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Weight loss and purpura
Case report
Weight loss and purpura Matthew D Snape, Susan M Sawyer, Margot C Nash A 15-year-old boy was admitted to hospital in July, 1998, with a history of weight loss, weakness, and a purpuric rash. His weight was 48 kg 6 months previously, 39·7 kg 3 weeks before admission, and 32·0 kg on admission. There was a 1-week history of lower limb myalgia on exertion, constipation, and slowing of speech and movements. 2 days before admission he developed a purpuric rash over his left lower chest which spread to the other side. There were no night sweats, headaches, polyuria, vomiting, or diarrhoea. He was appropriately concerned regarding his weight loss and both he and his mother reported that he had a good diet. He enjoyed cooking and planned to become a chef. Examination revealed a cachectic pubertal boy with a body mass index of 12 kg/m2 (figure). His pulse rate was 40/min, he was hypothermic (35·3ºC), and hypotensive (blood pressure 100/60 mm Hg). There was muscle wasting and decreased reflexes but no muscle tenderness. There was a purpuric rash predominantly on the left of his chest. Initial differential diagnoses included an intracranial or other neoplasm, dermatomyositis, and endocrine or renal dysfunction. Investigations showed a markedly elevated creatine kinase of 4322 U/L, thyroxin 6·6 pmol/L, thyroid stimulating hormone 1·40 mU/L, creatinine 0·121 mmol/L, urea 26·5 mmol/L, alanine aminotransferase 289 U/L, and unconjugated bilirubin 29 umol/L with otherwise normal liver function tests. He had thrombocytopenia (112⫻109/L) with a prothrombin time of 23·1 s. His erythrocyte sedimentation rate was 0 mm/h. An electrocardiogram showed sinus bradycardia. His urine had 2+ of protein and there was decreased corticomedullary differentiation on renal ultrasound. Further tests included an early morning cortisol of >1380 nmol/L and a cranial computed tomograph scan consistent with dehydration. On the ward, he was noted to have a preoccupation with his diet. He agreed with the suggestion that he was very thin but was also concerned about “becoming too fat”. He denied purging or excess exercise. He was not depressed. Dietary assessment revealed a limited intake with avoidance of fats and dairy products resulting in a caloric intake of 1000 Kcal/day, roughly one third of his nutritional requirements. After discussion with the boy and with his family, he readily increased the amount he ate. This resulted in resolution of his rash and other symptoms, appropriate weight gain, and return to normal of all his laboratory investigations as he gained weight. He best fulfils diagnostic criteria1 for “eating disorder not otherwise specified” because of his lack of resistance to resuming a Lancet 1999; 354: 1352 Royal Children’s Hospital, Victoria 3052, Australia (M D Snape S M Sawyer MD, M C Nash MD ) (e-mail: http://www.rch.unimelb.edu.au) Correspondence to: Dr M C Nash
1352
MB,
Patient on admission He gave permission for publication of this photograph.
normal diet. He was discharged after 14 days and continued to eat normally at home. He weighed 46 kg 2 months later; there was no evidence of mental ill health. Eating disorders are well known to cause hypothermia, bradycardia, and hypotension. Thrombocytopenia and thyroid, renal, and hepatic dysfunction2 are also recognised. There is a previous report of two patients with anorexia, myopathy, and purpuric rash in the absence of significant initial thrombocytopenia.3 Petechiae with normal platelet counts have also been reported in isolation in other patients with eating disorders,4 as has elevated creatine kinase.5 This case highlights the importance of including eating disorders in the differential diagnosis of many physical presentations in adolescents, even in males, and in the absence of an obvious history of restricted intake. References 1
American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th edition). Washington, DC: 1994. 2 Sharp CW, Freeman CPL. The medical complications of anorexia nervosa. Br J Psychiatry 1993; 162: 452–62. 3 Alloway R, Reynolds ER, Sporgo E, Russell GF. Neuropathy and myopathy in two patients with anorexia and bulimia nervosa. J Neurol Neusirg Psychiat 1985; 48: 1015–20. 4 Warren M, Vande Wiele R. Clinical and metabolic features of anorexia nervosa. Am J Obstet Gynecol 1973; 117: 435–99. 5 Alloway R, Shur E, Obrecht R, Russell GF. Physical complications in anorexia nervosa, haematological and neuromuscular changes in 12 patients. Br J Psychiatr 1988; 153: 72–75.
