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Biomedical subjects

Iwona Kozłowska

Publications and source records attributed to Iwona Kozłowska.

7 recordsLinked to original sources
PubMed2006

[Neurotoxicity of cyclosporine].

Using cyclosporine as an immunosuppressive drug allowed increasing survival of grafts as well as patients. Despite this drug is being safely used for many years, it can cause complications. The most often complications are nefrotoxicity, hepatotoxicity, diabetes mellitus, arterial hypertension and neurotoxicity. The most often manifestation of neurotoxicity are tremor, leucoencephalopathia, headache and even seizures. Among risk factors we can enumerate arterial hypertetension, low cholesterol level, hypomagnesemia and previous cerebrovascular insufficiency.

Cyclosporine↗
PubMed2005

[Resistance to activated protein C in a patient with multiple myocardial infarctions and stroke--a case report].

A case of a 49-year-old female with a history of two myocardial infarctions (MI) and ischaemic stroke is presented. The patient was admitted to the hospital due to a third acute MI. Laboratory investigations revealed resistance to activated protein C due to factor V Leiden mutation. Diagnosis and treatment of patients with this condition are discussed.

Activated Protein C Resistance↗
PubMed2005

[Anomalous pulmonary artery as a cause of wide, polycyclic pulmonary hilus--case report].

Changes of lymphatic system, vascular disease during pulmonary hypertension or aneurysms are very often considered to be a cause of wide pulmonary hilus. However, we should remember developmental anomaly of pulmonary artery, too. We present a case of a patient hospitalized very often due to necessity of diagnostic wide, polycyclic pulmonary hilus. Only digital subtraction angiography allowed us to know the reason of wide pulmonary hilus as the developmental anomaly of pulmonary artery.

Angiography, Digital Subtraction↗
PubMed2004

[Mitochondrial syndrome].

Mitochondrial syndrome is a metabolic disease, caused by punctiform mutations or depletions in nuclear and mitochondrial DNA. These genetic lesions alter mitochondrial oxidative phosphorylation, what leads to reduction in energy produced for cell activity. Particular severity of symptoms can be observed in organs and tissues highly dependent on oxygen metabolism. Symptoms can be seen in central and peripheral nervous system, skeleton muscles, pancreas, endocrine glands, kidneys and gastrointestinal tract. Diagnostics is difficult and expensive. It is based mainly on genetical assays and respiratory chain investigations in bioptate of skeleton muscles. So far the treatment is based on decreasing symptoms intensity. Presently studies are being conducted on gene treatment of this disorder, which aim is to provide evidence for efficacy of using respiratory chain co-factors in the treatment of mitochondrial syndrome.

DNA, Mitochondrial↗
PubMed2004

[The effect of lowering plasma homocysteine levels on some parameters of thrombotic activity in haemodialyzed patients with chronic renal failure].

This study was designed to check whether lowering plasma homocysteine concentration resulting from treatment is associated with decreased thrombotic activity in haemodialyzed patients. The study group included 38 patients undergoing chronic haemodialysis. Blood was collected after an overnight fast after two days of weekend intervals in haemodialysis. Tests were performed before and after eight weeks of combined treatment with vitamin B6 (100 mg/day, oral), vitamin B12 (1 mg s.c. once a week) and folic acid (15 mg/day, oral). Homocysteine, vitamin B12 and folic acid concentrations in serum, antithrombin, fibrinogen and protein C activity in plasma and thromboxane B2 levels in activated platelets were determined before and after treatment. Combined treatment resulted in a statistically significant decrease in plasma homocysteine concentration. No influence of this finding on parameters of thrombotic activity was found. The following conclusions were drawn: (1) Treatment with physiological doses of vitamin B12, B6 and folic acid effectively decreases homocysteine concentration in haemodialyzed patients with chronic renal failure. (2) Monitoring of treatment with concentrations of folic acid and vitamin B12 is unfounded as no significant correlations with homocysteine were revealed. (3) The decrease in homocysteine concentration in haemodialyzed patients does not affect thrombotic activity. Therefore, treatment with physiological vitamin doses should not be recommended for routine use.

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