Pooya Khan Mohammad Beigi - Acrodermatitis Enteropathica: A Clinicians Guide
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This new text provides insight and treatment options for the covered disease, including dozens of high quality photographs, illustrations, and clinical tables. Topics covered include the history of the disease, categories of the disorder, molecular analysis, epidemiology, effects on body systems, disorder symptoms, and treatment. Acrodermatitis Enteropathica is a rare disorder of zinc metabolism that occurs in one of two forms: inborn and acquired. If untreated, the disease is fatal and affected individuals may die within just a few years, but since there is no cure for the condition, it is critical that physicians are aware of the signs and symptoms related to AE and the appropriate treatments available for patients. A Comprehensive Guide to Acrodermatitis Enteropathica is the only book of its kind to give insight into this rare disorder. Written by and for dermatologists, pediatric specialists, and ObGYNs, this book contains one of the largest clinical research studies done on Acrodermatitis Enteropathica over the last decade.
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Part I
Overview of Disorder
Overview of Disorder
Springer International Publishing Switzerland 2015
Pooya Khan Mohammad Beigi and Emanual Maverakis Acrodermatitis Enteropathica 10.1007/978-3-319-17819-6_11. History of Acrodermatitis Enteropathica
Pooya Khan Mohammad Beigi 1, 2 and Emanual Maverakis 3
(1)
University of British Columbia, Vancouver, British Columbia, Canada
(2)
New York Medical College, Valhalla, NY, USA
(3)
University of California Davis, Sacramento, CA, USA
Acrodermatitis Enteropathica (AE) is an inherited autosomal recessive disorder which often presents in newborn infants [].
Except for the characteristic dermatitis, the symptoms of this disorder vary with age of the patient. Severe uncontrollable diarrhea, mood changes, anorexia, and neurological disorders are frequently reported in infants. Growth retardation, alopecia, weight loss, and recurrent infections have also been reported in toddlers and young children; and spontaneous remission may happen in adolescence [].
The disorder was first discovered in 1902 by Wende [].
Moynahan suggested that the absence of an enzyme called oligopeptidase in the intestine was responsible for the decreased serum zinc levels observed in AE patients []; however its mechanism is unknown and its main role in zinc absorption still needs to be elucidated.
In 2002 two independent studies showed that AE was due to homozygous or compound heterozygous mutations of SLC39A4 , a gene located on chromosomal region 8q24.3, which codes for the zinc-specific transporter ZIP4 (or hZIP4) [], where it enables the absorption of zinc from the intestinal lumen. Through its function and localization, ZIP4 plays a major role in human zinc homeostasis, which explains the broad clinical picture of acrodermatitis enteropathica.
References
Maverakis E, et al. Acrodermatitis enteropathica and an overview of zinc metabolism. J Am Acad Dermatol. 2007;56(1):11624. PubMed CrossRef
Puri N. A study of efficacy of oral zinc therapy for acrodermatitis enteropathica. Nasza dermatolologia online. 2013;4:1626. CrossRef
Van Wouwe JP. Clinical and laboratory diagnosis of acrodermatitis enteropathica. Eur J Pediatr. 1989;149(1):28. PubMed CrossRef
Aggett PJ. Acrodermatitis enteropathica. J Inherit Metab Dis. 1983;6 Suppl 1:3943. PubMed CrossRef
Wende GW. Epidermolysis bullosa hereditaria. J Cut Dis. 1902;20:53747.
Brandt T. Dermatitis in children with disturbances of the general condition and the absorption of food elements. Acta Derm. 1936;17:51346.
Danbolt N, Closs K. Acrodermatitis enteropathica. Acta Derm Venerol. 1942;23:12769.
