Biomedical subjects

Jean-Louis Wemeau

Publications and source records attributed to Jean-Louis Wemeau.

5 recordsLinked to original sources

PubMed2005

[Hyperthyroidism: current concepts and management].

Hyperthyroidism leads to an overproduction of thyroid hormones, which determine diverse expressions of thyrotoxicosis. However a high prevalence of mild and subclinical forms of hyperthyroidism are now recognised, since the biological measurement of thyroid hormones and TSH modified the diagnostic criteria. Clinical, biological, ultrasonographic and scintigraphic data allow the identification of the different causes of hyperthyroidism. This point is very important to assess the prognosis and to choose the right therapy. Graves' disease, solitary and multinodular toxic goiters constitute the main causes of hyperthyroidism, with iatrogenic thyrotoxicosis. Antithyroid drugs, surgery and radioactive iodine, are useful for the traditional forms of hyperthyroidism. But the choice of the therapy and the procedures for the follow-up has now a more rational background.

Antithyroid Agents↗

PubMed2004

[Congenital hypomagnesemia].

MORE PRECISE IDENTIFICATION: The progress in molecular genetics has led to better understanding of primitive magnesium deficiency. Transporters of this cation have been identified in the intestines and kidneys. The majority of congential hypomanesemia phenotypes have been correlated with a defect in magnesium transport. The primary deficiency of intestinal absorption of magnesium is responsible for hypomagnesemia and subsequent hypocalcemia. DEPENDING ON THE MECHANISM: Magnesium absorption defects in Henle's loop induce hypomagnesemia with hypercalciuria and nephrocalcinosis, autosomal dominant hypocalcemia or Bartter syndrome. In isolated dominant hypomagnesemia and Gitelman syndrome, an abnormality in the distal convoluted tubule explains the primitive hypomagnesemia, through renal leaking. Conversely, the mechanisms of recessive isolated hypomagnesemia remains unknown. ORIENTING GENETIC DIAGNOSIS: In a context of primitive hypomagnesemia, the clinical and biological presentation will orient genetic research leading to correct diagnosis. However, there are many border-line phenotypes and the pheno-genotype correlation is still imperfect.

Absorption↗

PubMed2004

[Pseudo-hypoaldosteronisms].

TWO FORMS: Pseudohypoaldosteronisms (PHA) are characterized by end-organ resistance to aldosterone inducing hyperkalemia and hyperaldosteronism. There are two forms of PHA classified according to the level of blood pressure with either hypotension (Type 1 PHA or PHA 1) or hypertension (Type 2 PHA or PHA 2). PHA 1: The association with hypotension and high renin level (PHA 1) is responsible for type 4 tubular acidosis and should suggest congenital or acquired excessive salt loss. Acquired forms are associated with salt wasting of urinary (nephropathy) or digestive (colon resection + ileostomy) origin. Congenital neonatal forms are either sporadic or autosomal dominant or recessive. Sporadic or autosomal dominant forms are caused by mutations in the mineralocorticoid receptor gene and generally remit with age. Autosomal recessive forms are caused by mutations in the gene encoding the amiloride-sensitive sodium channel and are clinically more severe with pulmonary symptoms. PHA 2: The association of hyperkalemia/hyperaldosteronism with high blood pressure should suggest PHA 2 or Gordon's syndrome, still called familial hyperkalemic hypertension. This form of low-renin hypertension is caused by mutations in the WNK genes (WNK 1 for PHA 2C and WNK 4 for PHA 2B), but other genes located on different loci are also involved. These WNK kinases constitute a new signalisation pathway that would regulate blood pressure and homeostasy of Na+, K+, H+ and Cl- ions.

Blood Pressure↗

PubMed2004

Profile and outcome of pure androgen-secreting adrenal tumors in women: experience of 21 cases.

BACKGROUND: The aim of the study was to determine the outcome and possible prognostic factors of pure androgen-secreting adrenal tumors (PASATs). METHODS: In a review of 801 adrenal operations from 1970 through 2003, 21 women with PASATs were divided into 2 groups, benign and undetermined tumors (Weiss score < or = 3) (BT = 11) and malignant tumors (Weiss > or =4 or nonresectable) (MT = 10). RESULTS: In both groups, age at presentation was similar. There were no differences concerning type of secretion, but increase in testosterone level was 2.6-fold greater in malignant tumors (MT) than benign tumors (BT). Imaging studies allowed diagnosis of malignancy in 4 of 10 MT. Size and weight were greater for MT than for BT (average, 13.7 vs 9.2 cm and 1462 vs 206 g). At follow-up (median, 17 y; range, 1 to 33 y) 2 of 11 patients with BT died of unrelated causes, and 9 of 11 are alive without recurrence; 5 of 10 patients with MT died of disease, and 3 are alive with disease; 7 of those 8 patients had stage III or IV disease and/or had a Weiss score of 6 or greater. Two patients with MT are alive without disease; both were Weiss 7, stage II and received mitotane postoperatively. CONCLUSIONS: PASATs of undetermined benign condition share the good prognosis of BT. Weiss score is diagnostic of malignancy. MacFarlane classification determines the prognosis, and long-term disease-free survivors at stages III/IV are never observed after operation only. Postoperative mitotane therapy might be beneficial at stage II.

Adolescent↗

PubMedDate not supplied

[Fundic endocrine tumors and atrophic gastritis: the value of antrectomy].

We report two cases of fundic endocrine tumors associated with fundic atrophic gastritis-related hypergastrinemia and treated by antrectomy. About twenty infracentimetric tumors were observed in each patient and restrictively involved fundic mucosa. Antrectomy induced normalization of gastrinemia and the disappearance of fundic tumors, as soon as the 4(th) and 7(th) month. No recurrence was observed during the 5-year and 18-month follow-up time, respectively. We therefore consider that antrectomy may be regarded as a useful alternative treatment in the management of atrophic gastritis-related fundic endocrine tumors.

Abdominal Pain↗