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A Sweet Source of Abdominal Pain T h e new england journal o f medicine clinical problem-solving A Sweet Source of Abdominal Pain Shari S. Rogal, M.D., M.P.H., Chinweike Ukomadu, M.D., Ph.D., Bruce D. Levy, M.D., and Joseph Loscalzo, M.D., Ph.D. In this Journal feature, information about a real patient is presented in stages (boldface type) to an expert clinician, who responds to the information, sharing his or her reasoning with the reader (regular type). The authors’ commentary follows. From the Clinical Pathological Conference A 25-year-old woman presented to her primary care physician for evaluation of ab- Series, Department of Medicine, Brigham dominal pain. Her discomfort had begun 6 months earlier and was localized to the and Women’s Hospital, and Harvard Medical School — both in Boston. Ad- right upper quadrant of the abdomen. She described a constant pressure unrelated to dress reprint requests to Dr. Levy at food intake that was associated with intermittent nausea and vomiting. She reported Brigham and Women’s Hospital, Harvard no change in urine or stools and no hematochezia, melena, dysphagia, anorexia, in- Institutes of Medicine Bldg., Ave. Louis Pasteur (HIM855), Boston, MA 02115, or crease in abdominal girth, early satiety, or change in weight. She also had no leth- at [email protected]. argy, fatigue, pruritus, jaundice, night sweats, fever, easy bruising, or bleeding. N Engl J Med 2011;364:1762-7. Copyright © 2011 Massachusetts Medical Society. Appropriate characterization of abdominal pain is the first step in identifying its cause. It is important to ask about the location of the pain and its quality, duration, relationship to meals, radiation, and any associated symptoms. In this patient, the pain is described as “pressure” in the right upper quadrant of the abdomen and is unrelated to meals; these characteristics decrease the likelihood that disorders of the gallbladder or bowel are the cause. Dyspepsia is a common cause of pain but tends to be intermittent and related to diet. Pain that feels like pressure is common with hepatic capsular stretch and raises the possibility that her discomfort is of An Interactive hepatic origin. Medical Case related to this The patient’s medical history was notable for type 1 diabetes mellitus, which had been Clinical Problem- diagnosed in childhood and was complicated by several episodes of diabetic ketoaci- Solving article is available at dosis, hypothyroidism, psoriasis, and a seizure disorder, as well as juvenile rheuma- NEJM.org toid arthritis, which was diagnosed when she was 18 months of age, after the devel- opment of arthritis in her right ankle and uveitis in both eyes. Her growth was normal despite eventual involvement of arthritis in both ankles and knees. She had been treated with naproxen, methotrexate, and glucocorticoids. Her current medications included carbamazepine, methotrexate, levothyroxine, and insulin. Her cumulative dose of methotrexate was 1.3 g. She reported no use of over-the-counter medications or herbal supplements. She worked as a nurse, was unmarried, and had no children. She smoked seven cigarettes a day and had done so for 10 years. She said she did not use alcohol or illicit drugs and had no history of blood transfusions, no occupational exposure to blood, and no tattoos. She was not sexually active and had no history of sexually transmitted infections. There was no family history of diabetes, arthritis, autoimmune diseases, or liver disease. Although it is possible that the patient’s nonspecific symptoms are due to gastritis or gastroparesis, her medical history supports a hepatic cause of her abdominal discomfort. Given prior episodes of diabetic ketoacidosis, she may have poorly con- trolled diabetes, which could have caused steatohepatitis and then hepatomegaly. The nausea and vomiting could be related to diabetes-induced gastroparesis or hepa- 1762 n engl j med 364;18 nejm.org may 5, 2011 The New England Journal of Medicine Downloaded from nejm.org by alieh pourdast on March 11, 2013. For personal use only. No other uses without permission. Copyright © 2011 Massachusetts Medical Society. All rights reserved. clinical problem-solving titis. She could have autoimmune hepatitis, which per deciliter (53.0 μmol per liter), and glucose 217 is more likely, given her sex and other autoim- mg per deciliter (12 mmol per liter). The level of mune disorders, including type 1 diabetes melli- alanine aminotransferase was 443 U per liter (nor- tus, juvenile rheumatoid arthritis, and hypothy- mal range, 7 to 52), aspartate aminotransferase roidism. Toxin-induced hepatitis is a possibility 218 U per liter (normal range, 9 to 30), alkaline and may have been caused by several of her med- phosphatase 145 U per liter (normal range, 38 to ications, including methotrexate, carbamaze pine, 118), total bilirubin 0.5 mg per deciliter (8.6 μmol glucocorticoids, and nonsteroidal anti inflam ma- per