Search PubMed⌕ Search

Biomedical subjects

L Favre

Publications and source records attributed to L Favre.

At least 55 records · Page 3Linked to original sources
PubMed1983

[Non-steroid anti-inflammatory agents, diuretics and kidney function: a warning].

On the basis of their own experience and data from the literature, the authors warn against the simultaneous administration of diuretic agents and non-steroidal antiinflammatory drugs. Apart from the drastic reduction in the natriuretic effects of some diuretics, this association may lead to acute non-oliguric renal failure in patients with one of the following predisposing factors: volemic depletion, effective circulating volume (cardiac insufficiency, liver cirrhosis), preexisting nephropathy (lupus erythematosus, chronic renal failure), or borderline renal function (geriatric patients, diabetics).

Acute Kidney Injury↗
PubMed1983

[Pseudo-Conn's syndrome due to intoxication with nonalcoholic pastis].

A case is reported in a patient who presented with hypertension and quadriparesis, both due to ingestion of a new beverage, non-alcoholic pastis (an anise-based aperitif), containing glycyrrhizinic acid. Consumers, especially if they are ex-alcoholics, diabetics or hypertensives, may develop potentially serious effects from hypermineralocorticism.

Aldosterone↗
PubMed1983

[Prostaglandins and arterial pressure].

Renal and vascular prostaglandins, which are vasoactive factors with local action, are implicated in the regulation of arterial blood pressure and might play a role in the genesis of arterial hypertension. By their properties of supervision on intrarenal blood flow, on renin secretion, on excretion of electrolytes and on the antidiuretic action of vasopressin, the prostaglandins E2 and I2 of renal origin indirectly control the blood pressure balance. In patients suffering from essential hypertension the urinary excretion level of renal prostaglandins is normal or diminished. When given to patients in pharmacological doses, prostaglandins exert a marked hypotensive effect. Non steroidal antiinflammatory drugs who act through inhibition of the synthesis of prostaglandins combat the action on blood pressure of several antihypertensive agents and lower natriuresis normally induced by some diuretics. These data show the diversity of action of the prostaglandins. By these properties, prostaglandins take part in control mechanisms on arterial blood pressure and facilitate the therapeutic use in patients suffering from hypertension.

Alprostadil↗
PubMed1983

Interaction of diuretics and non-steroidal anti-inflammatory drugs in man.

1. The influence of four diuretics on renal prostaglandins was investigated in a study designed in two parts (A and B): A, 24 normal subjects on a constant sodium intake received frusemide (80 mg daily), or hydrochlorothiazide (100 mg), or triamterene (200 mg) or spironolactone (300 mg); B, the same subjects were pretreated for 3 days with indomethacin (150 mg daily), which was continued during the 3 day administration of the respective diuretics and during a 2 day post-diuretic period. 2. In study A, only triamterene provoked a rise in urinary prostaglandins E2 and F2 alpha (+ 474 +/- SEM 92%, P less than 0.01, and + 192 +/- 7%, P less than 0.01). In study B, prostaglandins were significantly inhibited in all subjects. After indomethacin, the natriuretic effect of frusemide and spironolactone was reduced by 80 +/- 12% (P less than 0.01) and 54 +/- 11% (P less than 0.001), whereas the natriuresis induced by hydrochlorothiazide and triamterene was unchanged. No correlation was found between urinary PGE2 and F2 alpha and natriuresis. 3. When triamterene was associated with indomethacin, two subjects developed reversible acute renal failure. 4. Plasma renin activity and urinary aldosterone were stimulated by the four diuretics in study A, but their response was blunted in study B. Urinary antidiuretic hormone was not modified by diuretics but was suppressed by indomethacin. 5. Diflunisal, a structurally unrelated nonsteroidal anti-inflammatory drug, given to 12 of the subjects provoked similar interactions with frusemide, hydrochlorothiazide and spironolactone. 6. The results suggest that prostaglandins contribute to the natriuretic effects of frusemide and spironolactone, but not to those of hydrochlorothiazide and triamterene.

