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INTRODUCTION: Toxic hepatitis is a common cause of elevated liver enzymes. In the literature, there are case reports about the development of hypercholesterolaemia and related pseudohyponatremia as a result of the deterioration of lipoprotein excretion in the course of toxic hepatitis. In this article, we present a case of hyponatremia due to toxic hepatitis induced hypercholesterolaemia. CASE: The 58-year-old male patient was hospitalized 5 weeks ago at a different hospital because of hyperglycemia. After blood glucose regulation, atorvastatin, terbinafine, pancreatin, vildagliptin, desloratadine, domperidone were prescribed and discharged. Liver enzymes were found to be high in their follow-up and no specific factor was found in the etiology. T. bilirubin and d. bilirubin were found high and Na was found low in the patient who started jaundice 3–4 days ago. The patient was admitted to the clinic with the diagnosis of acute hepatitis. His medical history included toxic hepatitis due to terbinafine use (6 years ago), diabetes mellitus, hyperlipidemia, and onychomycosis. The patient was considered as toxic hepatitis due to terbinafine use because of its history of toxic hepatitis due to terbinafine use. Liver enzymes regressed in follow-up. In the patient with euvolemic hyponatremia, in the laboratory tests performed for etiology, aldosterone, plasma renin activity, sodium (24 hours in urine), cortisol (fasting), TSH were normal and measured serum osmolarity 275 mOsm/kg, calculated serum osmolarity 257 mOsm/kg, osmotic gap 18, urine osmolarity 618 mOsm/kg were found. Isoosmotic hyponatremia was considered. Total protein, albumin/globulin ratio, and lipid profile were re-studied despite normal results and T. cholesterol:1274 mg/dl, triglycerides:208 mg/dl, LDL:1160 mg/dl, total protein 5.53 g/dl, albumin 3.30 g/dl were found. The patient was considered to have pseudohyponatremia due to hypercholesterolemia. The measured serum viscosity was 2.55 cP. Because of he had abdominal pain, he was started lipid apheresis and had 3 sessions. Sodium and lipid profile of the patient improved, abdominal pain regressed. Hyponatremia and hypercholesterolemia were not observed during the follow-up period. DISCUSSION: Toxic hepatitis is a common cause of elevated liver enzymes. There are reports in the cases of cholestatic acute hepatitis that the lipoproteins are not discharged into bile and that hypercholesterolemia may develop in these patients. In the literature, there are case reports of hypercholesterolemia and associated pseudohyponatremia in cholestatic liver diseases. Our case also had cholestatic liver damage. The patient who had normal lipid profile and sodium level before liver injury was diagnosed pseudohyponatremia due to cholestatic liver injury related hypercholesterolemia. CONCLUSION: When hyponatremia is detected in patients presenting with cholestatic liver injury, pseudohyponatremia due to hypercholesterolemia should be kept in mind in addition to common etiologic factors.

INTRODUCTION: Giant cell hepatitis is a disease usually described in the newborn and rarely seen in adults. Various viruses, drugs and autoimmune diseases are responsible for etiology. In some case series, autoimmune liver disease is involved in the etiology of approximately 40% of cases. Clinical spectrum; changing from acute hepatitis to chronic liver disease, can lead to fatal liver failure. CASE: A 19-year-old man visited our hospital due to generalized symptoms. In 2013, a diagnosis of autoimmune hepatitis was made in the outside center. Medical treatmant with methylprednisolone, azathioprine and ursodeoxycholic acid was started. Patient was admitted to intensive care unit due to systemic infections and septic status. Therefore treatment of azatiopurine was discontinued. The patient developed hyponatremia and encephalopathy, and referred to our institution for evaluation of liver transplantation. On physical examination; the patient was lethargic and icteric, had flapping tremor, rales in the middle and upper zones of the lungs and generalized acid. (MELD score: 35, Child-Pugh score: 14 (C)). Coombs positive hemolytic anemia was present in the patient. When the liver pathology specimens from 2013 were re-evaluated; chronic active hepatitis which including multinuclear giant hepatocytes were reported. The patient was diagnosed as giant cell hepatitis and autoimmune hemolytic anemia. Intravenous methylprednisolone (40 mg) treatment was started. We planned liver transplantation for the patient due to chronic liver disease-acute exacerbation. But liver transplantation could not be done due to infection status. The patient have developed cardiac arrest secondary to pneumonia/sepsis and died on the 9th day of hospitalization. DISCUSSION: Giant cell hepatitis is a progressive disease which has high mortality. If the liver transplantation is not performed, survival would be approximately 50%. Giant cell hepatitis is a histopathological diagnosis that can be caused by many etiological factors rather than a specific disease. In the correct diagnosis and treatment of this pathology, both clinical and pathological examinations require more than routine examinations. Since the disease is progressive and mortality is high, liver transplantation should be considered during the follow-up period.

