There are pregnancy-related conditions which may or may not be hypertensive in origin but which can cause serious illness and diagnostic problems. One such condition is characterized by hemolysis, elevated liver enzyme activity, and low platelet count, and is known as the HELLP syndrome. There is disagreement as to whether the syndrome represents a separate disease entity or whether it is a part of the preeclamptic process. In either case, it is important to identify the variations correctly because they indicate a “sick” pregnancy in which both mother and baby are at grave risk.The present authors report the case of a woman who had some degree of pregnancy-induced hypertension, but in whom the presence of jaundice, abdominal pain, and a single gallstone was thought to represent a co-existent obstructive cholecystitis. Actually, she was suffering from a well-developed HELLP syndrome, and the gallstone was not related to her condition.The 26-year-old woman was admitted to a country hospital with pregnancy-induced hypertension and upper abdominal pain. Her blood pressure was 130/90 mm Hg, and she had ankle edema but no proteinuria. Her conjugated and total bilirubin levels, aspartate aminotransferase activity, and alkaline phosphatase activity were distinctly elevated. Because of her chemical state of jaundice and the repeated episodes of upper abdominal pain, a gall bladder ultrasound examination was performed on the 4th day after admission. This showed a solitary, large, mobile calculus within the gall bladder. Gall bladder, bile ducts, liver, and pancreas were normal in appearance. By the 5th day in hospital, the patient was jaundiced clinically and showed bile and urobilinogen in her urine.On the 8th hospital day, the patient's blood pressure was 140/100 mm Hg, and her urinary output was recorded as 300 ml in 24 hours. She had edema of the legs and sacrum, and she complained of pain in the right upper abdomen. She was transferred to the authors' hospital, where an investigation for HELLP syndrome was begun. A complete blood picture showed a hemoglobin level of 104 gm/liter (normal, 110–135 gm/liter), a platelet count of 49 × 109/liter (normal, 150–400 × 109/liter), and a reticulocyte count of 4.2 per cent (normal, 0.2–2.0 per cent). The numerous spherocytes and fragmented cells that were found were consistent with microangiopathic hemolysis. This was confirmed later by a reduced serum haptoglobin level of 0.2 gm/liter (normal, 0.45–2.35 gm/ liter). The multiple blood analysis showed mixed hyperbili-rubinemia, elevation of all liver enzyme activities, a distinctly raised uric acid level that was consistent with pre-eclampsia, and a reduced serum albumin level, which probably contributed to the patient's peripheral edema.Preparations were made to expedite delivery of the infant and within 3 hours of induction, the patient spontaneously delivered (vaginally), a live male infant weighing 2.34 kg, with Apgar scores of 7 and 10 at 1 and 5 minutes, respectively. The recorded blood loss at delivery was 250 ml.The next day the patient's blood pressure was settling, her hemoglobin level was 101 gm/liter, and her platelet count was 127 × 109/liter. By the 3rd postpartum day, however, her hemoglobin level had dropped to 82 gm/liter, and her platelet count had decreased to 63 × 109/liter. The blood film confirmed the continuing presence of microangiopathic hemolysis. The blood chemistry was improving, but the patient was still jaundiced. In view of the continuing nature of the HELLP process, four units of packed red blood cells were given to the patient.Subsequently, slow but steady improvement was made. On the 6th postpartum day, the patient's hemoglobin level was 114 gm/liter, and her platelet count was 164 × 109/ liter. She was discharged on the 20th day after delivery. The need for a cholecystectomy was to be decided by her general practitioner.