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Biomedical subjects

H Levesque

Publications and source records attributed to H Levesque.

At least 91 records · Page 5Linked to original sources

Acquired von Willebrand's syndrome associated with decrease of plasminogen activator and its inhibitor during hypothyroidism.

OBJECTIVES: In a prospective study we searched for von Willebrand's syndrome during hypothyroidism and investigated the effects of treatment with thyroid hormones on plasma concentrations or activities of the factors involved in von Willebrand's disease in addition to tissue plasminogen activator and plasminogen activator inhibitor 1. METHODS: Eleven patients with hypothyroidism were tested. Factor VIII coagulant activity (VIIIc), von Willebrand factor (vWf:Ag), von Willebrand factor activity (vWf:RCo), tissue plasminogen activator antigen (tPA) and plasminogen activator inhibitor activity (PAI) was monitored before and after correction of hypothyroidism by hormone supplementation. RESULTS: Five patients had laboratory evidence of type I von Willebrand's disease. The other six patients had concentrations or activities of the factors involved in von Willebrand's disease within the normal range. In all cases except one, during thyroxin treatment, von Willebrand factors returned to normal if initially low, or increased clearly if initially normal. With the correction of hypothyroidism, an increase of tPA was noted in the eleven patients, associated with a significant increase of PAI. CONCLUSION: Laboratory evidence of von Willebrand's disease is common during hypothyroidism. Study of plasminogen activator and its inhibitor suggest a decrease of von Willebrand factor synthesis during hypothyroidism.

Adult↗

A low molecular weight heparin decreases plasma aldosterone in patients with primary hyperaldosteronism.

Four patients with primary hyperaldosteronism were treated with nadroparin 4100 or 6150 antiXa IU daily for 4 days. Plasma and urine sodium and potassium, and plasma aldosterone and renin were monitored before, during and after the study. After four days of treatment, and for the following two days, plasma aldosterone was decreased (by a mean of 49% on Day 6), and urinary Na/K was increased (3.7-fold). The direction of the changes was reversed on Day 8. The study has confirmed the effect of low molecular weight heparin on aldosterone, and makes it unlikely that it is related to inhibition of angiotensin II stimulation in these patients, as renin could not be detected in their plasma.

Aged↗

[Acute thrombosis of the right renal vein. Two cases with coagulopathies].

We report two cases of renal vein thrombosis, unusual because of acute expression, right renal vein localization, absence of the usual renal or perirenal causes, surgical management and a never before reported etiology. In one case the thrombosis was secondary to primary antiphospholipid syndrome, in the other it was secondary to heparin associated thrombocythemia. In this case surgical management was performed during prostacyclin infusion.

Acute Disease↗

[Erythromelalgia in adults. Apropos of 16 cases].

The authors report sixteen consecutive cases of erythromelalgia, an infrequent disease in which local heat, redness, and pain develop in the hands and/or feet in recurrent attacks. The disease was essential in nine patients; in the remaining seven, the cause was a myeloproliferative syndrome (polycythemia vera in 3 cases and thrombocythemia in 1 case) or a drug (bromocriptine, nicardipine, and nifedipine, one case each). Acetylsalicylic acid was effective in only six of the nine essential cases. Intravascular platelet activation and aggregation with plugging of the arterioles has been suggested as the mechanism of erythromelalgia in patients with myeloproliferative disorders. Other, as yet unelucidated pathophysiologic events underlie the juvenile-onset forms, which usually fail to respond to acetylsalicylic acid.

Adult↗

[Influence of protein S deficiency on the arterial thrombosis risk].

Protein S is the cofactor of activated protein C which, together with the antithrombin system, is a major regulator of coagulation. Congenital protein S deficiency is an important risk factor for venous thrombosis. In this study of 105 patients with protein S deficiency, 64 had one of several thromboembolic accidents, including 14 arterial thrombotic accidents involving the central nervous system or the myocardium. These accidents occurred in young subjects (mean age: 25 +/- 13 years) only one-third of whom had another risk factor. This high frequency of arterial thrombosis associated with protein S deficiency calls for a prospective study in young subject with cerebral vascular accident or myocardial infarction.

Adolescent↗

Clinical correlations and prognosis based on hyaluronic acid serum levels in patients with progressive systemic sclerosis.

