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Hindawi Publishing Corporation Case Reports in Hepatology V olume 2011, Article ID 176894, 2 pages doi:10.1155/2011/176894 Case Report Acut e Liver Injury with Severe Coagulopath y in Marasmus Caus ed by a So matic Delu sional Disorder Lance L. St ei n 1 and Arun B. Je sudian 2 1 Piedmont Tr ansplant Institute, Piedmont Hospital, 1968 Peachtree Road NW, 77 Building, 6th Floor, Atlanta, GA 30309, USA 2 Division of Gastroenterology , New Y ork Presbyterian Hospital, Weill Medical College of Cornell University , 1305 Y ork Avenue, 4th Floor, New York, NY 10021, USA Correspondence should be addressed to Lance L. Stein, [email protected] Received 13 May 2011; Accepted 6 July 2011 Academic Editors: A. Grasso and C. Karaca Copyr ight © 201 1 L. L. Stein and A. B. Jesu dian. This is an open acce ss articl e distri buted under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Marasmus is a severe form of protein-calorie malnutrition characterized by the depletion of fat stores, muscle wasting, and the lack of edema. In developed countries, marasmus is often the result of anorexia nervosa. Abnormal transaminases with liver synthetic dysfunction have rarely been reported with anorexia nervosa. To our knowledge, we report the first detailed case of acute liver injury with severe coagulopathy (INR > 1.5) in a patient with marasmus due to self-induced calorie restriction caused by a somatic delusional disorder. This case highlights the severity of liver injury that may occur with significant weight loss from self-induced calorie restriction and the rapid normalization of this injury with treatment. It is important for clinicians to be aware of patterns of acute liver injury in patients with severe protein-calorie malnutrition, regardless of the underlying cause. 1. Intr oductio n Marasmus is a severe form of protein-calorie malnutrition characterized by the depletion of subcutaneous fat stores, muscle wasting, and the absence of edema. In developed coun tries, marasmu s is commonly the result of anor exia nervosa. Complications of marasmus include bradycardia, hypotension and hypothermia. Abnormal liver transaminas- es with liver synthetic dysfunction have rarely been reported to occur in anorexia nervosa. To our knowledge, we report the first case of acute liver injury with severe coagulopathy (INR > 1.5) in a patient with marasmus caused by a somatic delusional disorder. 2. Cas e Pr esentation A 43-year-old woman was admitted for the evaluation of a 25 kg weight loss resu lting in seve re protei n maln utrition due to inten tiona l calori e restric tion (300 Kcal/day) for six months. She had no previous medical or surgical history and was not receiving medicat ions. The patie nt belie ved that she developed an “autoimmune disease” that improved with self-induced calorie restriction. On presentation, the pat ien t wei ghe d 30.1 kg (BMI 11) , tempera ture 98.6 ◦ F, heart rate 75 bpm, and blood pre ssure 105 /68 mmHg. She was mark edly cachectic with temp oral wasti ng, scaph oid abdomen, and normal liver span without stigmata of cir- rhosis. She was normally oriented and asterixis was absent. Her admissi on laboratory testing reveale d AST (2895 U/L), AL T (1868U/L), alkaline phosp hatase (460U/L), bilirubin (2.9 mg/ dL), alb umi n (3.7 g/d L), INR (1.9), amyla se 188, lipase 322, CPK 535, normal TSH, negative viral hepatitis and autoimmune serologies, ceruloplasmin (17 mg/dL), and elevated 24-hour urine copper (117 mcg). Abdominal ultra- sound reveale d a hete rogen eous liver with patent vess els. A sli t lamp exa m fai led to rev eal Kayser-F lei sch er ring s. Ps yc hia try consu lta tio n dia gnos ed a somati c del usi ona l disorder. She did not fit the DSM-IV TR diagnostic criteria for anorexia nervosa. Five days after the initiation of oral ref eed ing and intr avenous vita min K, lab orat ory tes ting rev ealedAST(221 U/L), AL T (539 U/L), alk ali ne pho sph ata se (373 U/L), bil irubin (1. 3 mg/ dL), and INR (1.43). Duri ng her initial refeeding period, she had occasional episodes of bradycardia, hypothermia, hypotension, and EKG changes with inverted T waves and prolonged QTc. On hospital day 9, her transa minas es were improving but still 5–7 times the
