[An asymptomatic chronic hypokalaemia]. / Une hypokaliémie chronique asymptomatique.

We report the case of an asymptomatic patient presenting a severe chronic renal hypokalaemia. Once being sure of no diuretics use, two hypothesis can be mentioned for a normotensive patient presenting an hypokalaemia associated with a metabolic alcalosis: Bartter syndrome or Gitelman syndrome. The highlighting of low magnesaemia and hypocalciuria strongly concentrates the diagnosis on Gitelman syndrome. First, this has been strengthened by the results of renal function tests and later it has confirmed by molecular diagnosis with the identification of a known homozygous mutation on SLC12A3 gene. In the patient family, the same chromosomal abnormality has been found in the young sister. For these two patients the treatment ordered is an antikaliuretic diuretic, magnesium and potassium supplements. This case shows the difficulty to diagnose Gitelman syndrome: it is frequently mistaken for Bartter syndrome. The main differences between these two syndromes are magnesaemia and calciuria. Furthemore , patients with Gitelman syndrome are often asymptomatic, this explains why prevalence of this illness is probably underestimated.

Balance in ghrelin and leptin plasma levels in anorexia nervosa patients and constitutionally thin women.

Ghrelin, a 28-amino acid octanoylated peptide, has recently been identified in rat stomach as an endogenous ligand for the GH secretagogue receptor. In addition to GH-releasing properties, exogenous ghrelin injections exert orexigenic effects in both rodents and humans. As the endogenous peptide appears directly related to feeding behavior, we assessed its plasma levels in anorexia nervosa (AN) patients before and after renutrition and in constitutionally thin subjects with body mass indexes (BMIs) equivalent to those of AN women but with no abnormal feeding behavior. The relationships between plasma ghrelin levels and other neuroendocrine and nutritional parameters, such as GH, leptin, T3, and cortisol, were also investigated. In AN patients, morning fasting plasma ghrelin levels were doubled compared with levels in controls, constitutionally thin subjects, and AN patients after renutrition. Twenty-four-hour plasma ghrelin, GH, and cortisol levels determined every 4 h were significantly increased, whereas 24-h plasma leptin levels were decreased in AN patients compared with controls and constitutionally thin subjects. Both plasma ghrelin and leptin levels returned to control values in AN patients after renutrition. Constitutionally thin subjects displayed intermediate 24-h plasma ghrelin and leptin levels, significantly different from controls and AN patients, whereas GH and cortisol were not modified. Ghrelin was negatively correlated with BMI, leptin, and T(3) in controls, constitutionally thin subjects, and AN patients, whereas no correlation was found between GH and ghrelin or between cortisol and ghrelin. Ghrelin and BMI or T3 were still correlated after renutrition, suggesting that ghrelin is also a good nutritional indicator. Basal and GHRH-stimulated GH release were significantly increased in AN patients only. In conclusion, ghrelin is increased in AN and constitutionally thin subjects who display very low BMI but different eating behaviors, suggesting that not only is ghrelin dependent on body fat mass, but it is also influenced by nutritional status. Even though endogenous ghrelin is not strictly correlated with basal GH secretion, it may be involved in the magnitude of GHRH-induced GH release in AN patients.

Macroprolactinaemia associated with prolactin adenoma.

BACKGROUND: Macroprolactinaemia, defined as hyperprolactinaemia with a predominance of, or only, the big big prolactin (bbPRL) isoform, is considered idiopathic and poorly symptomatic. Since its association with a PRL adenoma is poorly documented, we examined a series of 13 patients with tumoral hyperprolactinaemia for the presence of macroprolactinaemia. METHODS: From a series of 36 patients with hyperprolactinaemia studied for PRL isoforms, we selected 13 with hyperprolactinaemia and a prolactinoma, and divided them into two groups on the basis of the predominant PRL isoform, the large PRL group (five patients), with a predominance of the big big PRL isoform, and the monomeric PRL (mPRL) group (eight patients), with a predominance of the mPRL isoform. Plasma PRL concentrations were measured by radioimmunoassay, while plasma PRL heterogeneity was studied by gel filtration chromatography. The plasma autoantibody-bound PRL and the histology of the tumours were also studied. RESULTS: Macroprolactinaemia was seen in five out of the 13 patients with a PRL adenoma. The clinical and biological characteristics of the groups with and without macroprolactinaemia were similar. In the large PRL group, no evidence for anti-PRL autoantibodies was found and the prolactinomas were either typical or exhibited unusual aggregates of immunoreactive PRL deposits, the latter suggesting the tumoral origin of these large forms. CONCLUSION: Our results suggest that PRL adenoma may be associated with macroprolactinaemia.

[Generic carbamazepine-induced subacute adrenal insufficiency?]. / Décompensation surrénalienne subaiguë induite par un médicament générique de la carbamazépine?

Iatrogenic causes of adrenal insufficiency in Addison's disease are exceptional. We report the case of a patient with a history of epilepsy (taking carbamazepine, Tégrétol LP) and Addison's disease (treated by hydrocortisone (HDC) 30 mg/d, Dectancyl 0,5 mg/d, Florinef 50 mg/d). Recent digestive disorders required emergency hospitalization. The physical examination was normal and laboratory tests showed hyponatremia, hyperkalemia, and elevated serum ACTH. The course was rapidly favorable after rehydration and up-titration of the drug regimen. No triggering factor was identified, but the Tégrétol LP had been replaced for 3 months by a generic drug with the same quantity of active ingredients and the same bioavailability, but with a different excipient (the generic drug was not encapsulated). Could these differences have increased the serum level of carbamazepine and lead to more rapide HDC metabolism by enzymatic induction? Could poorer digestive tolerance have decreased HDC absorption? The hypothesis of carbamazepine overdosage is unlikely because the assay remained within the therapeutic range and hyperkaliemia would favor adrenal decompensation. In conclusion, this single case cannot prove drug interaction but does point out the importance of being prudent when modifying a well--tolerated regimen in a patient with Addison's disease.