Adult↗
PubMed1983

Influence of a prostaglandin inhibitor and a mineralocorticoid on the antidiuretic and hormonal response to an osmolar load.

To examine the influence of prostaglandins (PGs) and sodium-volume status on the urinary excretion and action of arginine-vasopressin (AVP), we studied the response to a hypertonic saline infusion (2.5% NaCl, 0.06 ml/kg/min for 3 h) in 8 healthy males under three different conditions: 1) on an ad libitum salt diet (C), 2) after 4-day treatment with indomethacin (IDM) 150 mg/d, 3) after 4-day treatment with fluorohydrocortisone (9 alpha FF) 0.6 mg/d. The rise of urine osmolality and the decrease of free water clearance were identical in all three studies. Basal urinary PGE2, PGF2 alpha and AVP were decreased during IDM and unchanged during 9 alpha FF, compared to C. The increment of urinary AVP was similar during C and IDM but significantly greater with 9 alpha FF (P less than 0.02) although urinary PGs were higher at the end of the infusion. In conclusion, despite markedly different hormonal patterns and sodium status in the three protocols, the antidiuretic response to an osmolar load is preserved suggesting an adaptive mechanism maintaining a constant balance between AVP and PGs.

Adult↗
PubMed1982

Urinary prostaglandins, vasopressin, and kallikrein excretion in healthy children from birth to adolescence.

The urinary excretion of PGE2, PGF2 alpha, arginine-vasopressin, and kallikrein was measured in 58 healthy subjects aged 2 days to 13 years. In contrast to the activity of the renin-angiotensin-aldosterone system, which is known to decrease from birth, urinary excretion of PGE2, PGF2 alpha, vasopressin, and kallikrein significantly increased with age. These changes were not correlated to urine volume, natruresis, or glomerular filtration rate. Correction of the values by body surface area obliterated the differences for PGs and vasopressin, but not for kallikrein.

Adolescent↗
PubMed1982

Association of coarctation of the thoracic aorta with fibromuscular dysplasia of the renal arteries: a case report.

The case of a 25-year-old woman with coarctation of the thoracic aorta and combined bilateral fibromuscular dysplasia of the renal arteries is reported. Although marked hemodynamic changes induced by the coarctation were probably pre-existent, hypertension was revealed only during the last month of her first pregnancy and was spontaneously corrected 2 months post partum. Surgical treatment of the thoracic coarctation did not influence blood pressure which remained normal.

Adult↗
PubMed1982

Mineralocorticoid escape in man: role of renal prostaglandins.

The role of renal prostaglandins (PGE2 and PGF2 alpha) and kallikrein in the renal escape from excess mineralocorticoid has been evaluated in 10 normal volunteers on a high sodium diet. Escape from 9-alpha-fluorohydrocortisone (9-alpha-FF) administered for 12 days (0.6 mg daily) occurred within 4-5 days when 345 +/- 50 mmol sodium had accumulated. Indomethacin, a cyclooxygenase inhibitor, was then administered for 3 days while maintaining 9-alpha-FF. This was followed by a further cumulative gain of 105 +/- 28 mmol sodium after which escape resumed. Potassium balance remained negative throughout the study. Both PGE2 and PGF2 alpha excretion increased significantly under 9-alpha-FF from respective control values of 220 +/- 50 and 818 +/- 86 ng/24 h. to 610 +/- 317 and 1213 +/- 132 ng/24 h at the time of escape. Concomitantly urinary kallikrein increased from 1.1 +/- 0.2 to 2.5 +/- 0.3 units/24 h. Creatinine clearance increased from a mean baseline value of 111 +/- 4 to 123 +/- 4 ml/min during the same period. Indomethacin produced an inhibition of prostaglandin excretion without significant alteration of kallikrein excretion. Overall these results and particularly the transient sodium retention induced by indomethacin at the time of mineralocorticoid escape, suggest that prostaglandins may contribute to the escape phenomenon, whereas the role of kallikrein does not appear to be determinant.