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Hindawi Publishing CorporationCase Reports in Hepatology Volume 2011, Article ID 176894, 2 pagesdoi:10.1155/2011/176894
Case Report Acute Liver Injury with Severe Coagulopathy in MarasmusCaused by a Somatic Delusional Disorder
Lance L. Stein1 and Arun B. Jesudian2
1 Piedmont Transplant Institute, Piedmont Hospital, 1968 Peachtree Road NW, 77 Building, 6th Floor, Atlanta, GA 30309, USA 2 Division of Gastroenterology, New York Presbyterian Hospital, Weill Medical College of Cornell University, 1305 York Avenue,
4th Floor, New York, NY 10021, USA
Correspondence should be addressed to Lance L. Stein, [email protected] 13 May 2011; Accepted 6 July 2011
Academic Editors: A. Grasso and C. Karaca
Copyright © 2011 L. L. Stein and A. B. Jesudian. This is an open access article distributed under the Creative CommonsAttribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.
Marasmus is a severe form of protein-calorie malnutrition characterized by the depletion of fat stores, muscle wasting, and the lack of edema. In developed countries, marasmus is often the result of anorexia nervosa. Abnormal transaminases with liver syntheticdysfunction have rarely been reported with anorexia nervosa. To our knowledge, we report the first detailed case of acute liverinjury with severe coagulopathy (INR > 1.5) in a patient with marasmus due to self-induced calorie restriction caused by a somaticdelusional disorder. This case highlights the severity of liver injury that may occur with significant weight loss from self-inducedcalorie restriction and the rapid normalization of this injury with treatment. It is important for clinicians to be aware of patternsof acute liver injury in patients with severe protein-calorie malnutrition, regardless of the underlying cause.
1. Introduction
Marasmus is a severe form of protein-calorie malnutritioncharacterized by the depletion of subcutaneous fat stores,muscle wasting, and the absence of edema. In developedcountries, marasmus is commonly the result of anorexianervosa. Complications of marasmus include bradycardia,hypotension and hypothermia. Abnormal liver transaminas-es with liver synthetic dysfunction have rarely been reportedto occur in anorexia nervosa. To our knowledge, we report
the first case of acute liver injury with severe coagulopathy (INR > 1.5) in a patient with marasmus caused by a somaticdelusional disorder.
2. Case Presentation
A 43-year-old woman was admitted for the evaluation of a 25 kg weight loss resulting in severe protein malnutritiondue to intentional calorie restriction (300 Kcal/day) for six months. She had no previous medical or surgical history and was not receiving medications. The patient believedthat she developed an “autoimmune disease” that improvedwith self-induced calorie restriction. On presentation, the
patient weighed 30.1 kg (BMI 11), temperature 98.6◦F,heart rate 75 bpm, and blood pressure 105/68 mmHg. Shewas markedly cachectic with temporal wasting, scaphoidabdomen, and normal liver span without stigmata of cir-rhosis. She was normally oriented and asterixis was absent.Her admission laboratory testing revealed AST (2895 U/L),ALT (1868 U/L), alkaline phosphatase (460 U/L), bilirubin(2.9 mg/dL), albumin (3.7 g/dL), INR (1.9), amylase 188,lipase 322, CPK 535, normal TSH, negative viral hepatitisand autoimmune serologies, ceruloplasmin (17 mg/dL), and
elevated 24-hour urine copper (117 mcg). Abdominal ultra-sound revealed a heterogeneous liver with patent vessels.A slit lamp exam failed to reveal Kayser-Fleischer rings.Psychiatry consultation diagnosed a somatic delusionaldisorder. She did not fit the DSM-IV TR diagnostic criteriafor anorexia nervosa. Five days after the initiation of oralrefeeding and intravenous vitamin K, laboratory testingrevealed AST (221 U/L), ALT (539 U/L), alkaline phosphatase(373 U/L), bilirubin (1.3 mg/dL), and INR (1.43). Duringher initial refeeding period, she had occasional episodes of bradycardia, hypothermia, hypotension, and EKG changeswith inverted T waves and prolonged QTc. On hospital day 9, her transaminases were improving but still 5–7 times the
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2 Case Reports in Hepatology
Figure 1: H&E stain at 400x shows mild acute hepatitis with rareacidophil bodies (long arrow) and increased mitotic figures (shortarrow) in the hepatic lobule.