The serum levels of hyaluronic acid (sHA) were measured using an affinoimmunoenzymatic assay in patients with distal (n = 16) and proximal (n = 15) progressive systemic sclerosis (PSS) and in 31 controls. The severity of PSS was evaluated using a standardized organ-involvement score. The mean sHA was significantly higher in the patients with PSS than in controls (mean +/- SD:80 +/- 43.4 micrograms/l vs. 42.3 +/- 19.1 micrograms/l, P less than 0.001). sHA was significantly higher in patients with proximal PSS than in patients with distal PSS (106.4 +/- 44.6 micrograms/l vs. 55.4 +/- 23.8 micrograms/l, P less than 0.001). A positive correlation was found between sHA and the disease score (r = 0.67, P less than 0.001). sHA was also correlated with lung diffusion capacity for carbon monoxide (r = 0.70, P less than 0.001), but only in the those patients who had abnormal lung function, and therefore presumably had lung PSS involvement. We suggest that sHA could be an indicator of the degree of systemic involvement in PSS. Its prognostic value and possible use in the follow up of patients with PSS remain to be clarified.

Adult↗

[Hyaluronic acid. Usefulness and perspectives of its serum assay].

Hyaluronic acid (hyaluronan or HA) is a major component of connective tissue synthesized by fibroblasts. Some progress has been made in recent years in the understanding of its metabolism, regulation and physiological role. The development of specific and sensitive assay methods has shown that the HA plasma level is increased in a wide variety of disorders. This increase may be due to decrease hepatic clearance, excessive synthesis (systemic sclerosis, inflammatory arthropathies, psoriasis, cancers, etc.), or even to an increased hyaluronidase activity in certain cancers. The major use of HA assays at the moment is in the evaluation of the evolutivity of those diseases where the HA increase relates to their activity. It seems to be of no diagnostic activity, at least for the time being.

Acute Kidney Injury↗

Evolution of atenolol kinetics when hypothyroidism is corrected.

A single oral dose of atenolol 100 mg was given to 7 hypothyroid patients (4 F, 3 M), before and after correction of hypothyroidism, mean delay 3.5 months (2 to 6.5 months). There was no change in the elimination parameters of atenolol, but the maximal plasma atenolol concentration was increased (1.66 to 7.37 mg.l-1) as was the AUC (14.9 to 52.1 mg.l-1.h) when the hypothyroidism had been treated. Only one patient differed: he had had a supra-selective vagotomy, and had similar curves before and after treatment of the hypothyroidism, both being similar to the plasma concentration curves found in the other patients after correction of the hypothyroidism. The results suggest an increase in the bioavailability of atenolol when hypothyroidism is corrected. The findings in the patient with vagotomy suggest that the decreased bioavailability during hypothyroidism might be related to changes in intestinal pH. Further studies are needed of the impact of hypothyroidism on gastric and pancreatic or biliary function and its consequences for drug absorption, and drug pharmacokinetics.

Adult↗

[Vasoactive factors of endothelial origin].

The discovery of powerful vasoactive compounds synthetized by the vascular endothelium has led to the elaboration of new physiopathological concepts. We review the present state of knowledge about the role, potential therapeutic virtues, and physiopathological consequences of the three major endothelial vasoactive factors: 1. Prostacyclin (PG12), a powerful vasodilator, and the most potent known inhibitor of platelet aggregation, derived from arachidonic acid metabolism: 2: Endothelium-derived relaxing factor (EDRF) a powerful vasodilator thought to be a short-acting nitroxide; 3: Endothelin, a 21 amino-acid peptide with potent vasoconstricting properties.

Arteriosclerosis↗

[Idiopathic hypereosinophilic syndrome with predominant digestive manifestations or eosinophilic gastroenteritis? Apropos of 2 cases].

We report two cases of hypereosinophilic syndrome with predominant gastrointestinal signs, which could have been mistaken for eosinophilic gastroenteritis. In the first case, the patient presented with eosinophilic ascites; documentation of pulmonary involvement allowed to easily establish the diagnosis. In the second case, the patient presented with diarrhea and malabsorption; gastrointestinal and pancreatic involvement seemed isolated. Cases reported as eosinophilic gastroenteritis in the literature with polyvisceral involvement raise the possibility of hypereosinophilic syndrome. We suggest that diffuse eosinophilic gastroenteritis could in fact be an isolated manifestation of the idiopathic hypereosinophilic syndrome.

Adult↗