liter), total protein 7.4 mg per deciliter, albu- tory drugs; she reports no alcohol use. Apart from min 4.4 g per deciliter, and globulin 3.0 mg per her work as a nurse, she has no obvious risk fac- deciliter. Amylase and lipase levels were normal. tors for viral hepatitis. There is no family history The white-cell count was 6630 per cubic millime- of liver disease, which reduces but does not elim- ter, with a normal differential count; hematocrit inate the possibility of an inherited disorder, such 38.5%, with a mean corpuscular volume of 110 fl as hemochromatosis, Wilson’s disease, or alpha1- and a red-cell distribution width of 14.6%; and antitrypsin deficiency. platelet count 383,000 per cubic millimeter. Levels of vitamin B12 and folic acid were normal. The in- On physical examination, the patient was a thin, ternational normalized ratio was 0.9. anicteric woman who was not in acute distress. She was afebrile; her pulse was 109 beats per min- The most significant abnormalities are the ele- ute, blood pressure 122/90 mm Hg, weight 46 kg vated hepatic enzyme levels; the patient also has (101 lb), and height 152 cm (60 in.). The jugular a high mean corpuscular volume, an elevated ra- venous pressure was not elevated. Examination tio of blood urea nitrogen to creatinine, and hy- of the heart and lungs was unremarkable. The ab- perglycemia. The differential diagnosis at this domen was nondistended and soft, with normal point includes common causes of chronic liver bowel sounds. She had mild tenderness on palpa- injury: drug-induced hepatitis, viral hepatitis, and tion in the right upper quadrant, with no rebound inherited iron-overload disorder. Also under con- or guarding. Murphy’s sign was absent. The liver sideration is nonalcoholic fatty liver disease — was palpable 3 to 4 cm below the costal margin, specifically, nonalcoholic steatohepatitis, a sub- with a measured span of 14 cm at the midclavicu- type of nonalcoholic fatty liver disease in which lar line. The edge of the liver was smooth. The fatty infiltration of the liver is accompanied by spleen was not palpable, and there was no evi- evidence of other liver injury, including inflam- dence of ascites. Examination of the skin revealed mation and fibrosis. Given her history of autoim- scaly plaques on her scalp, ears, and the extensor mune disorders, autoimmune hepatitis is also a surfaces of her arms and legs. She had no vesicular concern. In addition, acquired glycogen deposi- lesions, palmar erythema, leg edema, or spider tion disease merits consideration, given the pres- angiomata. The results of neurologic examina- ence of type 1 diabetes mellitus. Less common tion, including mental status, were normal. causes of hepatitis and hepatomegaly include thyroid disease, celiac sprue, the Budd–Chiari Physical examination reveals an enlarged liver syndrome, and deposition diseases of the liver, but no evidence of an enlarged spleen, making it such as amyloidosis, sarcoidosis, and Gaucher’s less likely that the patient has severe portal hyper- disease. tension from cirrhosis or an infiltrative process The possibility of drug-induced hepatitis (both of which are common causes of hepato- should be assessed by obtaining a thorough megaly and splenomegaly). Congestive hepatopa- medical history of the patient and her family, thy is also unlikely, given her normal cardiovas- with attention to over-the-counter medications cular examination. and herbal supplements (e.g., kava, pennyroyal, comfrey, and germander). In addition, her use of Laboratory studies showed that the sodium level medications with potential hepatotoxic effects was 137 mmol per liter, potassium 4.1 mmol per raises some concerns. Methotrexate has been re- liter, chloride 97 mmol per liter, bicarbonate 31 ported to cause liver injury, but her cumulative mmol per liter, blood urea nitrogen 29 mg per dose of less than 1.5 g makes this unlikely. Al- deciliter (10.4 mmol per liter), creatinine 0.6 mg though carbamazepine can cause hepatitis, it also n engl j med 364;18 nejm.org may 5, 2011 1763 The New England Journal of Medicine Downloaded from nejm.org by alieh pourdast on March 11, 2013. For personal use only. No other uses without permission. Copyright © 2011 Massachusetts Medical Society. All rights reserved. T h e new england journal o f medicine seems unlikely to be the culprit here, since the The serologic findings rule out chronic hepatitis associated hepatitis is often severe. B and C, and the positive result for hepatitis B Wilson’s disease occurs in young adults and surface antibody is consistent with prior vaccina- should be considered in any patient younger tion. Iron overload is unlikely, given the normal than 40 years of age with unexplained hepatitis. iron studies; the aminotransferase levels are also A decreased ceruloplasmin level and Kayser– higher than in typical cases of iron-overload dis- Fleischer rings (brownish copper deposits around ease.
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