Acrodermatitis enteropática y desnutrición proteica posterior a cirugía bariátrica / Enteropathic acrodermatitis and proteic nuttrution after bariatric surgery

La utilización de la cirugía bariátrica ha ido en aumento por su efectividad a largo plazo en el mantenimiento del peso perdido, en la reducción drástica de comorbilidades y mortalidad global. El bypass biliopancreático es una de las técnicas bariátricas más eficaces para la pérdida y mantenimiento del peso con menor restricción dietética. Se presenta un caso clínico de una mujer intervenida previamente de by-pass biliopancreático y que presento signos de malnutrición por deficiencia del zinc. Se describe la evolución de la enferma y se discuten las características y repercusiones que la deficiencia produce en la paciente

The use of bariatric surgery has been increasing due to its long-term effectiveness in maintaining lost weight, in drastically reducing comorbidities and overall mortality. Biliopancreatic bypass is one of the most effective bariatric techniques for weight loss and maintenance with less dietary restriction. We present a clinical case of a woman who had previously undergone biliopancreatic bypass and had signs of zinc malnutrition. The evolution of the patient is described and the characteristics and repercussions that the deficiency produces in the patient are discussed

Zinc deficiency and toxicity in pediatric practice.

PURPOSE OF REVIEW: Zinc is a commonly overlooked deficiency in developed countries, occurring in infants, children, and adolescents during critical growth periods. The purpose of this review is to present the evidence of zinc deficiencies and toxicities as well as treatment in pediatrics. RECENT FINDINGS: During the last decade, the significance of zinc deficiency in childhood growth, morbidity, and mortality has been recognized by a number of large-scale supplementation trials in underdeveloped countries. Recognition of the recent nationwide shortage of injectable zinc available for total parenteral nutrition supplementation over the last 2 years focused attention on the possibility of zinc deficiency in the United States. SUMMARY: Although primarily thought of as a problem reserved for underdeveloped countries, zinc deficiency has increasing pediatric prevalence in the USA. Zinc is an essential trace element in the body that is responsible for numerous structural, catalytic, and biochemical functions. Deficiencies can occur because of poor dietary intake, long-term parenteral nutrition without supplementation, and enteral causes such as malabsorption. Zinc deficiency is closely associated with stunting, respiratory infections, diarrhea, and dermatitis. Deficiency is hard to define solely by the serum levels. Clinicians should utilize a combination of serum zinc levels, presenting signs and symptoms, and nutritional intake via oral, enteral, and parenteral routes to accurately assess the deficiency risk and diagnosis.

Misdiagnosed food allergy resulting in severe malnutrition in an infant.

As food allergies become increasingly prevalent and testing methods to identify "food allergy" increase in number, the importance of careful diagnosis has become even more critical. Misdiagnosis of food allergy and inappropriate use of unproven testing modalities may lead to a harmful food-elimination diet. This case is an example of an infant who was placed on an overly restrictive elimination diet at the recommendation of her health care providers, resulting in kwashiorkor and acquired acrodermatitis enteropathica.

Severe dermatitis with loss of epidermal Langerhans cells in human and mouse zinc deficiency.

Zinc deficiency can be an inherited disorder, in which case it is known as acrodermatitis enteropathica (AE), or an acquired disorder caused by low dietary intake of zinc. Even though zinc deficiency diminishes cellular and humoral immunity, patients develop immunostimulating skin inflammation. Here, we have demonstrated that despite diminished allergic contact dermatitis in mice fed a zinc-deficient (ZD) diet, irritant contact dermatitis (ICD) in these mice was more severe and prolonged than that in controls. Further, histological examination of ICD lesions in ZD mice revealed subcorneal vacuolization and epidermal pallor, histological features of AE. Consistent with the fact that ATP release from chemically injured keratinocytes serves as a causative mediator of ICD, we found that the severe ICD response in ZD mice was attenuated by local injection of soluble nucleoside triphosphate diphosphohydrolase. In addition, skin tissue from ZD mice with ICD showed increased levels of ATP, as did cultured wild-type keratinocytes treated with chemical irritants and the zinc-chelating reagent TPEN. Interestingly, numbers of epidermal Langerhans cells (LCs), which play a protective role against ATP-mediated inflammatory signals, were decreased in ZD mice as well as samples from ZD patients. These findings suggest that upon exposure to irritants, aberrant ATP release from keratinocytes and impaired LC-dependent hydrolysis of nucleotides may be important in the pathogenesis of AE.

Nutrition and bullous skin diseases.