Background/aim: Many autoimmune diseases occur concomitantly with celiac disease (CD). We aimed to determine the frequency of Sjögren's syndrome (SS) in CD patients based on SS-specific serology verified by minor labial salivary biopsy. Materials and methods: Eight-two patients with CD were included in the study. After examination for objective evidence of sicca complex, all patients were tested for serological presence of rheumatoid factor (RF) and antinuclear antibodies (ANAs) and for ANA profile. Minor labial salivary biopsy was performed for patients with positive serology and/or clinical signs of SS. Results: Of the patients included, 24 (29.3%) had dry eye symptoms while 20 (24.4%) had dry mouth symptoms. Dry eye was detected by Schirmer test in 10 patients (12.2%) and by ocular staining score in only 2 patients (2.4%). All samples were negative for RF while 12 (14.6%) samples were positive for ANAs. Of 82 patients with CD, the diagnosis of SS was established in only one patient (1.2%), while one patient (1.2%) was diagnosed with morphea and 4 patients (4.9%) were classified as having undifferentiated connective tissue disease. Conclusion: The prevalence of SS in CD is low, so there is no need for serologic screening of all patients with CD for SS.

Amaç: Diyabetik ve non-diyabetik kişilerde anksiyete vedepresyon prevalansının sosyo-demografik ve klinik risk faktörleri ile ilişkiliolarak belirlenmesi Yöntemler: Bu kesitsel ankete dayalı çalışmaya toplam 217 tip 2diabet hastası (ortalama (SS) yaş: 53.7(8.1) yıl, %56.7’si kadın) ve non-diyabetik100 sağlıklı kontrol (ortalama (SS) yaş: 36.9(10.6) yıl, %67.0’si kadın) dahiledildi. Hastane Anksiyete ve Depresyon Ölçeği (HADS) için anksiyete (HADS-A) vedepresyon (HADS-D) alt ölçek skorları sosyo-demografik ve diyabete ilişkinözellikler bağlamında diyabetik ve non-diyabetik hastalarda, değerlendirildi. Bulgular: Sınırda veya anormal anksiyete ve depresyonprevalansları açısından diyabetik (sırasıyla %42.4 ve %35.5) ve non-diyabetik(sırasıyla %49.0 ve %39.0) gruplar arasında anlamlı bir farklılık saptanmadı. Diyabetikgrupta, kadın cinsiyeti (sırasıyla, p, Objective: To determine theprevalence of anxiety and depression in diabetic versus non-diabetic persons inrelation to socio-demographic and clinical risk factorsMethods: A total of 217 patientswith type 2 diabetes mellitus (mean(SD) age: 53.7(8.1) years, 56.7% werefemales) and 100 age-matched non-diabetic control subjects (mean(SD) age:36.9(10.6) years, 67.0% were females) were included in this cross-sectionalquestionnaire based survey. Hospital Anxiety and Depression Scale (HADS)subscale scores for anxiety (HADS-A) and depression (HADS-D) were evaluated indiabetic patients in comparison to non-diabetics as well as in relation tosocio-demographic and diabetes related characteristics.Results: Similar prevalence of anxiety and depression was noted in diabetic(42.4% and 35.5%, respectively) and non-diabetic (49.0% and 39%, respectively)groups. In the diabetic group, female gender (p

Fifty six years old male patient admitted to our clinic with cholangitis due to anastomosis stricture after liver transplantation. Percutaneous transhepatic cholangiography (PTK) was performed and imipenem was started. Teicoplanin was added to treatment at 10th day because of fewer and elevated WBC. Tonic clonic epileptic seizures was developed 1 day after the teicoplanin was started. Cranial CT, MRI and EEG is performed. Only chronic ischemic changes was seen in MRI. At laboratory analysis, serum sodium level was 124 mEq/L and was corrected. Levetiracetam was started. The patient was entubated because of metabolic asidosis due to repeated epileptic seizures. Because of seizures started after teikoplanin and that we could not find any etiologic factor, we thought that seizure was induced by teicoplain. The drug was stopped and seizures ended. But the patient died due to ventilator associated pneumonia. Teicoplanin induced seizure must be kept in mind in infected patients with seizures., Elli altı yaşında erkek hasta karaciğer nakli sonrası anastomoz darlığı ve kolanjit tanısı ile kliniğimize başvurdu. Hastaya perkütan transhepatik kolanjiografi (PTK) yapıldı. Kolanjit tanısı ile imipenem başlandı. Ancak ateş ve beyaz küre değerinde yükseklik olması üzerine imipenem tedavisinin 10. gününde teikoplanin eklendi. İlaç başlandıktan bir gün sonra tonik klonik epileptik nöbetleri oldu. Kranial bilgisayarlı tomografi (BT), elektroensefalografi (EEG) ve kranial magnetik rezonans görüntüleme (MRG) çekildi. Sadece MRG’de kronik iskemik değişiklikler saptandı. Laboratuvar analizinde kan sodyum 124 mEq/L saptanan hastaya replasman tedavisi yapıldı. Hastaya levetiracetam başlandı. Epileptik atakları tekrarlayan hastada metabolik asidoz gelişti ve entübe edildi. Teikoplanin verilmesinden hemen sonra başlaması ve diğer etiyolojik faktörlerin dışlanması nedeniyle nöbetlerin teikoplanine bağlı olabileceği düşünüldü ve hastanın ilacı kesildi. İlaç kesilmesi sonrası nöbetler kesildi. Ancak ventilatöre bağlı pnömoni gelişen hasta exitus oldu. Enfekte ve teikoplanin alan bir hastada nöbet varlığında ilaca bağlı nöbet akılda tutulmalıdır.