Adult↗
PubMed1982

Reversible acute renal failure from combined triamterene and indomethacin: a study in healthy subjects.

As part of a study on the interaction between diuretics and renal prostaglandins, four healthy medical students receiving indomethacin for 8 days were also given triamterene for 3 days. Whereas renal function was initially normal in all four subjects, creatinine clearance decreased in two by 62% and 72% after concomitant administration of the two drugs, and was only restored to normal after 4 weeks. In control periods when triamterene or indomethacin was given alone renal function was preserved in all subjects. Urinary prostaglandin E2 was stimulated by triamterene and inhibited by indomethacin in all four subjects; both changes were more marked in the two sensitive subjects. Thus prostaglandin inhibition by indomethacin may unmask triamterene toxicity and contribute to the pathogenesis of the renal failure observed in sensitive subjects. As alternative therapy is readily available, avoidance of this potentially nephrotoxic association is recommended.

Acute Kidney Injury↗
PubMed1980

Primary aldosteronism with bilateral adrenal adenomas.

An unusual case of primary aldosteronism with bilateral single adenomas is reported. The two tumors were revealed by computerized axial tomography and subsequently confirmed by surgical exploration. Spironolactone therapy prior to the operation induced the formation of spironolactone bodies in only one of the two adenomas. As it has been postulated that these cytoplasmic inclusions may reflect the activity of the adenomatous cells, the presence of the bodies in a single adenoma would indicate a unilateral source of the hyperaldosteronism. Thus, the existence of spironolactone bodies could corroborate the data of functional localizing tests more closely than the morphological findings of computerized tomography.

Adenoma↗
PubMed1979

[Bartter's syndrome: Recurrence in the course of a treatment inhibiting prostaglandin synthesis].

Two adults with Bartter's syndrome were treated first with propranolol and a potassium-sparing diuretic and then with indomethacin for 22 months. Inhibition of prostaglandin synthesis by indomethacin, confirmed by a fall in urinary excretion rate of prostaglandins E2 and F2 alpha, induced a marked decrease in plasma renin activity and aldosterone excretion rate and an increase in plasma potassium. While the first patient was well controlled by this therapy, the second had elevation of prostaglandin excretion after 8 months associated with a relapse of symptomatic hypokalemia. Reintroduction of propranolol in addition to indomethacin led to renormalization of plasma potassium. A therapeutic trial with another prostaglandin synthesis inhibitor, meclofenamate, also produced partial correction of hyperreninemia and hypokalemia but only for a short time. From these observations it is concluded that (1) inhibition of renal prostaglandins by indomethacin or meclofenamate represents an effective but transient therapy for Bartter's syndrome, and (2) while prostaglandin secretion may elude pharmacological inhibition, the addition of propranolol restores complete inhibition and the therapeutic benefits of the previous treatment.

Adult↗
PubMed1979

Gigantism associated with a pituitary tumour secreting growth hormone and prolactin and cured by transsphenoidal hypophysectomy.

An 18-year old male is reported who presented with a history of a growtn spurt over the year preceding his admission. His height was above the 97th percentile, and he had incompletely developed secondary sexual characters. Pituitary evaluation demonstrated a moderately elevated level of growth hormone (hGH) not suppressible by a glucose load and not stimulable by TRH or by L-DOPA. Serum prolactin (PRL) concentration was also increased while gonadotrophin, thyroid and adrenal function were all subnormal. There was clear radiological evidence of a large pituitary tumour with suprasellar extension and transsphenoidal total hypophysectomy was performed. A mixed chromophobe and acidophilic adenoma was found and both growth hormone and prolactin were demonstrable in different cells of the tumour by the immunoperoxidase technique. Post-operatively the patient has hypopituitarism and levels of growth hormone and prolactin have remained low or undetectable after 6 months. Thus early diagnosis and surgical treatment of gigantism of this mixed hGH-PRL secreting pituitary tumour was associated with a cure, which contrasts with the unfavourable outcome of many of the patients previously reported.

Adenoma, Acidophil↗