Abstract
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.