investigation of plasma glucose-6-phosphate dehydrogenase, 6-phoshogluconate dehydrogenase, glutathione reductase in premenauposal patients with iron deficiency anemia

Iron is an essential element that is necessary for all cells in the body. Iron deficiency anemia [IDA] is one of the most common nutritional disorders in both developed and developing countries. The glutathione pathway is paramount to antioxidant defense and glucose-6-phosphate dehydrogenase [G6PD]-deficient cells do not cope well with oxidative damage. The goal of this study was to check the activities of G6PD, 6-phosphogluconate dehydrogenase, glutathione reductase in patients with IDA. We analyzed the plasma samples of 102 premenopausal women with IDA and 88 healthy control subjects. Glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activity as compared to the reduction of NADP +, glutathione reductase activity was performed based on the oxidation of NADPH. 2 ml of plasma were used in all analyzes. SPSS program was used for all of the statistical analysis. Diagnosis of iron deficiency in patients belonging to the analysis of blood were ferritin 3.60 +/- 2.7 ng / mL, hemoglobin 9.4 +/- 1.5 mg / dl and hematocrit 30.7 +/- 4.1% ratio; in healthy subjects ferritin 53.5 +/- 41.7 ng/ml, hemoglobin level 13.9 +/- 1.3 mg / dl and hematocrit ratio 42 +/- 3.53%. When compared to healthy subjects the glutathione reductase level [P < 0.001] was found to be significantly higher in patients with IDA. IDA patients with moderate and severe anemia had lower GR activity when compared to IDA patients with mild anemia. But the plasma levels of glucose-6-phosphate dehydrogenase [P<0,600] and 6-phosphogluconate dehydrogenase [P < 0.671] did not show any differences between healthy subjects and in patients with IDA. It was shown that Glucose-6-Phosphate Dehydrogenase and 6-Phosphogluconate Dehydrogenase have no effect on iron-deficiency anemia in patients. The plasma GR levels of premenopausal women with IDA were found to be higher compared to healthy subjects, which could be secondary to erythrocyte protection against oxidative stress being commonly seen in IDA

hepatitis C-positive patient with new onset of nephrotic syndrome and systemic amyloidosis secondary to common variable immunodeficiency

Common variable immunodeficiency [CVID] is a heterogenous group of predominantly antibody-deficiency disorders that make up the greatest proportion of patients with symptomatic primary hypogammaglobulinemia. The rare coincidence of amyloidosis and hypogammaglobulinemia has been reported previously. Contrary to the usual insidious, slowly progressive disease following hepatitis C infection, a rapidly progressive cirrhotic form can develop in hypogammaglobulinemic patients. We report a HCV-positive patient with a new onset of nephrotic syndrome and systemic amyloidosis secondary to CVID. Blood analyses showed serum creatinine of 1.8 mg/dL and serum albumin of 3.1 gm/dL; 24-h urinary protein was 11 800 mg/day. Serum immunoglobulin levels were IgG 340 mg/dL, IgM 18 mg/dL, IgA 11 mg/dL. Duodenal biopsy revealed AA-type amyloidosis with potassium permanganate and Congo red staining. After a month of antiproteinuric therapy, the proteinuria was reduced to 3350 mg/day