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Biomedical subjects

N Galezowski

Publications and source records attributed to N Galezowski.

8 recordsLinked to original sources
PubMed1991

[Thrombosis of renal veins].

According to whether they are acute or progressive, complete or partial, uni- or bilateral, renal venous thromboses have quite various clinical expressions and biological consequences. The diagnosis is readily suggested by acute pain in the side with an increase in the size of one or both kidneys, associated with hematuria, proteinuria, or in case of renal failure, which is characteristic of acute bilateral thrombosis. On the other hand, chronic thrombosis of a renal vein is sometimes suggested only when complications such as pulmonary embolism occur. This explain why it is often discovered on autopsy. The diagnosis is confirmed on the basis of radiology, with ultrasound combined with vascular Doppler becoming increasingly important. Renal venous thrombosis may have various causes: disorders in renal blood flow, especially in the acute forms in newborns; hypercoagulability, in particular in nephrotic syndromes and above all in extramembranous glomerulonephritis; extension of vena cava thrombosis; retroperitoneal diseases involving the renal pedicle or extension of a renal tumor. The treatment of renal vein thrombosis is mainly medical and based on anticoagulants. The role of fibrinolytic treatment is controversial. Surgery is exceptional.

Humans↗
PubMed1990

[Congenital atrioventricular block and maternal autoimmune diseases].

Congenital heart block is rare; it is acquired in utero, definitive and, more often than not, complete. It can be diagnosed by the appearance of fetal bradycardia around the 23rd week of gestation, during ultrasonographic monitoring of pregnancy. Heart block is usually associated with the presence of anti-Ro and/or anti-La antibodies in the mother's serum. These maternal immunological abnormalities can be isolated or associated with an autoimmune disease, usually systemic lupus erythematosus, but also Sjögren's syndrome, or more rarely still, an as yet unclassified connective tissue disease. Anti-Ro and anti-La antibodies cross the placental barrier and react with a fetal heart, leading to acute fetal myocarditis by the 17th week of gestation. When severe, it is lethal, otherwise it can result in degeneration and endocardial fibroelastosis, disrupting conduction and leading to congenital heart block. The ideal treatment would be prevention with corticosteroids. When the mother is Ro or La antibody-positive before pregnancy, elimination of these circulating antibodies can be attempted by treatment with 0.5 mg/kg body wt/d of prednisolone for 3 months. If the treatment is successful, corticotherapy can be prescribed early in the pregnancy to try to protect the fetus. However, there is not always a relationship between maternal anti-Ro antibodies and fetal heart block. If the Ro/La antibody-positive woman is already pregnant, but before her 17th week, it is possible to prescribe dexamethasone, which crosses the placenta and remains active, sometimes in association with plasmapheresis.

Antibodies, Antinuclear↗
PubMed1988

[Polymyositis].

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Adolescent↗
PubMed1987

[Complications of infections attributed to cytomegalovirus in a group of 52 kidney transplant patients].

Cytomegalovirus (CMV) infection after renal transplantation was studied over a one year period in 52 patients receiving immunosuppressive drugs. During the infectious episodes, viral shedding was systematically detected in the blood and urines by culture on MRC5 cells and CMV antibodies were titrated in the serum by ELISA (IgG: M. A. Bioproducts, IgM: immunocapture Wellcome) and compared to the initial antibody titer determined the day of transplantation. Primary CMV infection was observed in 6 of 22 seronegative patients, attested by CMV shedding from urine and/or blood and by the emergence of CMV IgM antibodies. This primary infection was severe, including at least 4 of the following features: fever greater than 38 degrees C, neutropenia, thrombocytopenia, cytolytic hepatitis, pneumonia, impaired renal function, neurological syndrome, usually occurring about 6 weeks after transplantation. Reactivation was found in 12 of 30 seropositive patients, as shown by excretion of CMV in the urine and significant rise of specific antibodies. This reactivation occurring about 9 weeks after surgery was symptomatic in 5 patients with severe illness and associated with the presence of IgM antibodies in 2 cases. Rise of CMV antibodies was observed in 10 seropositive patients without excretion of virus. It coincided with symptomatic infection in only three patients who displayed severe symptoms, with presence of CMV IgM antibodies in one case. As previously reported, we confirm that CMV infection is a frequent complication of organ transplantation. It may be clinically silent in renal transplant patients or cause problems ranging from fever to pneumonia or retinitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