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P Cauchie

Publications and source records attributed to P Cauchie.

32 records · Page 2Linked to original sources
PubMed1987

Urea treatment for water retention in hyponatremic congestive heart failure.

We have studied the efficiency of urea in the treatment of hyponatremia and hydrosaline retention in a 76-year-old man with chronic ischemic congestive heart failure. Since increase of furosemide worsened the hyponatremia (120 mmol/l), 30 g/day of urea was added and induced the following changes: progressive weight loss (6.5 kg in one week), increased diuresis (from 0.750 to 1.950 l/day), increased salt excretion (from 40 to 165 mmol sodium/day) and correction of the hyponatremia (120 to 136 mmol/l). Blood urea and creatinine serum concentrations rose moderately without significant change in creatinine clearance (32 to 38 ml/min). No adverse effects related to urea administration were observed. Urea intake seems to be useful in the management of hyponatremia in our patient with cardiac failure.

Aged↗
PubMed1986

Role of vagal neuropathy in the hyponatraemia of alcoholic cirrhosis.

The hyponatraemia common in decompensated cirrhosis arises in part from secretion of antidiuretic hormone attributed to a decrease in effective blood volume. Baroreceptors send inhibitory impulses to the midbrain and hypothalamus through the vagus and glossopharyngeal nerves. Since vagal neuropathy often occurs in chronic alcoholism, this might theoretically contribute to the inappropriate secretion of antidiuretic hormone, which might in turn induce hyponatraemia. In a prospective study including 34 patients with cirrhosis a high incidence of vagal neuropathy was found in the alcoholics (64%) and a clear cut increase in the incidence of hyponatraemia in patients with evidence of vagal damage and ascites (seven of eight patients (88%); p = 0.02). Results of a retrospective study of 64 patients with cirrhosis and ascitic decompensation showed hyponatraemia in 17 (50%) of 34 alcoholics but in only four (13%) of 30 patients with non-alcoholic disease (p = 0.006). Vagal neuropathy in alcoholic cirrhosis may contribute to the low serum sodium concentrations commonly found in these patients.

Ascites↗
PubMed1986

Relationship between aldosterone and sodium, potassium, and uric acid clearance in cirrhosis with and without ascites.

We have suggested that cirrhotic patients with high uric acid clearances had an increased effective vascular volume. This hypothesis was tested by studying the relationship between the excretion of uric acid, sodium, potassium, and aldosterone in cirrhosis. In 29 consecutive cirrhotic patients, of whom 17 had ascites, and in a control group, the logarithm of urinary sodium and aldosterone excretion highly correlated in control (r = -0.79, p less than 0.001) and cirrhotic patients without (r = -0.72, p less than 0.01) and with (r = -0.80, p less than 0.001) ascites. The regression line significantly shifted to the left in the cirrhotic patients (p less than 0.001). The urinary ratio K/K + Na also correlated with urinary aldosterone in controls (r = +0.66, p less than 0.001) and in cirrhotic patients (r = +0.77, p less than 0.001); this regression line shifted to the right in cirrhosis patients (p less than 0.02). The fractional uric acid excretion significantly correlated with urinary aldosterone only in cirrhotic patients (r = -0.76, p less than 0.001). These data confirmed the existence of hypoaldosteronism in many cirrhotic patients and are consistent with tubular hypersensitivity to aldosterone and emphasize the major role of the effective vascular volume in the control of urid acid clearance in cirrhosis.

Adult↗
PubMed1986

Treatment of hyponatremic cirrhosis with ascites resistant to diuretics by urea.

We have studied the efficacy of urea in the treatment of hyponatremia and hydrosaline retention in cirrhotic patients with ascites resistant to diuretics. In 5 patients with hyponatremia and ascites resistant to a major diuretic treatment (200-400 mg spironolactone combined with 40-160 mg furosemide/day for 4 of them), urea intake (30-90 g/day) induced the following changes: the daily weight changed from a gain of 0.01 +/- 0.06 kg/day to a loss of 1.03 +/- 0.12 kg/day (p less than 0.001) (mean +/- SEM), serum sodium concentration rose from 128 +/- 1.3 to 133 +/- 1.4 mmol/l (p less than 0.01), sodium output increased from 24 +/- 4 to 82.5 +/- 11 mmol/day, diuresis increased from 1.05 +/- 0.10 to 2.24 +/- 0.24 liters/day (p less than 0.01). Despite an important weight loss, the creatinine clearance did not change significantly (53.6 +/- 4.5 ml/min before and 70.0 +/- 8.2 ml/min during urea). In patients responding to classical diuretics, urea as a monotherapy was less effective. From the 6 patients with resistant ascites, only 1 developed prerenal uremia after urea treatment. In order to enhance urea efficacy, it is important to take it together with a long-loop diuretic. Intermittent urea intake seemed to be useful in cirrhotic patients with hyponatremia associated with ascites resistant to diuretics and with low or normal blood urea concentrations.

Adult↗
PubMed1986

Platelet survival in myelodysplastic syndromes.

A platelet survival study with indium-111 oxine was performed in 6 patients with a myelodysplastic syndrome. A markedly shortened platelet life-span (range 0.50-2.65 days; normal 6.5-12 days) was obtained in each case. Platelet production ranged from 53,100 to 430,800 platelets/mm3/day (normal 66,200 +/- 14,600). A second isotopic study was performed in 1 case with platelets from a normal compatible donor. The nearly complete normalisation of the platelet life-span (from 0.85 to 5.50 days) indicates an intracorpuscular origin of the defect.

Adult↗
PubMedDate not supplied

Severe thrombophilic diathesis starting with hepatic vein thrombosis (BUDD-CHIARI syndrome) in a family with a new Protein S gene mutation.

We report the case of a 26-year-old man with a chronic Budd-Chiari syndrome with ascites, caused by a hereditary Protein S deficiency, in a Turkish family with consanguinity. In this family, the father, the two sisters and the young brother suffered from severe venous thrombosis of the limbs, with pulmonary embolism in two of them. Those thrombotic events are caused by a hitherto not reported mutation in the PROS 1 gene on chromosome 3, resulting in a severe familial Protein S deficiency. No other thrombophilic defect was detected in the family, despite extensive investigation. Furthermore, we observe hereditary twenty-nail dystrophy in this family, the two genes probably segregating independently. Prophylaxis is discussed.

Adult↗