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Biomedical subjects

M Karmochkine

Publications and source records attributed to M Karmochkine.

At least 37 records · Page 2Linked to original sources
PubMed1998

Thrombomodulin: an overview and potential implications in vascular disorders.

Thrombomodulin (TM), a high affinity thrombin receptor present on endothelial cell membrane, plays an important role as a natural anticoagulant. It acts as a cofactor of thrombin-catalyzed activation of protein C, and inhibits the procoagulant functions of thrombin. TM is also located in other cells (keratinocytes, osteoblasts, macrophages,...) where it might be involved in cell differentiation or in inflammation. In the presence of cytokines, activated neutrophils and macrophages, endothelial TM is cleaved enzymatically, releasing soluble fragments which circulate in the blood and are eliminated in urine. Plasma TM level (pTM) can be measured using a two-site enzyme-linked immunosorbent assay (ELISA). pTM level is regarded as a molecular marker reflecting injury of endothelial cells. It is often increased in case of diffuse endothelial damage as in disseminated intravascular coagulation, diabetic microangiopathy, Plasmodium falciparum and rickettsial infections. pTM is also a predictive marker of hypertensive complications in pregnancy. In several systemic inflammatory diseases, pTM levels are correlated to the activity of the disease.

Antibodies, Monoclonal↗
PubMed1998

[Episcleritis and brucellosis. Apropos of a case].

A 35-year-old man presented a case of recurrent episcleritis revealing brucellosis. No concurrent diagnosis other than brucellosis could account for the episcleritis. Moreover his status was dramatically improved by specific antibiotherapy. A review of the literature showed that uveitis and optic neuropathies are the most common ocular manifestations of brucellosis. To the best of our knowledge, this is the first case of episcleritis associated with brucellosis.

Adult↗
PubMed1997

[Thrombomodulin: physiology and clinical applications (excluding systemic diseases)].

Thrombomodulin (TM) is a proteoglycan present on the surface of endothelial and mesothelial cells where it acts as a strong anticoagulant. TM is also located in other cells (keratinocytes, osteoblasts, mononuclear phagocytes...) where it might be involved in cell differentiation or inflammatory processes. The damage of endothelial cells releases cleavage fragments. Plasma TM appears to be a marker of endothelium damage. Plasma TM has been investigated in several disorders: it is usually increased in the case of diffuse endothelial damage.

Cardiovascular Diseases↗
PubMed1996

Plasma levels of thrombomodulin in pulmonary hypertension.

BACKGROUND: Long-standing pulmonary hypertension (PH) leads to structural alterations of the pulmonary vasculature and its endothelium, and occlusion of small vessels by microthrombi. In patients with PH, the search for factors inducing or worsening endothelium damage and in situ thrombi is still ongoing. Thrombomodulin (TM), an endothelial cell membrane protein, is a receptor for thrombin and a major anticoagulant proteoglycan. PURPOSE: To analyze plasma TM levels in patients with different forms of severe PH. PATIENTS: We prospectively studied 32 consecutive patients with PH referred for heart, lung, or heart-lung transplantation: 11 patients with primary PH (group 1), 11 patients with secondary precapillary PH (Eisenmenger's syndrome, group 2) and 10 patients with secondary postcapillary PH due to congestive heart failure (group 3). Thirty-eight healthy subjects were also studied as a control group. METHODS: Plasma concentrations of TM were measured by an immunoenzymatic technique that uses two anti-TM monoclonal antibodies that have a strong avidity and react with different epitopes of the molecule. RESULTS: Thrombomodulin plasma levels decreased in all patients with precapillary PH, and this decrease was highly significant compared with controls (26 +/- 2 versus 44 +/- 2 ng/mL, P = 0.0001). In primary PH, the TM decrease was only significant in males whereas in the Eisenmenger's syndrome TM values were the lowest of all the patients studied, with mean values twice as low as controls (22 +/- 2 versus 44 +/- 2 ng/mL, P = 0.0001). In contrast, in postcapillary PH, studied only in males, TM levels were increased (85 +/- 17 versus 54 +/- 3 ng/mL, P = 0.02). Patients with precapillary PH had more severe disease than patients with postcapillary PH, with higher pulmonary artery pressure and pulmonary vascular resistance (P < 0.001). There was no correlation between TM plasma levels and all hemodynamic variables. CONCLUSION: We found low levels of plasma TM in patients with precapillary PH but not in postcapillary PH compared with healthy controls. This may be related to the severity of PH and may contribute to the initiation or worsening of in situ thromboses frequently found in pulmonary hypertension. Further studies should analyze whether other markers of endothelial cell damage are correlated with plasma TM levels in patients with precapillary pulmonary hypertension.