Autoimmune and nonautoimmune bullous diseases can both be associated with significant morbidity and mortality. Although our understanding of the pathogenic mechanisms of these diseases has increased tremendously, there is still much to learn about the various factors affecting their onset, course, and therapy. In recent years, increasing information has been published about the effect of vitamins, minerals, and other nutrients on bullous skin diseases. Some factors are believed to be inducers (thiol and phenol-containing foods in pemphigus), whereas others are believed to be protective (antioxidants in cutaneous porphyrias). This contribution reviews the evidence in the literature of the role of various dietary factors in bullous diseases, including the nonautoimmune and the deficiency dermatoses. Additional studies and new investigations are needed to provide a better understanding of the specific associations of dietary factors with bullous diseases and better management for patients affected by these conditions.

Acrodermatitis acidemica secondary to malnutrition in glutaric aciduria type I.

We encountered a patient with glutaric aciduria type I (GA-I) associated with skin lesions resembling acrodermatitis enteropathica (AE). This child was being fed with a low-protein diet when the skin disorder developed. A deficiency in plasma levels of essential amino acids, particularly isoleucine, and zinc was confirmed. Supplementation of a high-caloric, protein-rich diet together with zinc, selenium and vitamins led to a prompt improvement of the skin lesions. We assume that in our patient the skin lesions were the result of malnutrition, rather than being primarily associated with the underlying metabolic disease. To our knowledge, no other report is so far available concerning GA-I complicated by skin eruptions.

[Acrodermatitis enteropathica-like changes in a patient with parenteral nutrition]. / Acrodermatitis-enteropathica-ähnliche Hautveränderungen durch parenterale Ernährung.

A patient on long term parenteral nutrition developed acrodermatitis enteropathica-like skin changes. Just as in the autosomal recessive disorder, acrodermatitis enteropathica, the lesions in our patient were caused by zinc deficiency. Replacement therapy with zinc led to rapid improvement.

The effects of diet and zinc treatment on the fatty acid composition of serum lipids and adipose tissue and on serum lipoproteins in two adolescent patients with acrodermatitis enteropathica.

In two adolescent patients with acrodermatitis enteropathica fatty acid spectra in serum lipids and adipose tissue and serum lipoprotein concentrations were followed for about 7 yr. One patient was treated by diet and iv infusions of high amounts of linoleic acid and later by different doses of zinc. The other boy was given only varying doses of zinc. Extra supply of linoleic acid raised its concentrations in serum triglycerides, cholesterol esters, phospholipids, and adipose tissue lipids from low to normal or high levels. In both patients linoleic acid in serum lipids was sensible to the dose of zinc, decreasing when it was low and increasing when it was high. Serum triglycerides increased when the supply was low and was normalized when high doses were given. High-density lipoprotein cholesterol, however, remained low throughout the study. We conclude that in acrodermatitis enteropathica zinc thus seems to be of importance in regulating linoleic acid and serum lipoprotein metabolism.

Cystic fibrosis manifesting with acrodermatitis enteropathica-like eruption. Association with essential fatty acid and zinc deficiencies.

A refractory dermatitis resembling acrodermatitis enteropathica was the manifesting sign in a 5-month-old male infant with cystic fibrosis, preceding pulmonary and gastrointestinal tract symptoms by two months. The eruption was clearly nutritionally responsive. Biochemical evidence was shown for deficiencies of zinc, essential fatty acids, and protein. Altered prostaglandin metabolism was also demonstrated.

Acute zinc depletion syndrome during parenteral hyperalimentation.

Zinc is an essential trace element whose malabsorption in early childhood may result in a skin disorder known as acrodermatitis enteropathica. Cutaneous lesions typical of acrodermatitis enteropathica have been described during total parenteral nutrition on zinc-deficient intravenous solutions in both adults and children. This condition has been named the "acute zinc depletion syndrome." A case is described in which a patient, despite a zinc intake of double the daily requirement, manifested the acute zinc depletion syndrome during therapy with combined liquid diet plus parenteral hyperalimentation. Predisposing factors in this individual included a short bowel syndrome and a large oral load of calcium lactate. Zinc metabolism is reviewed with attention to alterations in disease and during hyperalimentation. The clinical manifestations, predisposing factors, therapy and prevention of the acute zinc depletion syndrome are discussed.

[Acrodermatitis enteropathic treated with zinc sulfate. Report of a case]. / Acrodermatitis enteropática tratada con sulfato de zinc. Reporte de un caso

A case is reported of a girl with acrodermatitis enteropathica who was treated succesfully with zinc sulfate at 75 mg/day PO. A remarkable increase in weight was evident through the course of 12 months of treatment, reaching the percentile 50 by the age of 3 years; however the height remained close to percentile 3. Possibly, the zinc deficiency is secondary to a selective defect in the metal absorption. Treatment with zinc sulfate in these patients substitutes with greate advantages the use of diiodohydroxyquin. Possibly, zinc supplements must be given for a life time to these patients.