ZINC-DEFICIENCY DURING PARENTAL NUTRITION - SKIN MANIFESTATIONS AND IMMUNE INCOMPETENCE IN A PREMATURE-INFANT

Deficiency of trace elements during total parenteral nutrition (TPN) has emerged with the transition from use of crude hydolysates to the use of purified mixtures of crystalline L-amino acids unsupplemented with trace elements. A 1.4-kg neonate had an ischemic segmental ileal volvulus with diffuse peritonitis that necessitated bowel resection (13 cm) and temporary ileostomy. Prolonged total (including plasma and intralipid) and supplemental parental nutrition induced a good anabolic response. After 3 mo, excessive ileostomy drainage developed and failed to respond to cessation of enteral feedings, but at 3.5 mo birth weight had almost doubled. At that time, skin lesions consistent with acrodermatitis enteropathica appeared and spread quickly. Topical and systemic treatment for secondary skin infection did not ameliorate or halt spread of the lesion. Immune deficiency (IgG 107 mg/dl) was treated with fresh frozen plasma, without improvement. Plasma zinc (40 μg/dl) and alkaline phosphatase (27 IU) were below normal range. Zinc sulfate oral therapy produced a dramatic improvement in 36 hr and complete disappearance of the skin lesions within 1 wk. Concurrently, ileostomy drainage decreased, irritability subsided, and appetite improved, with elevation of IgG, zinc, and alkaline phosphatase to normal levels. Zinc is a structural and functional component of various enzyme systems essential for metabolism. Zinc deficiency, in this case, developed as a result of inadequate intake, excessice loss of zinc-containing enzymes in pancreatic and intestinal fluids, and utilization of available zinc in the anabolic tissue growth response to TPN. Fast repletion of immune mechanisms enhanced control of skin infections and healing. © 1978 Grune & Stratton, Inc.