A rare cause of dilated cardiomyopathy: hypocalcemia

SUMMARY Dilated cardiomyopathy (DCM) is characterized by systolic dysfunction and is usually idiopathic. A rare cause of reversible DCM is hypocalcemia. Calcium plays a key role in myocardial contraction. Hypocalcemia can lead to a decrease in contraction, left ventricular systolic dysfunction, and heart failure with reduced ejection fraction (EF). Hypocalcemia-related reversible DCM reports are rare. Herein, we present two cases with heart failure caused by hypocalcemia developed due to hypoparathyroidism. The first case presented with severe heart failure and an extremely low serum calcium level (4.4 mg/dL) due to idiopathic hypoparathyroidism. The second case, which was also admitted with heart failure due to hypocalcemia, had iatrogenic hypoparathyroidism due to a subtotal thyroidectomy. In both cases, patients had reduced left ventricular systolic functions (EF was 33% and 42%, respectively). After calcium replacement and heart failure treatment, calcium levels were normalized. A significant and rapid improvement in heart failure was achieved in both cases (EF 60% and 50%, respectively). Serum calcium levels should always be measured in patients with heart failure, and the etiology of hypocalcemia should be sought. In addition to the standard pharmacotherapy of heart failure with reduced EF, calcium supplementation is essential for treating these patients.

Malnutrition treatment and follow-up in clinical nutrition outpatient clinics associated with increased muscle mass.

OBJECTIVE: Clinical nutrition outpatient clinics (CNOCs) are the mainstay of the nutrition bundle in hospitals. They are important for the diagnosis, treatment, and follow-up of outpatients with malnutrition (MN) and sarcopenia. The aim of this study was to evaluate changes in muscle mass during the treatment of MN in patients admitted to CNOCs. METHODS: A total number of 1118 patients were included in this retrospective cohort descriptive study. Data including medical history, weight loss, anthropometric measurements, MN diagnosis (according to ESPEN definition), nutrition treatment, bioelectrical impedance analysis and laboratory examinations were noted for the first admission and the follow-up. RESULTS: This retrospective, cohort descriptive study included 1118 patients. The mean age of the participants was 54 ± 22 y (18-101 y) and half of the patients were men. Of the 1118 patients, 37,7% were ≥65 y of age. Cancer (32.2%) was the most frequent diagnosis followed by diabetes (16.7%) and dementia (11.3%). MN prevalence was 51.6%. Protein- and energy-enriched diet, oral enteral nutrition supplementation, tube enteral feeding, and parenteral nutrition were used in 42.7%, 69.6%, 11%, and 2.7% of the patients with MN, respectively. Skeletal muscle mass was significantly increased in MN, cancer, neuromuscular diseases (NMD) and patients ≥65 y of age in the first 6 mo, and could be maintained during the next 6 mo of follow-up. Patients with cancer, chronic kidney disease, and NMD and those ≥65 y of age were able to increase their body mass index. CONCLUSIONS: MN treatment and follow-up can restore muscle mass especially in patients ≥65 y of age and in those with chronic diseases. CNOCs are beneficial in the treatment and follow-up of MN.

A rare cause of dilated cardiomyopathy: hypocalcemia.

Dilated cardiomyopathy (DCM) is characterized by systolic dysfunction and is usually idiopathic. A rare cause of reversible DCM is hypocalcemia. Calcium plays a key role in myocardial contraction. Hypocalcemia can lead to a decrease in contraction, left ventricular systolic dysfunction, and heart failure with reduced ejection fraction (EF). Hypocalcemia-related reversible DCM reports are rare. Herein, we present two cases with heart failure caused by hypocalcemia developed due to hypoparathyroidism. The first case presented with severe heart failure and an extremely low serum calcium level (4.4 mg/dL) due to idiopathic hypoparathyroidism. The second case, which was also admitted with heart failure due to hypocalcemia, had iatrogenic hypoparathyroidism due to a subtotal thyroidectomy. In both cases, patients had reduced left ventricular systolic functions (EF was 33% and 42%, respectively). After calcium replacement and heart failure treatment, calcium levels were normalized. A significant and rapid improvement in heart failure was achieved in both cases (EF 60% and 50%, respectively). Serum calcium levels should always be measured in patients with heart failure, and the etiology of hypocalcemia should be sought. In addition to the standard pharmacotherapy of heart failure with reduced EF, calcium supplementation is essential for treating these patients.