ACTA ENDOCRINOLOGICA (BUC)

Context. Severe hypertriglyceridemia (SH), which calls for a triglyceride (TG) level above 1000 mg/dL, remains an important health issue. While some data exist to offer combination of heparin, insulin and fenofibrate as a reasonable treatment option, safety and benefits of this therapy have not been accurately weighted, largely due to the limited sample size of the relevant studies. Aim. Assess the efficacy and safety of the heparin, insulin and fenofibrate combination in the treatment of patients with SH. Patients - Methods. Patients aged ≥18 years with TG level above 1000 mg/dL and adequate organ function were included. Triglyceride levels were measured immediately before the treatment and on the 3rd and 6th days of the treatment. Treatment dosage, duration, response and side effects were assessed. Patients with hypertriglyceridemia presenting with acute pancreatitis were treated additionally with lipid apheresis. Results. A total of 42 patients were included. Of these, 85.8% came to medical attention with some kind of secondary hypertriglyceridemia causes. The baseline median TG value of the cases was 2141.0 mg/ dL (1026-12250). There were 6 patients (14.3%) with acute pancreatitis at presentation. In patients without pancreatitis, with administration of insulin infusion, unfractionated heparin infusion and fenofibrate capsule, median TG values decreased to 921 mg/ dL (190-6400) on the 3rd day and to 437 mg/ dL (112-1950) on the 6th day of the treatment (p<0.0001, Friedman test). Potential toxicities related to insulin, heparin and fenofibrate combination treatment including hypoglycemia, hemorrhage, rise in creatine kinase levels, hepato - and nephrotoxicity were not observed. Conclusion. In this trial involving patients with SH, our data suggest that insulin, heparin and fenofibrate combination therapy was safe and effective.

Background. Langerhans cell histiocytosis (LCH) is a rare group of neoplastic diseases resulting from Langerhans dendritic cells. The most common site (80%) is bones. Thyroid gland involvement is exceedingly rare and usually expected to be seen as a part of multisystemic disease. Case Report. We present a 45 year old male patient operated due to multinodular goiter and neck pain, and diagnosed with LCH in his postoperative pathologic examination. As a result of the systemic screening performed after the pathological diagnosis, the disease was interestingly localized to the thyroid gland. Systemic involvement did not develop in the two-year follow-up of the patient who did not receive additional chemotherapy treatment. Conclusion. It is difficult to diagnose LCH in the thyroid gland before surgery. Although surgical treatment with or without chemotherapy is recommended, surgery is not recommended alone since it is generally systemic involvement. However, in primary thyroid LCH cases limited to the thyroid gland, we recommend that only total thyroidectomy treatment should be kept in mind.

Hypothyroidism is a common endocrine disease with characteristic symptoms and signs such as fatigue, weight gain, intolerance of cold, constipation, depression, mental slowdown and muscle cramps. Myopathic changes are observed in 30-80% of patients with hypothyroidism, but muscular hypertrophy with muscle stiffness has been reported in less than 10% of patients. Hoffmann’s syndrome is a specific form of the hypothyroid-associated myopathy, rarely seen. Symptoms of this syndrome include proximal muscle weakness, hypertrophies in extremities, stiffness, muscle cramps, spontaneous muscle pain; and are associated with increased muscle enzymes. These findings can be seen at any time during hypothyroidism. Hofmann’s syndrome has a very good prognosis. Its response to hormone replacement therapy is very good. Therefore, in patients with myopathylike symptoms, considering in the differential diagnosis that the myopathy may be a reflection of hypothyroidism will facilitate the diagnosis and treatment. In this case, we aimed to present together Hashimoto thyroiditis and muscular hypertrophy, which is an atypical presentation of hypothyroidism and rarely seen in the literature, namely Hoffmann’s syndrome.

COVID-19 is a viral disease that is recognized now as a pandemic by the World Health Organization. It is known that some viral infections may trigger autoimmune diseases. It has been revealed that COVID-19 may also lead to the pathogenesis of some autoimmune diseases, including Type 1 DM (T1DM) and autoimmune thyroid diseases. Here, we aimed to present a young female patient with COVID-19, who we followed up in our clinic, who presented with diabetic ketoacidosis (DKA), and developed Hashimoto’s disease during the treatment process. In order to emphasize that COVID-19 may trigger the emergence of T1DM, that it may mask nonspecific DKA symptoms like nausea and vomiting, that it may cause delay in diagnosis of DKA, and also to emphasize the importance of evaluating other autoimmune diseases accompanying COVID-19, we found it appropriate to present this case.

Background. Drug induced thrombocytopenia is mostly related with nonsteroidal\r\nanti-inflammatory drugs (NSAID), anticonvulsants, sulfonamides, diuretics, cinchona\r\nalkaloid derivatives, penicillamine and gold salts. Oral sulfonylureas such as glibenclamide,\r\nchlorpropamide and glimepiride are known to induce thrombocytopenia.\r\nCase report. We report a 42 year old female admitted to emergency department with\r\na complaint of hematochesia. She has been using oral gliclazide for three years. Laboratory\r\nresults revealed bicytopenia: haemoglobin=8.9 g/dL (N=12.3-15.3), white blood count\r\n(WBC)=12100/&#956;L (N=4400-11300), platelet count=4000/&#956;L (N=150000-450000). All\r\nexaminations to etiology of thrombocytopenia were negative including autoimmune,\r\ninfectious (viral-bacterial) and haematological diseases. Colonoscopic examination showed\r\n50% construction of the lumen in the first 15 cm segment of the colon by an ulcerovegetant\r\nmass. Pathological examination was reported as adenocarcinoma. Thrombocyte levels\r\nincreased on the 4th day after stopping gliclazid treatment.\r\nConclusions. It is the first case of gliclazid induced thrombocytopenia in literature. So\r\nwe recommended that platelet count should be regularly checked in all patients receiving\r\nsulfonylurea drugs including gliclazid.