Tag Archives: reactive oxygen species

Hereditary hemochromatosis: Retrospective study on clinical data from Emergency County Hospital Mures

DOI: 10.2478/amma-2022-0031

Objective: Hereditary hemochromatosis, or primary hemochromatosis, is a recessive genetic liver disorder caused by iron accumulation in tissues. This study evaluates patients with hereditary hemochromatosis to determine correlations between clinical and laboratory data.
Methods: The data analyzed in this study was gathered from the discharge records from 2019 to 2021 of the Gastroenterology Department of the Mures Country Emergency Clinical Hospital. 15 patients with hemochromatosis were sampled during the studied period.
Results: Hepatic cirrhosis is present in 67% of the studied group of patients, 40% of patients presented hypertension and 20% of patients showed diabetes mellitus and portal hypertension. Positive correlations were obtained between serum iron and alkaline phosphatase (r=0.8536), between serum iron and lactate dehydrogenase (r=0.7381), and between serum iron and urea (r = 0.79). Positive, strong correlation between ferritin and serum iron (r=0.7719), GOT (r=0.778) and GPT (r=0.6108). total bilirubin and direct bilirubin (r = 0.85), between total bilirubin and GOT (r = 0.68) and GPT (r = 0.82).
Conclusions: Excess iron stored is influencing organ function trough reactive oxygen species, the hepatic signs being a main participant in the clinical presentation, while serum iron cause damage to other tissues such as myocardium, pancreas and kidneys. Treatment for hemochromatosis includes phlebotomies, and iron chelation with Deferoxamine.

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Flow Cytometry Assessment of Bacterial and Yeast Induced Oxidative Burst in Peripheral Blood Phagocytes

DOI: 10.1515/amma-2017-0020

Objective: The aim of this study was to verify in our laboratory conditions the performance criteria of a commercial kit (PhagoburstTM, Glycotope Biotechnology) as described by the producers. We have also partially altered the use of the available kit by introducing a non-opsonized Candida albicans stimulus, in addition to the opsonized Escherichia coli stimulus provided by the manufacturer.
Material and methods: The peripheral blood samples of 6 clinically healthy adults were tested in triplicate according to the manufacturer recommendations. The intra-assay imprecision, as well as the ranges of neutrophil and monocyte burst activation triggered by various stimuli, were assessed.
Results: The activation range of granulocytes and monocytes was similar to the one described by the producer in the presence of E. coli (granulocytes: 78.45-99.43% versus 99.6-99.95%, average %CV of 1.53% versus 0.1%, monocytes: 54.63-92.33% versus 81.80-96.67, average %CV 6.92% versus 1.1%). The leukocyte range of activation in the presence of non-opsonized C. albicans was comparable to the one triggered by the fMLP (N-formyl-methionyl-leucyl-phenylalanine) stimulus.
Conclusion: The intra-assay precision obtained in our laboratory conditions, as well as the ranges of activated leukocytes, are comparable to the ones described by the producer when using E. coli as a stimulus. The present study shows that introducing an extra fungal stimulus for burst oxidation assessment could provide additional information regarding the non-specific cellular immune response, particularly in patients at risk for candidemia.

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