An Unusual Case of Hyperemesis Gravidarum

Author Information
Gupta AS.
(Professor. Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)


An interesting case of hyperemesis gravidarum with elevated hepatic aminotransferases is reported. Despite complete cessation of vomiting the patient’s liver aminotransferases kept rising. All investigations to detect any underlying liver disease were futile. She eventually responded to oral administration of a multivitamin.


Hyperemesis gravidarum is pernicious vomiting of pregnancy that can lead to dehydration, ketoacidosis of starvation, alkalosis, electrolyte imbalance, weight loss, altered liver or renal function and Wernicke’s encephalopathy.[1] It can result in deficiency of vitamins and nutrients due to reduced intake or poor absorption. B complex vitamins are important coenzymes in enzymatic reactions. They are required for normal energy metabolism, thiamine more than the others. Wernicke encephalopathy is a well documented complication of thiamine deficiency in patients of hyperemesis gravidarum.

Case Report

Twenty one year old Gravida 1 presented with a complaint of hyperemesis gravidarum at 8 weeks of pregnancy. She had had persistent vomiting for one week.  She was admitted, kept nil by mouth and was infused with intravenous crystalloids including Ringer lactate solution. Doxylamine and pyridoxine were administered at 8 hour intervals orally with sips of water. On admission her pulse rate was 96/min., BP was 90/60 mm of Hg, tongue was moist, respiratory rate was 18/min. Her uterus was anteflexed, soft and corresponding to 8 weeks size. Her laboratory parameters were as follows: Hb 11.5 g/dl, WBC 7600/mm3. TSH was 1.35 μIU/mL, random blood sugar was 110 mg%, uric acid 3.2 mg%, BUN 11 mg%, serum creatinine 0.8 mg%, SGOT 115 U/L, SGPT 91 U/L, serum electrolytes within normal limits. Urinary ketones were small. After admission the patient had no further episodes of vomiting and she was started on dry carbohydrate diet after 24 hours and oral doxylamine and pyridoxine were continued three times a day. As her liver enzymes were marginally elevated they were repeated. Her serial serum hepatic aminotransferases levels are shown in the table below.

Serial laboratory serum hepatic aminotransferases levels

2nd Jan 14
Day 1
Day 3
Day 6
Day 9
Day 12
Day 15
Day 17
Day 81

Her serum bilirubin, creatinine, BUN, electrolytes, coagulation profile were normal on serial measurements. The liver enzymes showed a rising trend. The patient had no further episodes of vomiting. Her condition was stable and she was tolerating dry solids orally. She was continued on oral doxylamine and pyridoxine three times a day. A coexisting liver disorder was suspected. A gastroenterologist’s opinion was obtained. As per his advise, viral markers, ultrasound (USG) abdomen, ANA, Anti-ds DNA and Anti smooth muscle antibody testing (ASMA) were obtained. All viral markers (HbsAg, HCV, HIV, IgM HbcAb, and IgM HEV) were negative. Autoimmune markers like ANA, Anti-ds DNA, and ASMA (Interglandular Actin Fibers, Muscularis Mucosa, Muscle layers of blood vessels) were all negative. USG abdomen was normal. Liver was normal in size and echo texture. Hepato- portal color Doppler was also normal. Hepatic veins were normal. Middle and lower hepatic vein had common ostia. Right hepatic vein was normal. Spleen was normal. As the liver enzymes showed a rising trend over 12 days and all tests indicating any other liver pathology were negative we were in a dilemma about terminating her pregnancy. However before that we decided to give a multivitamin orally. The contents of that multivitamin were vitamin B1 10mg, vitamin B2 10 mg, Nicotinamide 100 mg, vitamin B6 3 mg, calcium pantothenate 50 mg, Folic acid 1.5 mg, vitamin B12 15 mcg, vitamin C 150 mg. We gave her one tablet of this multivitamin daily and then repeated the liver enzymes after 3 days. The liver enzymes gradually decreased and normalized over the next 15 days. The patient was discharged after a stay of 19 days. The pregnancy is ongoing and is uncomplicated.


Nausea vomiting is common is the first trimester of pregnancy. Incidence of hyperemesis gravidarum is about 0.1-2% pregnancies.[1] Of these about 50% patients have evidence of liver dysfunction as evidenced by deranged liver aminotransferases.[2] The liver enzymes normalize after vomiting resolves. If liver dysfunction persists an underlying liver pathology is to be evaluated.[3] In our patient despite having no vomiting her liver enzymes kept deteriorating. All investigations to detect any underlying viral, autoimmune or ischemic pathology were done but no cause for the rising aminotransferases could be found. B group of vitamins act as a cofactor in many of the chemical reaction in the liver. Use of thiamine for prevention of Wernicke’s encephalopathy is well documented.[4] B complex vitamins have a wide role in enzymatic, non enzymatic regulatory roles. Thiamine is an important cofactor in energy metabolism and is naturally present in the liver.[5] One of the hypothesis of alteration of liver function in patients of hyperemesis is the affect on the fatty acid oxidation in the mitochondria. Starvation also results in increase in circulating fatty acids due to increased lipolysis.[2] Thiamine pyrophosphate, a derivative of thiamine, is required for the carbohydrate metabolism and the Kreb’s cycle. Deficiency of this vitamin may increase the fatty acid metabolism.[6] Niacin is supposed to reduce the triglyceride and secretion of very low density and low density lipoproteins.[7] Riboflavin is believed to be involved in the biosynthesis of coenzyme A reducing  the oxidative stress.[8] Administration of the B complex tablet in this case  may have corrected the energy metabolism and reduced the fatty acid metabolism allowing the liver enzymes to correct themselves. It may be worth trying to administer a multivitamin tablet in cases of hyperemesis gravidarum patients who fail to recover their liver function despite cessation of vomiting.  This may be because the deficiency of the one or more components of the B group of vitamins, especially where they are not stored in the body like thiamine, may persist due to inadequate dietary intake even after vomiting stops. However, we noted a significant decline in the liver enzymes on continuous administration of the B complex tablet in our patient.


B complex administration in intractable elevation of liver aminotransferases is worth a trial especially in those cases of hyperemesis gravidarum whose liver function continues to deteriorate even after control of vomiting and no other cause for the abnormal liver function is detected.


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Gupta AS. An Unusual Case of Hyperemesis Gravidarum. JPGO 2014 Volume 1 Number 5 Available from: