glucose 6 phosphate dehydrogenase/fáradtság

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A new glucose-6-phosphate dehydrogenase deficiency variant, G6PD Mizushima, showing increases in serum ferritin and cytosol leucine aminopeptidase levels.

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We made a diagnosis of glucose-6-phosphate dehydrogenase (G6PD) deficiency with a new mutation of 848A→G (exon 8) in a 16-year-old male patient presenting with severe hemolysis. He was administered a diclofenac sodium suppository (50 mg) at the time of first visit to our hospital because of pyrexia.

I.V. ascorbic acid for treatment of apparent rasburicase-induced methemoglobinemia in a patient with acute kidney injury and assumed glucose-6-phosphate dehydrogenase deficiency.

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OBJECTIVE A case of apparent rasburicase-induced methemoglobinemia and acute kidney injury treated with i.v. ascorbic acid because of suspected glucose-6-phosphate dehydrogenase (G6PD) deficiency is reported. CONCLUSIONS A 46-year-old African-American man with a recent diagnosis of multiple myeloma

Glucose-6-phosphate dehydrogenase deficiency presented with convulsion: a rare case.

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Red blood cells carry oxygen in the body and Glucose-6-Phosphate Dehydrogenase protects these cells from oxidative chemicals. If there is a lack of Glucose-6-Phosphate Dehydrogenase, red blood cells can go acute hemolysis. Convulsion is a rare presentation for acute hemolysis due to

A hemolysis trigger in glucose-6-phosphate dehydrogenase enzyme deficiency. Vicia sativa (Vetch).

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Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme, playing an important role in the redox metabolism of all aerobic cells. It was reported that certain medications, fava beans, and infections can trigger acute hemolytic anemia in patients with G6PD deficiency. An 8-year-old male patient was

[Clinical Features and Laboratory Data Analysis of Glucose-6- Phosphate Dehydrogenase Deficiency].

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OBJECTIVE To explore clinical features and laboratory data of glucose-6-phosphate dehydrogenase（G6PD）deficiency and to investigate the relationship between them. METHODS Clinical data of 43 patients with G6PD deficiency was analyzed, the statistical method was applied to investigate the relationship

Fatal haemolytic crisis with microvascular pulmonary obstruction mimicking a pulmonary embolism in a young African man with glucose-6-phosphate dehydrogenase deficiency.

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We report a fatal case of haemolytic crisis mimicking a pulmonary embolism in a previously healthy 42-year-old African man. The patient was admitted to hospital with fatigue, shortness of breath and jaundice lasting for 2 days. Laboratory tests were consistent with haemolysis and inflammation. The

Case Report: A Case of Primaquine-Induced Hemoglobinuria in Glucose-6-Phosphate Dehydrogenase-Deficient Malaria Patient in Southeastern Bangladesh.

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We herein report the first case of Mediterranean glucose-6-phosphate dehydrogenase (G6PD) variant from Bangladesh. A boy had been admitted to hospital and was diagnosed with uncomplicated Plasmodium vivax infection and treated with 30 mg/kg body weight (BW) chloroquine for 3 days and 4.8

Review and drug therapy implications of glucose-6-phosphate dehydrogenase deficiency.

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The pathophysiology, diagnosis, and medication-use implications of glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common enzyme deficiency in humans, are reviewed. Originally identified as favism in patients who experienced hemolysis after ingestion of fava beans, G6PD deficiency

Amifostine administration during radiotherapy for cancer patients with genetic, autoimmune, metabolic and other diseases.

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Amifostine is a broad-spectrum cytoprotective agent approved for protection against cisplatin toxicities and radiation-induced xerostomia; strong clinical evidence exists that amifostine protects normal mucosa and lung from radiation damage. Hypotension, nausea/vomiting, fatigue and fever/rash are

[13-year old girl with fever 6 months after returning from sub-Saharan Africa].

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METHODS A 13-year-old girl presented with regular fevers, 6 months after a prolonged trip through Africa. The patient reported relapsing fevers at 48 hour intervals. Each febrile episode was followed by pronounced fatigue and a subsequent recovery back to her usual state of health. She reported

Blood glutathione status during exercise: effect of carbohydrate supplementation.

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Blood glutathione status and activities of antioxidant enzymes have been investigated during prolonged exercise with or without carbohydrate (CHO) supplementation. Eight subjects cycled at approximately 70% of maximal oxygen uptake to fatigue [134 +/- 19 (SE) min] on the first occasion (control,

Free radical theory of erythrocyte aging.

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Mature, circulating mammalian erythrocytes have a finite lifespan. The molecular mechanism that determines removal of cells from the circulation remains unknown, but probably involves recognition of senescence antigens by phagocytes, either directly or via an antibody/complement-mediated pathway. It

[Metabolism of thyroid gland cells as affected by prolactin and emotional-physical stress].

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A study was made of the role of prolactin (PRL) in the regulation of thyroid function in intact animals and in those exposed to stress (swimming was used as physical exercise). A single daily dose of 125 micrograms of PRL per 100 g of body mass was injected subcutaneously in 0.5 ml of saline

Acute haemolytic anaemia and myolysis due to G6PD deficiency.

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A 2-year-old African-American male patient with sickle cell trait developed cough, red coloured urine, pallor and fatigue. The patient was hospitalised. Diagnostic workup showed that he was glucose 6 phosphate dehydrogenase (G6PD) deficient in erythrocytes. He also had chest X-ray findings of

Aseptic meningitis, hemolytic anemia, hepatitis, and orthostatic hypotension in a patient treated with trimethoprim-sulfamethoxazole.

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OBJECTIVE The case of a patient who developed aseptic meningitis, hemolytic anemia, hepatitis, and orthostatic hypotension simultaneously during treatment with trimethoprim-sulfamethoxazole is described. BACKGROUND A healthy 37-year-old African- American man was receiving treatment with

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