Adolescent↗
PubMed1996

High prevalence of antiphospholipid antibodies in precapillary pulmonary hypertension.

OBJECTIVE: To assess prevalence and clinical associations of various antiphospholipid antibodies (aPL) in patients with primary and secondary pulmonary hypertension. METHODS: A prospective trial of aPL in 38 consecutive patients with pulmonary hypertension. Nine patients had primary pulmonary hypertension. Twenty-nine patients had pulmonary hypertension secondary to different etiologies: left heart failure, 8; congenital heart defect, 11; various lung diseases, 10. The search for aPL directed against 4 phospholipids (cardiolipin, phosphatidylserine, inositol, ethanolamine) was by ELISA. RESULTS: Eleven patients (29%) had aPL, with various phospholipid specificities. Mean pulmonary artery pressure and mean pulmonary vascular resistance of aPL positive patients were not different from those of aPL negative patients. Mean pulmonary wedge pressure was significantly lower in aPL positive patients than those without aPL. Positive aPL were detected only in patients with precapillary pulmonary hypertension (11/30; 36.6%). The prevalence of aPL in primary (4/9; 44%) was not significantly different from aPL in secondary (7/29; 24%) pulmonary hypertension. There was no association between the presence of aPL and prior thrombosis or recurrent fetal losses. CONCLUSION: The frequent positivity of aPL in precapillary pulmonary hypertension, irrespective of its cause and severity, suggests the existence of an associated endothelial disease. These antibodies might play a role in the initiation and/or progression of in situ thromboses frequently observed in precapillary pulmonary hypertension. Our results reinforce the necessity of longterm anticoagulant treatment in these patients.

Adolescent↗
PubMed1995

[Antiphospholipid antibodies: cause of thrombosis or an epiphenomenon?].

Antiphospholipid antibodies (aPL) present in systemic lupus erythematosus and the primary antiphospholipid syndrome are a well-known risk factor for thrombosis. Most of them require the presence of a cofactor, beta 2-glycoprotein I for anticardiolipin antibodies, prothrombin for lupus anticoagulant. These aPL are of the "immune" type. APL are also found in various non-immunological conditions, in which repeated endothelial or membranous damages appear to be frequent, but thromboses are rare. Most of these aPL are cofactor-independent, except those induced by chlorpromazine, and might belong to "natural" antibodies.

Animals↗
PubMed1995

[Apoptosis].

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Apoptosis↗
PubMed1995

[Human parvovirus B19 infection. Update].

Pathogenicity of parvovirus B19 has been demonstrated. The spectrum of clinical manifestations varies according to the age and immune status of affected patients. Parvovirus B19 is the aetiologic agent of erythema infectiosum in children. In normal adults, it is responsible for acute, bilateral and symmetrical arthritis, although chronic arthritis can develop. Parvovirus B19 has a particular tropism for erythroid precursors: in patients with underlying hemolysis, it induces transient aplastic crisis; in immunosuppressed patients the virus can lead to chronic pure red cell aplasia. Hydrops fetalis is one of the most severe manifestation of the infection. Diagnosis of recent parvovirus B19 infection is based upon serology and PCR, especially in immunosuppressed patients in whom polyvalent intravenous immunoglobulins must be started. The link between parvovirus B19 and systemic vasculitis is questioned.

Acute Disease↗