Neldner KH, Hambidge KM. Zinc therapy of acrodermatitis enteropathica. N Engl J Med. 1975;292(17):87982. PubMed CrossRef
Moynahan EJ. Letter: acrodermatitis enteropathica: a lethal inherited human zinc-deficiency disorder. Lancet. 1974;2(7877):399400. PubMed CrossRef
Aggett PJ, et al. The therapeutic effect of amphotericin in acrodermatitis enteropathica: hypothesis and implications. Eur J Pediatr. 1981;137(1):235. PubMed CrossRef
Hurley LS, et al. Zinc-binding ligands in milk and intestine: a role in neonatal nutrition? Proc Natl Acad Sci U S A. 1977;74(8):35479. PubMedCentral PubMed CrossRef
Evans GW, Johnson PE. Characterization and quantitation of a zinc-binding ligand in human milk. Pediatr Res. 1980;14(7):87680. PubMed CrossRef
Kry S, et al. Identification of SLC39A4, a gene involved in acrodermatitis enteropathica. Nat Genet. 2002;31(3):23940. PubMed CrossRef
Wang K, et al. Homozygosity mapping places the acrodermatitis enteropathica gene on chromosomal region 8q24.3. Am J Hum Genet. 2001;68(4):105560. PubMedCentral PubMed CrossRef
Springer International Publishing Switzerland 2015
Pooya Khan Mohammad Beigi and Emanual Maverakis Acrodermatitis Enteropathica 10.1007/978-3-319-17819-6_22. Epidemiology and Etiology
Pooya Khan Mohammad Beigi 1, 2 and Emanual Maverakis 3
(1)
University of British Columbia, Vancouver, British Columbia, Canada
(2)
New York Medical College, Valhalla, NY, USA
(3)
University of California Davis, Sacramento, CA, USA
2.1 Epidemiology
AE is not specific to any ethnic population, as cases have been reported from all around the world [].
Even though AE is not as prevalent in the United States as it is in countries with high rates of consanguinity, acquired zinc deficiency has been reported in American newborns and children. There have been several studies that reported of American infants having exceptionally low hair and plasma zinc levels [].
Lactation, alcoholism, old age, and metabolic disorders are associated with zinc deficiency in the American adult demographic []. In the light of this, more research and attention should be devoted to increasing knowledge, raising awareness, and correction of these nutritional problems.
2.2 Etiology
2.2.1 Molecular Etiology of AE
Presently, AE is considered a treatable disorder since it can be simply managed with zinc supplementation once diagnosed. As a result of the profound effects this disease has on human physiology, which are particularly pronounced in infants, medical science still considers it as one of the most intriguing and interesting disorders. AE is suggested to have an autosomal recessive mode of inheritance by genealogic data [].
AE presents a multitude of opportunities for research; however, at present only rare cases are referred to academic medical centers since this disorder is easily treatable. Consequently, the study of this disorder is rarely done. Two main hypotheses are proposed. One is based on a problem of zinc bioavailability and the other on an intrinsic defect of zinc transport by the affected individual.
2.2.2 Hypothetical Etiology 1: The Alteration of Zinc Bioavailability
As patients with AE can obtain only a small amount of zinc through dietary sources, supplementing the diet with sufficient amounts of zinc can raise the level of zinc in blood plasma to a normal level and result in the resolution of the disorder. Although the amount of zinc in breast milk and infant formula are roughly equal, the zinc in breast milk has been observed to be more absorbable by infants with AE and this phenomenon has become an interesting matter among dermatologists, pediatricians, and medical researchers [].
To date, research has indicated that the zinc absorption process is very complex. Research laboratory results illustrate that the zinc binding ligand found in human milk facilitates zinc absorption in the intestine and the ligands presence results in high bioavailability of zinc in human milk [). 
Figure 2.1
Molecular structure of picolinic acid
Evans and Johnson found the concentration of picolinic acid, a zinc binding ligand, in human milk to be much higher than that in either bovine milk or infant formulas. The higher concentration of picolinic acid in human milk could result in the formation of additional zinc picolinate complexes which would be more absorbable by the intestine compared to ionic zinc or zinc complexed with other ligands [). 
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