which 41 men aged over 50 years with adult onset hypopituitarism and GH deficiency during rhGH replacement were examined. Serum PSA and IGF-I were measured at baseline and at latest follow-up. RESULTS: Mean serum PSA remained unchanged during rhGH replacement, with a median follow-up of 2 years. No correlation was found between the individual changes in serum IGF-I and changes in serum PSA. CONCLUSIONS: These data are reassuring thus far regarding the safety of GH replacement in relation to the prostate in this patient group.