Search PubMed⌕ Search

Biomedical subjects

M Thibonnier

Publications and source records attributed to M Thibonnier.

79 records · Page 5Linked to original sources

[Hyponatremia after very heavy beer drinking (author's transl)].

Severe water and electrolyte disturbances were observed in a patient after a bout of very heavy beer drinking (30 liters in 6 days). On admission she was found to have hypokalemia (2.2 mEq/I), metabolic alkalosis (pHa: 7.55-total CO2: 40 mEq/I), and more particularly hyponatremia (109 mEq/I), responsible for the typical neurological signs of water intoxication (hyponatremic encephalopathy). There was a positive cumulative return of sodium (570 mEq) and chloride (900 mEq) levels, and normal conditions were restored without significant modifications in water balance or weight. No other etiology, apart from the beer, was discovered. Heavy drinking of beer alone can therefore provoke chloride and sodium depletion, probably because beer, which is poor in NaCl, must produce urinary loss of these electrolytes. The high osmolarity of beer may explain this latter phenomenon. This particular cause of hyponatremia should be recognized, if only to avoid confusing the clinical signs of alcoholic intoxication with those due to water intoxication.

Alcoholic Intoxication↗

[Phaeochromocytoma: localisation by computerised scanner tomography. 5 cases (author's transl)].

In five patients with a phaeochromocytoma, axial computerised scanner tomography made it possible to localise the tumour without ambiguity, even when intravenous urography had been interpreted as normal. Although all the tumours diagnosed were relatively large (between 3 and 9 cm), this is nevertheless a non-invasive examination, free of danger and worthy of consideration in the preoperative assessment of a case of phaeochromocytoma.

Adrenal Gland Neoplasms↗

Abnormal regulation of antidiuretic hormone in idiopathic edema.

Idiopathic edema is characterized by impaired water excretion, particularly in the upright posture. Indirect evidence has shown that antidiuretic hormone is involved in this disease. For this reason, we measured urinary arginine vasopressin by radioimmunoassay before and during water loading (15 ml/kg) in 10 normal women and in 10 subjects with idiopathic edema in both the supine and upright postures. Daily sodium intake was 100 meq. Renin and aldosterone were concomitantly investigated, and abnormally high values were observed both in the recumbent and upright postures. Basal values for urinary arginine vasopressin were identical in control subjects and in patients with idiopathic edema. The water load significantly reduced urinary arginine vasopressin in normal women in both positions, but in those with idiopathic edema only in the supine position. In those with idiopathic edema, assumption of the upright posture was accompanied by a transient decrease in glomerular filtration, a major decrease in osmolar clearance and no decrease in urinary arginine vasopressin after water loading. Significant correlations were established between urinary arginine vasopressin and osmolar or volemic parameters in normal women, but these correlations were not found in those with idiopathic edema in either position. Arginine vasopressin regulation was abnormal in idiopathic edema, and this hormone was believed to play a part in the pathogenesis of this disease.

Adult↗

Pharmacokinetic studies of nifedipine tablet. Correlation with antihypertensive effects.

A tablet form of nifedipine was given to eight hypertensive hospitalized men (Stage I or II WHO, 45 +/- 10 years old). After an initial placebo test, 20, 40, and 60 mg of nifedipine were given at 8.00 a.m. in random order at 72-hour intervals in a single administration double-blind crossover study. Blood pressure and heart rate were measured twice by the same observer every 20 minutes from 7.00 a.m. to 8.00 a.m. and then hourly until 8.00 p.m., first with the patients recumbent and again after 1 minute of standing. Plasma nifedipine levels were assayed in samples drawn hourly from 8.00 a.m. to noon, every 2 hours from noon to 8.00 p.m., and at 24 and 48 hours after drug ingestion. The three doses all lowered blood pressure significantly. The reduction during recumbency was significantly larger (-18%) and lasted longer (12 hours) after 60 mg than after 20 mg (-11% at 7 hours). The three doses caused similar increases in heart rate (+29% to +38%), the maximum occurring at the second hour and lasting for 5 hours. The peak plasma concentrations and areas under the plasma concentration time curve were dose-dependent; kinetics were linear between 20 and 60 mg, and the half-life of nifedipine tablets was close to 10 hours. The decrease in mean arterial blood pressure correlated strongly with plasma nifedipine levels (r = 0.61; n = 190; p less than 0.001). Four patients experienced mild side effects (headaches, flushes, drowsiness, or weakness). The tablet form of nifedipine had a potent antihypertensive action that lasted longer than that of the capsule formulation.

Administration, Oral↗

[Sensitive radioimmunoassay for plasma arginine vasopressin (author's transl)].

Using an ion exchange resin, a sensitive radioimmunoassay for plasma arginine vasopressin (AVP) was developed. This assay was characterized by the absence of blank values, an excellent recovery rate, great sensitivity (0.1 pg of AVP was significantly detected) and reproducibility. In 8 normal men, plasma AVP after overnight dehydration was 1.57 +/- 0.17 pg/ml and dropped to 0.58 +/- 0.11 pg/ml after 20 ml/kg oral water loading. Significant correlations between plasma AVP levels and plasma or urinary osmolality confirm the validity of this assay. In complete pituitary diabetes insipidus (n = 4) plasma AVP was undetectable whereas it was frankly increased in Schwartz-Bartter syndrome (3 to 33 pg/ml, n = 8).

Adult↗