AMIODARONE AND THYROID DYSFUNCTION.

Thyroid gland has a key role in maintaining the body homeostasis. Thyroxine is the main hormone secreted from the thyroid gland, its effect being predominantly achieved after the intracellular conversion of thyroxine to triiodothyronine, which exhibits a higher affinity for the receptor complex, thus modifying gene expression of the target cells. Amiodarone is one of the most commonly used antiarrhythmics in the treatment of a broad spectrum of arrhythmias, usually tachyarrhythmias. Amiodarone contains a large proportion of iodine, which is, in addition to the intrinsic effect of the medication, the basis of the impact on thyroid function. It is believed that 15%-20% of patients treated with amiodarone develop some form of thyroid dysfunction. Amiodarone may cause amiodarone-induced hypothyroidism (AIH) or amiodarone-induced thyrotoxicosis (AIT). AIT is usually developed in the areas with too low uptake of iodine, while AIH is developed in the areas where there is a sufficient iodine uptake. Type 1 AIT is more common among patients with an underlying thyroid pathology, such as nodular goiter or Graves' (Basedow's) disease, while type 2 mostly develops in a previously healthy thyroid. AIH is more common in patients with previously diagnosed Hashimoto's thyroiditis. Combined types of the diseases have also been described. Patients treated with amiodarone should be monitored regularly, including laboratory testing and clinical examinations, to early detect any deviations in the functioning of the thyroid gland. Supplementary levothyroxine therapy is the basis of AIH treatment. In such cases, amiodarone therapy quite often need not be discontinued. Type 1 AIT is treated with thyrostatic agents, like any other type of thyrotoxicosis. If possible, the underlying amiodarone therapy should be discontinued. In contrast to type 1 AIT, the basic pathophysiological substrate of which is the increased synthesis and release of thyroid hormones, the basis of type 2 AIT is destructive thyroiditis caused by amiodarone, desethylamiodarone as its main metabolite, and an increased iodine uptake. Glucocorticoid therapy is the basis of treatment for this type of disease.

Hypertriglyceridemia-induced pancreatitis treated with continuous insulin infusion-Case series.

OBJECTIVE: There are no definitive treatment guidelines for hypertriglyceridemia (HTG)-induced acute pancreatitis (AP). The aim of this retrospective study was to evaluate the efficacy of insulin in decreasing triglyceride (TG) levels in patients with HTG-induced AP. DESIGN: We included 17 cases of HTG-induced AP treated with continuous insulin aspart for 4 days. PATIENTS: Fifteen patients were male, two were female. The mean TG level at admission was 56.53 ± 25.29 mmol/L. The mean APACHE II score was 10.2 ± 5.7, Ranson 4.2 ± 1.7 and Balthazar 6.5 ± 2.6, implying a severe form of the disease. METHODS: In an 8-year period, 17 patients with a diagnosis of HTG-induced AP were treated with a continuous infusion of 5% dextrose and insulin aspart in an attempt to lower TG levels. TG levels were assessed on admission, the second and fourth day of therapy. The patient outcome, complications and recurrence of AP were monitored. RESULTS: A significant reduction of TG levels was observed in all patients on Day 4. All patients survived, with one forming a giant pseudocyst as a disease complication, one needing haemodialyses treatment due to an acute kidney injury, and one developing acute respiratory distress syndrome that required mechanical ventilation for 4 days. All patients recovered completely. CONCLUSION: Our study showed that continuous insulin aspart infusion decreases TG levels in HTG-induced AP from a mean TG level of 56.53 mmol/L on Day 1 to 21.75 mmol/L on Day 2 and finally to 6.86 mmol/L on Day 4. We consider this therapy very efficient, safe, simple to administer and monitor.