upper limit of normal and a liver biopsy was performed. Theliver biopsy revealed mild non-specific acute hepatitis withintrasinusoidal and mild centrilobular perivenular fibrosis,
focal necroinflammatory foci, acidophil bodies (long arrow),and increased mitotic figures in the hepatic lobules (shortarrow) (Figure 1). Dry copper weight was 53.8 ug/g. ATP7BPCR gene testing was negative for Wilson’s disease.
3. Discussion
Mild elevations in serum aminotransferase levels have beenreported in up to 60% of patients with anorexia nervosa[1]. However, severe acute liver injury with coagulopathy has rarely been described in the Western literature [2–4].Coagulopathy that is not improved after vitamin K repletionappears to coincide with multiorgan dysfunction as seen
in our patient [5–7]. The exact pathogenic mechanism of hepatocyte injury is unclear but has been proposed to becaused by hepatic hypoperfusion or more recently due tohepatocyte autophagy [3, 8, 9].
In summary, this is the first reported case of acuteliver injury with severe coagulopathy due to protein-caloriemalnutrition caused by a somatic delusional disorder. Theclinical presentation and liver histology are similar toreported cases of acute liver injury due to anorexia nervosa.Recognition of the patterns of acute liver injury, whichcan occur in the absence of hypotension in patients withsevere protein-calorie malnutrition is important, regardlessof the underlying cause. Treatment consists of hemodynamic
support, cautious refeeding, and electrolyte replacement.After appropriate refeeding and weight gain of 4 kg, ourpatient had normalization of transaminases and coagulationfactors by hospital day 30.
Conflict of Interests
The authors have no financial conflict of interests to disclose.
Authors’ Contribution
All authors have participated in the clinical care and in thepreparation of this paper.
References
[1] S. Umeki, “Biochemical abnormalities of the serum in anorexianervosa,” The Journal of Nervous and Mental Disease, vol. 176,no. 8, pp. 503–506, 1988.
[2] S. Furuta, Y. Ozawa, K. Maejima et al., “Anorexia nervosa withsevere liver dysfunction and subsequent critical complications,”
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[4] J. Rivera-Nieves, K. Kozaiwa, C. R. Parrish, J. Iezzoni, and C.L. Berg, “Marked transaminase elevation in anorexia nervosa,”Digestive Diseases and Sciences, vol. 45, no. 10, pp. 1959–1963,2000.
[5] L. Di Pascoli, A. Lion, D. Milazzo, and L. Caregaro, “Acuteliver damage in anorexia nervosa,” The International Journal of Eating Disorders, vol. 36, no. 1, pp. 114–117, 2004.
[6] L. Nordgren and C. von Scheele, “Hepatic and pancreaticdysfunction in anorexia nervosa: a report of two cases,”
Biological Psychiatry , vol. 12, no. 5, pp. 681–686, 1977.[7] Y. Ozawa, T. Shimizu, and Y. Shishiba, “Elevation of serumaminotransferase as a sign of multiorgan-disorders in severely emaciated anorexia nervosa,” Internal Medicine, vol. 37, no. 1,pp. 32–39, 1998.
[8] J. Dowman, R. Arulraj, andI. Chesner, “Recurrent acute hepaticdysfunction in severe anorexia nervosa,” The International
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F. Contaldo, “Severe acute liver damage in anorexia nervosa:two case reports,” Nutrition, vol. 22, no. 5, pp. 572–575, 2006.
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