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Biomedical subjects

J F De Plaen

Publications and source records attributed to J F De Plaen.

10 recordsLinked to original sources
PubMed1992

An unusual cause of factitious mineralocorticoid excess.

The presence of hypokalaemia in hypertensive patient must prompt a search for increased mineralocorticoid activity. We describe and discuss the observation of a patient with biological markers of hypermineralocorticoidism, despite low plasma and urinary aldosterone levels, and suppressed plasma renin activity. This typical syndrome of apparent mineralocorticoid excess was secondary, in our patient, to prolonged administration of a mineralocorticoid-containing nasal spray.

Alkalosis↗
PubMed1991

Mineralocorticoids in the management of primary adrenocortical insufficiency.

Plasma renin activity (PRA) and plasma volume (PV) were determined in 22 adult patients treated for Addison's disease (AD) and reporting at the clinic for follow-up. Mean PRA was thrice the upper limit of normal (9.1 +/- 7.1 ng/ml/h (SD)) and mean PV was decreased (87% +/- 11 (SD)), consistent with residual hypovolemia in most patients, despite conventional treatment with both fluorocortisol (FF) and cortisone acetate. There was an inverse relationship between PRA and PV. Both PRA and PV were significantly correlated with FF dosage. On the other hand, no correlation was found between PV and either systolic or diastolic blood pressure (BP), while PRA was significantly correlated with systolic but not diastolic BP. Four patients were persistently hypertensive (diastolic BP greater than 100 mmHg) with elevated PRA in 3, associated with a definitely low PV in two cases. Two of these patients were progressively taken off FF, so as to control BP. Thus, in view of the not infrequent occurrence of arterial hypertension in AD patient on conventional treatment, we would warn against attempts at normalizing PV and PRA by means of FF, irrespective of BP in asymptomatic cases. In fact, when hypertension develops, reduction or sometimes withdrawal of FF may be recommended as a first therapeutic step.

Addison Disease↗
PubMed1990

The effect of membrane characteristics on tumour necrosis factor kinetics during haemodialysis.

We measured serum beta 2-M and TNF alpha before and after a 4-h haemodialysis performed on two membranes with different characteristics, either cuprophane (n = 40) or polyacrylonitrile (AN69) (n = 31). Kinetic studies including determinations at 0, 15, 30, 60 and 240 min were also performed during haemodialysis sessions on cuprophane (n = 14) and AN69 (n = 12). After a 240-min haemodialysis, TNF alpha increased on cuprophane (21.95 +/- 3.46 to 37.20 +/- 4.60 pg/ml, P less than 0.001) but remained stable on AN69 (16.70 +/- 2.60 to 19.90 +/- 2.90 pg/ml, NS). Kinetic studies revealed that on cuprophane, beta 2-M increased progressively from 40.72 +/- 4.41 to 45.71 +/- 4.77 mg/l (P less than 0.001) at 240 min with a significant increase already noted at 60 min. TNF alpha remained stable during the first 60 min but increased significantly at 240 min (34.14 +/- 6.60 to 49.71 +/- 8.78 pg/ml, P less than 0.001). The percentage increment in TNF alpha (50.5%) was significantly greater at 240 min than the percentage increment in beta 2-M (13.4%), a finding suggestive of net generation of TNF alpha. On AN69, beta 2-M decreased progressively from 31.82 +/- 2.70 to 27.30 +/- 2.26 mg/l (P less than 0.001). TNF alpha decreased transiently at 15 min but returned subsequently to control values (0 and 240 min: 25.00 +/- 3.81 and 29.75 +/- 3.59 pg/ml respectively, NS). Our data suggest a net release of TNF alpha during cuprophane but not during polyacrylonitrile haemodialysis. This release might play a role in the stimulation of beta 2-M production and thus in the genesis of dialysis amyloidosis.

Acrylic Resins↗
PubMed1977

Relationship between blood level of atenolol and pharmacologic effect.

Thirty-five hypertensive patients were treated with atenolol in weekly increasing doses (25, 50, 100, and 200 mg thrice daily). Factors determining the blood level of the drug were studied along with the relationship between blood level, the degree of cardiac beta blockade, and the antihypertensive effect of the drug. The blood level obtained varied with the daily dose, the time of blood sampling during the day, the body weight, and the creatinine clearance. The degree of beta blockade was assessed by measuring maximum-exercise tachycardia and was correlated with the blood level of atenolol. The reduction of the maximum exercise heart rate was independent of age. The hypotensive effect was not closely correlated with the blood level. Three days after the termination of long-term atenolol treatment, blood levels and beta blockage were still detectable.

Adult↗
PubMed1976

Comparative potency of atenolol and propranolol as beta-adrenergic blocking agents in man.

The comparative potency of two beta-blockers, propranolol and atenolol, in the inhibition of exercise tachycardia and isoproterenol-tachycardia has been studied in two groups of hypertensive patients, using oral doses which were increased weekly. A linear correlation was observed between the reduction in exercise tachycardia and the dose of each drug, up to a daily dose of propranolol 480 mg and atenolol 600 mg. Propranolol was slightly (0.7/1) more potent in decreasing maximal exercise tachycardia than atenolol when tested in low doses (below 100 mg); at higher doses (480 mg) no differences were found. However, atenolol was 10 times less potent than propranolol in blocking isoprenaline-induced tachycardia, which seems to be related to the cardioselectivity of atenolol.

Adult↗
PubMed1976

Relative value of beta blockers and thiazides for initiating antihypertensive therapy. Beta blockers or thiazides in hypertension.

Fifty-five patients with mild to moderate, renal or essential hypertension were admitted to a double blind cross-over trial of 18 weeks, involving treatment periods with placebo, the thiazide bendrofluazide (15 mg daily) and the beta blocker atenolol (600 mg daily). Compared to the placebo period (190/117 mm Hg) the hypotensive effect of atenolol (-24/16 mm Hg) was more pronounced than the hypotensive effect of bendrofluazide (-17/6 mm Hg). Arguments in favor of initiating antihypertensive drug therapy with beta blocker were its more powerful hypotensive effect, the quicker onset of its action, less metabolic disturbance, decreased frequency of complaints and patient's preference. On thiazides body weight and the frequency of swollen ankles decreased. Plasma renin concentration was not found to have a strong predicting power for the hypotensive effect of atenolol or bendrofluazide but low renin patients showed a more pronounced blood pressure decrease on bendrofluazide and high renin patients, especially essential hypertensives, on atenolol. While these points can be a guide to therapy today, the preference of one drug over the other must eventually be based on their relative efficacy in decreasing morbidity and mortality from the hypertensive disease.

Adrenergic beta-Antagonists↗
PubMed1976

The relationship between beta-blockade, hyporeninaemic and hypotensive effect of two beta-blocking agents.

In two consecutive series of hypertensive patients the hypotensive effect, the hyporeninaemic effect and the blockade of cardiac beta-receptors was studied using weekly increasing doses of propranolol or atenolol. With both beta-blockers, cardiac blockade and hypotensive effect increased in a parallel fashion when the dosage was increased suggesting that the hypotensive effect is related to cardiac beta-blockade. On the other hand lack of parallelism between the hypotensive effect and the hyporeninaemic effect suggests that the hypotensive effect was not related to a major extent to the hyporeninaemic effect of the drugs in the dosage range studied here.

Adrenergic beta-Antagonists↗