Hepatic Fe overload has often been reported in patients with advanced alcoholic liver disease. However, it is not known clearly whether it is the effect of alcohol that is responsible for such overload. To address this lacuna, a time-course study was carried out in mice in order to determine the effect of alcohol on Fe homoeostasis. Male Swiss albino mice were pair-fed Lieber-DeCarli alcohol diet (20 % of total energy provided as alcohol) for 2, 4, 8 or 12 weeks. Expression levels of duodenal and hepatic Fe-related proteins were determined by quantitative PCR and Western blotting, as were Fe levels and parameters of oxidative stress in the liver. Alcohol induced cytochrome P4502E1 and oxidative stress in the liver. Hepatic Fe levels and ferritin protein expression dropped to significantly lower levels after 12 weeks of alcohol feeding, with no significant effects at earlier time points. This was associated, at 12 weeks, with significantly decreased liver hepcidin expression and serum hepcidin levels. Protein expressions of duodenal ferroportin (at 8 and 12 weeks) and divalent metal transporter 1 (at 8 weeks) were increased. Serum Fe levels rose progressively to significantly higher levels at 12 weeks. Histopathological examination of the liver showed mild steatosis, but no stainable Fe in mice fed alcohol for up to 12 weeks. In summary, alcohol ingestion by mice in this study affected several Fe-related parameters, but produced no hepatic Fe accumulation. On the contrary, alcohol-induced decreases in hepatic Fe levels were seen and may contribute to alcohol-induced suppression of hepcidin.
Background:Pneumatic tube system (PTS) is commonly used in hospital settings to transport blood samples to diagnostic laboratories. At our blood center, we receive blood requisitions via the PTS, but units are carried to the ward by human courier. Recently we considered using the PTS for transporting blood units. Since, there are reports of hemolysis in blood samples sent through the PTS, we evaluated this system for transporting red cell units.Aims:The aim was to assess the effect of PTS transport on the quality of packed red cell units.Materials and Methods:A total of 50 red blood cells units (RBC), (25 non-irradiated and 25 irradiated) were subjected to transportation through the PTS. The control arm in the study was age-matched RBC units not subjected to PTS transport. Each RBC unit was evaluated for hemoglobin (Hb), lactate dehydrogenase, potassium and plasma hemoglobin (Hb). The paired t-test was used to compare these parameters, and the P value was calculated.Results and Conclusion:The percentage of hemolysis after transportation through PTS was below the recommended guidelines. Delivery of the blood unit to the wrong station, bags lying unattended at the destination were few of the problems that had to be addressed. To conclude, though the PTS is a safe means of transporting blood products with reduction in the turn-around-time, it must be validated before use.
Vitamin D toxicity also known as hypervitaminosis D was previously believed to be rare. But with an increase in vitamin D supplementation several cases have been reported in literature. Fat soluble vitamins like Vitamin D, due to their ability to accumulate in the body, have a higher potential for toxicity than water soluble vitamins. The main clinical consequence of vitamin D toxicity is hypercalcemia. In this report we describe an adult female patient who developed very high serum Vitamin D levels (746 ng/mL, RI: 20 to 50) as a result of medication error. Inspite of such high serum concentrations the patient was without any clinical symptoms and had normal serum calcium. We critically discuss the mechanism of toxicity and hypothesize the possible molecular/metabolic factors which might have been responsible for this nontoxic presentation. This case study highlights the fact that physicians need to consider the risk of medication errors while prescribing Vitamin D therapy. Clinical trials to study Vitamin D toxicity in humans is not possible ethically. Thus the evidence base regarding the safety profile of Vitamin D supplementation in humans has been build through case reports. This review of the paradoxical clinico-laboratory manifestation of hypervitaminosis D could possibly contribute to existing literature.
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