Background and objectives: Endothelial dysfunction has been proposed to be an underlying mechanism of the pronounced cardiovascular morbidity in end-stage liver disease (ESLD), but clinical evidence is still limited. In this study, we investigated the association of circulating levels of asymmetric dimethylarginine (ADMA) and nitric oxide (NO) with estimated cardiovascular risk in patients with ESLD awaiting liver transplantation. Materials and Methods: ADMA and NO levels were measured in the sera of 160 adult ESLD patients. The severity of hepatic dysfunction was assessed by the model for end-stage liver disease (MELD) score. The cardiovascular risk was estimated with the European Society of Cardiology Systematic Coronary Risk Estimation (SCORE) index, which was used to dichotomize patients in the subgroups depicting higher and lower cardiovascular risk. Results: Severe hepatic dysfunction (MELD ≥ 18) was present in 38% of the patients, and a higher cardiovascular risk was present in almost half of the patients (N = 74). ADMA and NO both significantly increased with the progression of liver disease and were independently associated with higher cardiovascular risk. Fasting glucose also independently predicted a higher cardiovascular risk, while HDL cholesterol and the absence of concomitant hepatocellular carcinoma were protective factors. Conclusions: These results suggest a remarkable contribution of the deranged arginine/NO pathway to cardiovascular risk in patients with end-stage liver disease.
Methods: This non-randomised prospective study included 77 patients of age ≥ 12 years with confirmed diagnosis of iron deficiency anemia between January 2018 & January 2019. Detailed history was taken & examination performed for signs & etiology of IDA. The cut-off serum ferritin level for IDA diagnosis was < 15 ng/ml. Pregnant females and patients with concurrent vitamin B12 deficiency were excluded. All patients were treated with Injection Ferric Carboxymaltose (FCM) by I.V. infusion over 30 minutes in day care. Total dose of parenteral iron was calculated according to Ganzoni Formula: Total iron deficit (mg) = 2.4 x body weight (kg) x [target haemoglobin -actual haemoglobin (g/dl)] + 500 mg (depot iron). The maximum dose of FCM administered in a single infusion was 1000 mg. Patients with total iron dose > 1000 mg received two divided doses one week apart. Patients also received oral folic acid at 5 mg/day dose for at least 3 weeks. Appropriate workup for etiology of IDA was performed in all patients. Therapeutic response was assessed after 3 weeks of first FCM dose & was defined as hemoglobin increase of ≥ 2 g/dl from baseline. Results: The median age of patients was 33 years (range 16 -75 years) and majority (78%) were females. The median baseline hemoglobin was 5 g/dl (range 2.0 -8.6 g/dl). Therapeutic response was achieved in 100% patients. Mean increase in haemoglobin at 3 weeks was 4.2 g/dl (range 2.8 -5.5 g/dl). One patient had mild headache during FCM infusion. There was no infusion-related toxicity or any other adverse event. Summary/Conclusion: In our study, intravenous ferric carboxymaltose was found to be highly effective & safe alternative to oral iron for treatment of iron deficiency anemia, with excellent patient compliance. It is ideally suited for patients who require rapid replenishment of iron stores.
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