Hipocalcemia e síndrome convulsiva em alcoólatras: uma associaçäo frequentemente näo diagnosticada / Hypocalcemia and convulsive syndrome in alcoholics: an association frequently not diagnosed

Hipocalcemia é um fator importante contribuinte para a epilepsia, e estudos anteriores mostraram que o etanol diminui o cálcio plasmático. Objetivo. Estabelecer a prevalência de hipocalcemia na populaçao convulsiva em geral e identificar um subgrupo específico de risco para hipocalcemia. Métodos. Realizamos um estudo prospectivo de dosagem de cálcio ionizado plasmático em 78 pacientes consecutivos admitidos no Serviço de Emergência da Escola Paulista de Medicina devido à síndrome convulsiva. Desses pacientes, 22 por cento eram alcóolicas. Foi também dosado o cálcio ionizado plasmático numa populaçao de 44 alcoólatras nao-convulsivos em seguimento ambulatorial. Resultados. Uma alta prevalência de hipocalcemia foi encontrada na populaçao alcoólatra convulsiva (32 por cento), em contraste com os convulsivos nao-alcoólatras e o grupo alcoólatra nao-convulsivo (ambos os grupos sem distúrbio do cálcio). O cálcio ionizado plasmático do grupo de alcoólatras convulsivos teve valores significantemente menores que o grupo de convulsivos nao-alcoólatras (p<0,05) [mediana de 1,20; variaçao entre 1,04 e 1,32 mmoI/L/; mediana de 1,24; variaçao entre 1,16 e 1,29 mmol/L, respectivamente]. O grupo de alcoólatras nao-convulsivos apresentou valores de cálcio ionizado entre 1,17 e 1,32 mmol/L, com mediana de 1,26mmol/L. Estes valores nao diferiram dos obtidos nos convulsivos nao-alcoólatras, mas foram significantmente maiores que os do grupo de alcoólatras convulsivos (p<0,05). Os níveis de paratormônio sérico, funçao hepática, fosfatemia e amilasemia estavam normais em todos os pacientes estudados. Conclusao. Estes estudo mostra a importância da dosagem de cálcio plasmático em pacientes alcoólatras com síndrome convulsiva e sugere que a correçao da hipocalcemia possa ser medida importante a ser adotada nestes casos.

Prevalence and magnitude of osteopenia in patients with prolactinoma

1. The association between hypogonadism and osteoporosis has been reported. We conducted a study to establish the prevalence and magnitude of osteopenia in patients with prolactinoma and the relationship of bone loss with the duration of hypogonadism. 2. We measured the bone mineral density (BMD) of spine and femur (a site that has not been analyzed earlier) in 35 patients with prolactinoma using a dual-energy X-ray absorptiometer. The patients were classified as normal BMD and low BMD (osteopenics). 3. Seventeen patients (48 per cent ) showed osteopenia. The mean bone loss in the different regions was: spine, 13 per cent ; femoral neck, 15 per cent ; trochanter, 11 per cent ; Ward's, 22 per cent . This difference was only significant when the spine and Ward's region were compared. The duration of hypogonadism was significantly greater in the low-BMD group (11.3 vs 4.9 years) when compared to the normal BMD group. There was a positive relationship between the duration of hypogonadism and magnitude of bone loss in both spine and femur (P = 0.04; r = 0.6). 4. A high prevalence of osteopenia in both spine and femur was found in patients with prolactinoma, and was highly associated with the duration of hypogonadism. Early treatment of this condition seems important to prevent bone loss

Do impaired glucose tolerance and diabetes mellitus interfere with the interpretation of the growth hormone response to the oral glucose tolerance test ?

The ability of glucose to suppress growth hormone (GH) secretion is well known and the glucose test is widely used for the diagnosis of acromegaly. However when suspected acromegaly is associaterd with diabetes mellitus (DM) or impaired glucose tolerance (IGT) the interpretation of the GH response to the oral glucose tolerance test (OGTT) may be difficult. Recently, Haltori et al. (Journal of clinical endocrinology and metabolism, 70: 771-778, 1990), using a highly sensitive (1.5 ng/l) polyclonal antibody-based immunoenzymometric assay, found no differences in the GH response to glucose load among control, IGT and DM patients. We employed a less sensitive (100 ng/l) but monoclonal antibody-based immunoenzymometric assay to measure the serum GII levels of 19 normal subjects, 11 patients with DM and 11 patients with IGT to determine the effect of glucose intolerance on the GH response to the OGTT. Complete suppression of GH (<0.1 ug/l) was achieved in 73% o9f the controls with a mean nadir of 0.17 ñ 0.16 ug/l (range, <0.1-0.6 ug/l). GH was completely suppressed in 82% of the the diabetes with a mean nadir of 0.58 ñ 1.21 ug/l (range, <0.1-4.0 ug/l). However, complete suppression occurred in only 27% of the IGT patients with a nadir of 1.09 ñ 2.08 ug/l (range, 0.1-7.0 yg/l), which was statisticaly higher than observed for controls and diabetics. We conclude that plasma GH plasma GH levels after glucose loading of IGT patients should be interpreted with caution because an abnormal response can be detected when some sensitive immunometric assays are employed