THE LANCET • Vol 354 • October 16, 1999
Weight loss and purpura Matthew D Snape, Susan M Sawyer, Margot C Nash A 15-year-old boy was admitted to hospital in July, 1998, with a history of weight loss, weakness, and a purpuric rash. His weight was 48 kg 6 months previously, 39·7 kg 3 weeks before admission, and 32·0 kg on admission. There was a 1-week history of lower limb myalgia on exertion, constipation, and slowing of speech and movements. 2 days before admission he developed a purpuric rash over his left lower chest which spread to the other side. There were no night sweats, headaches, polyuria, vomiting, or diarrhoea. He was appropriately concerned regarding his weight loss and both he and his mother reported that he had a good diet. He enjoyed cooking and planned to become a chef. Examination revealed a cachectic pubertal boy with a body mass index of 12 kg/m2 (figure). His pulse rate was 40/min, he was hypothermic (35·3ºC), and hypotensive (blood pressure 100/60 mm Hg). There was muscle wasting and decreased reflexes but no muscle tenderness. There was a purpuric rash predominantly on the left of his chest. Initial differential diagnoses included an intracranial or other neoplasm, dermatomyositis, and endocrine or renal dysfunction. Investigations showed a markedly elevated creatine kinase of 4322 U/L, thyroxin 6·6 pmol/L, thyroid stimulating hormone 1·40 mU/L, creatinine 0·121 mmol/L, urea 26·5 mmol/L, alanine aminotransferase 289 U/L, and unconjugated bilirubin 29 umol/L with otherwise normal liver function tests. He had thrombocytopenia (112⫻109/L) with a prothrombin time of 23·1 s. His erythrocyte sedimentation rate was 0 mm/h. An electrocardiogram showed sinus bradycardia. His urine had 2+ of protein and there was decreased corticomedullary differentiation on renal ultrasound. Further tests included an early morning cortisol of >1380 nmol/L and a cranial computed tomograph scan consistent with dehydration. On the ward, he was noted to have a preoccupation with his diet. He agreed with the suggestion that he was very thin but was also concerned about “becoming too fat”. He denied purging or excess exercise. He was not depressed. Dietary assessment revealed a limited intake with avoidance of fats and dairy products resulting in a caloric intake of 1000 Kcal/day, roughly one third of his nutritional requirements. After discussion with the boy and with his family, he readily increased the amount he ate. This resulted in resolution of his rash and other symptoms, appropriate weight gain, and return to normal of all his laboratory investigations as he gained weight. He best fulfils diagnostic criteria1 for “eating disorder not otherwise specified” because of his lack of resistance to resuming a Lancet 1999; 354: 1352 Royal Children’s Hospital, Victoria 3052, Australia (M D Snape S M Sawyer MD, M C Nash MD ) (e-mail: http://www.rch.unimelb.edu.au) Correspondence to: Dr M C Nash
1352
MB,
Patient on admission He gave permission for publication of this photograph.
normal diet. He was discharged after 14 days and continued to eat normally at home. He weighed 46 kg 2 months later; there was no evidence of mental ill health. Eating disorders are well known to cause hypothermia, bradycardia, and hypotension. Thrombocytopenia and thyroid, renal, and hepatic dysfunction2 are also recognised. There is a previous report of two patients with anorexia, myopathy, and purpuric rash in the absence of significant initial thrombocytopenia.3 Petechiae with normal platelet counts have also been reported in isolation in other patients with eating disorders,4 as has elevated creatine kinase.5 This case highlights the importance of including eating disorders in the differential diagnosis of many physical presentations in adolescents, even in males, and in the absence of an obvious history of restricted intake. References 1
American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th edition). Washington, DC: 1994. 2 Sharp CW, Freeman CPL. The medical complications of anorexia nervosa. Br J Psychiatry 1993; 162: 452–62. 3 Alloway R, Reynolds ER, Sporgo E, Russell GF. Neuropathy and myopathy in two patients with anorexia and bulimia nervosa. J Neurol Neusirg Psychiat 1985; 48: 1015–20. 4 Warren M, Vande Wiele R. Clinical and metabolic features of anorexia nervosa. Am J Obstet Gynecol 1973; 117: 435–99. 5 Alloway R, Shur E, Obrecht R, Russell GF. Physical complications in anorexia nervosa, haematological and neuromuscular changes in 12 patients. Br J Psychiatr 1988; 153: 72–75.
THE LANCET • Vol 354 • October 16, 1999