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Transitional Year

Training Level

Resident PGY 1


Henry Ford Hospital


History A 30-year-old white male with history of alcoholism complicated by cirrhosis who presented to an outside hospital with loss of consciousness after being found down in excrement and urine for an unknown amount of time. Patient’s course was complicated by pancreatitis, urosepsis, spontaneous bacterial peritonitis, and hepatic encephalopathy. Patient was transferred to Henry Ford Hospital for further management, and dermatology was consulted for a one-year history of pruritic rash on the arms and legs with concern for scabies. Examination: Patient appeared thin and malnourished. He was intubated with 2+ pitting edema to his mid-thighs. On his scalp, lateral neck, right abdomen, bilateral dorsal hands extending onto the dorsal forearms, dorsal feet, bilateral inner thighs and the entirety of his scrotum, the patient had well-demarcated pink plaques with cracked riverbed-appearing scale. There was no involvement of the axillae, interdigital finger or toe web spaces, mons pubis, or umbilicus. Course and therapy: Zinc level was found to be markedly decreased at 35 mcg/dL [normal: 70-150 mcg/dL], confirming a diagnosis of acrodermatitis enteropathica (AE). HIV 4th generation Ag/Ab was found to be nonreactive. Alkaline phosphatase was found to be elevated at 735 IU/L [normal: 44-147 IU/L]. Patient was treated with oral zinc replacement at 1.5 mg/kg/day as well as topical petrolatum as needed. Patient had improvement of his zinc level from 35 mcg/dL to within normal limits at 80 mcg/dL within three weeks. Discussion: Acrodermatitis enteropathica is a condition resulting from zinc deficiency characterized by sharply demarcated, symmetric erythematous patches and plaques with erosions and scale-crust in a peri-oral, genital, and acral distribution. Severe deficiency may be accompanied by alopecia, diarrhea, depression, hypogonadism, and immunosuppression. AE may be inherited as an autosomal recessive gene mutation in SLC39A4 leading to deficiency in an intestinal zinc transporter protein. This process often presents in neonates when weaning from breast milk to formula or in cases of low maternal breast milk zinc concentrations. AE, however, may also be acquired secondary to decreased nutritional intake or increased excretion/malabsorption leading to zinc deficiency. Risk factors for decreased nutritional zinc intake include limited resources, alcoholism, anorexia nervosa, vegan diets, and diets high in mineral-binding phytates. Risk factors for increased excretion include intestinal malabsorption, liver disease, renal disease, Crohn’s disease, cystic fibrosis, and sickle cell disease. Diagnosis is made based on clinical features and serum zinc level < 60 mcg/dL. In our patient, his zinc level was found to be significantly lower at 35 mcg/dL. Typically in AE, given that serum alkaline phosphatase (ALP) is a zinc-dependent enzyme, a decreased ALP is expected. Our patient’s ALP was found to be elevated, likely secondary to concomitant pancreatitis. Appropriate treatment is with oral zinc replacement at 1-2 mg/kg/day of elemental zinc with cutaneous improvement expected in weeks to months. Extracutaneous improvement often shows within 24 hours of beginning treatment. Our patient was treated with 1.5 mg/kg/day of oral elemental zinc, with improvement in his cutaneous lesions seen within 3 weeks.

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Acquired Acrodermatitis Enteropathica Secondary to Nutritional Deficiency from Alcoholism