Hiponatremia severa como primera manifestación de hipopituitarismo / Hypopituitarism initially presenting as severe hyponatremia

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Effects of normalization of GH hypersecretion on lipoprotein(a) and other lipoprotein serum levels in acromegaly.

BACKGROUND & AIMS: Lipoprotein(a) has been recognized as an important risk factor for cardiovascular disease. Lipoprotein(a) has been found to be elevated in sera of acromegalic patients, possibly contributing to the increased incidence of coronary heart disease found in these patients. In the present study we sought to determine the effects of GH hormonal status on lipoprotein(a) and other lipid parameters, including lipoprotein lipase (LPL) activity. DESIGN: Cross-sectional study. PATIENTS: Twenty acromegalic patients, with either active (n = 12) or controlled (n = 8) acromegaly, were studied. Twenty-nine healthy subjects served as control group for serum lipid measurements. MEASUREMENTS: Serum GH, IGF-1, IGF binding protein-3 (IGFBP-3) and insulin levels were measured in patients. Insulin resistance was measured by the homeostatic model assessment (HOMA). Plasma total cholesterol, triglycerides, HDL-lipids, apolipoproteins A-I and B, lipoprotein(a) and lipoprotein lipase activity were also measured. RESULTS: The highest lipoprotein(a) levels were observed in patients with active acromegaly, followed by patients with controlled acromegaly, whose lipoprotein(a) concentrations were still significantly higher than those of the control group (means +/- SEM: active acromegaly, 0.67+/-0.13 g/l; controlled acromegaly, 0.41+/-0.12 g/l; controls 0.17+/-0.02 g/l; P<0.05). There were no differences in other lipid and lipoprotein values among the groups. In patients, significant correlations were observed between lipoprotein(a) and basal GH levels (r = 0.56, P<0.02), mean GH levels (r = 0.48, P<0.05) and with insulin resistance estimated by HOMA (r = 0.62, P<0.01). No correlations were found between lipoprotein(a) and IGF-1 or IGFBP-3 levels. CONCLUSIONS: Our present results demonstrate that both active acromegalic patients and those with controlled disease have elevated serum lipoprotein(a) concentrations. The findings might suggest that the present biochemical criteria for cure of acromegaly are not strict enough to result in the normalization of all the undesirable metabolic changes found in this disease, and also that significant cardiovascular risk may persist despite successful treatment of acromegaly.

[Levothyroxine treatment of the solitary thyroid nodule]. / Tratamiento con levotiroxina del nódulo tiroideo solitario.

The aim of this study was to review all published randomized clinical trials evaluating the efficacy of suppressive therapy with levothyroxine for solitary thyroid nodules. No significant differences were observed in reducing the volume of benign solitary cold thyroid nodules between the placebo and levothyroxine groups.

Tratamiento con levotiroxina del nódulo tiroideo solitario / Levothyroxine treatment of the solitary thyroid nodule

El propósito de esta revisión es comprobar la eficacia del tratamineto supresor con levotiroxina (LT4) en los nódulos tiroideos solitarios fríos (NTSF). Para ello se seleccionaron los cuatro únicos trabajos publicados entre 1962 y 1996 con diseño prospectivo, randomizado, controlado por placebo, con medición objetiva del tamaño nodular y tipificación por punción aspiración con aguja fina. De estos cuatro estudios, tres conseguían niveles de tirotropina (TSH) suprimida, según los autores. El volumen nodular no disminuyó tras LT4 en los 99 casos de tipo coloide incluidos en el análisis tanto cuantitativo (T de Student no pareada) (Media ñ DT: 2,72 ñ 0,86 ml antes vs 2,57 ñ 0,87 ml después) como por métodos cualitativos (disminución = 50 porciento vs disminución < 50 porciento, Chi2 = 1,18; p = ns). A pesar del resultado negativo, antes de alcanzarse conclusiones definitivas, debieran llevarse a cabo ensayos multicéntricos y que cumplan los criterios de diseño antes referidos (AU)

[Hypoparathyroidism]. / Hipoparatiroidismo.

Hypoparathyroidism (HP) is caused by abnormalities of parathyroid hormone secretion, disordered parathyroid function and pseudohypoparathyroidism. The term pseudohypoparathyroidism describes a set of syndromes in which the effects of parathyroid hormone are blunted or absent. Patients with HP are hypocalcemic and hyperphosphatemic.