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Childhood Dermatitis Herpetiformis: a Case Report and Review of the Literature

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Childhood Dermatitis Herpetiformis: a Case Report and Review of the Literature CONTINUING MEDICAL EDUCATION Childhood Dermatitis Herpetiformis: A Case Report and Review of the Literature Julie T. Templet, MD; John Patrick Welsh, MD; Carrie Ann Cusack, MD GOAL To understand dermatitis herpetiformis (DH) in children to better manage patients with the condition OBJECTIVES Upon completion of this activity, dermatologists and general practitioners should be able to: 1. Describe the prevalence of DH in children. 2. Discuss the clinical presentation of DH in children. 3. Explain methods of diagnosing DH. CME Test on page 479. This article has been peer reviewed and approved Einstein College of Medicine is accredited by by Michael Fisher, MD, Professor of Medicine, the ACCME to provide continuing medical edu- Albert Einstein College of Medicine. Review date: cation for physicians. November 2007. Albert Einstein College of Medicine designates This activity has been planned and imple- this educational activity for a maximum of 1 AMA mented in accordance with the Essential Areas PRA Category 1 CreditTM. Physicians should only and Policies of the Accreditation Council for claim credit commensurate with the extent of their Continuing Medical Education through the participation in the activity. joint sponsorship of Albert Einstein College of This activity has been planned and produced in Medicine and Quadrant HealthCom, Inc. Albert accordance with ACCME Essentials. Drs. Templet, Welsh, and Cusack report no conflict of interest. The authors report no discussion of off-label use. Dr. Fisher reports no conflict of interest. Dermatitis herpetiformis (DH) is a chronic pru- autoimmune diseases and lymphoma, accurate ritic cutaneous eruption associated with gluten- diagnosis and treatment are imperative. sensitive enteropathy (celiac disease [CD]) and We present a case of DH in a 6-year-old Latino immunoglobulin A (IgA) deposition in the skin. boy previously diagnosed with atopic dermatitis While the disease is not uncommon among and recurrent urticaria. Our aim is to highlight the adolescents, DH is rarely seen in prepubertal various cutaneous presentations of DH and encour- patients. Children with DH present similarly to age clinicians to consider this diagnosis in young adults; however, uncommon skin findings have patients with recalcitrant atypical skin disease. been reported. Because of an increased risk for Cutis. 2007;80:473-476. Accepted for publication March 2, 2007. Dr. Templet is a dermatologist, Center for Sight, Sarasota, Case Report Florida. Dr. Welsh is a dermatologist, Division of Dermatology, A 6-year-old Latino boy presented with a history Western Pennsylvania Hospital, Pittsburgh. Dr. Cusack is Assistant Professor, Drexel University College of Medicine, of pruritic skin lesions (beginning at the age of Philadelphia, Pennsylvania. 9 months) previously diagnosed as atopic dermatitis Reprints not available from the authors. and recurrent urticaria. His pediatrician prescribed VOLUME 80, DECEMBER 2007 473 Childhood Dermatitis Herpetiformis Figure 1. Patient at presentation, with excoriated edem- atous papules on the buttocks. topical steroids and oral diphenhydramine hydro- chloride, without improvement. On examination, the patient had few excoriated edematous papules on his buttocks (Figure 1) and urticarial plaques on his Figure 2. Neutrophils in the papillary dermis with clefting upper extremity. His skin was xerotic but lacked any at the dermoepidermal junction (H&E, original magnifi- lichenified plaques or papules in the antecubital and cation 340). popliteal fossae. The patient denied any associated nausea or diarrhea. Family history was negative for disease (CD). HLA typing was not performed. A atopy and autoimmune disease. The mother reported complete blood count with differential blood count, that the patient was, at one time, “small for his age” comprehensive metabolic panel, thyroxine, thyroid but is now closer in size to his peers. stimulating hormone, and thyroglobulin antibodies A punch biopsy was obtained from an urticarial were all within reference range. The patient was plaque on his arm and treatment was initiated with initiated on a gluten-free diet and subsequently desonide cream 0.05% twice daily to the affected developed fewer lesions and reduced pruritus. areas. The biopsy revealed collections of neutrophils in the papillary dermis as well as clefting at the Comment dermoepidermal junction (Figure 2). A second DH is a cutaneous manifestation of CD, which is an biopsy for direct immunofluorescence (DIF) was immune-mediated enteropathy caused by gluten sen- performed from perilesional gluteal skin. This speci- sitivity. The symptoms of childhood CD include per- men exhibited granular immunoglobulin A (IgA) sistent diarrhea, failure to thrive, abdominal pain, and deposits in the papillary dermis, thus confirming the vomiting. Iron deficiency anemia also may be present diagnosis of dermatitis herpetiformis (DH). as well as other sequelae of malabsorption. Although Evaluation by a gastroenterologist who performed patients with DH usually do not have gastrointestinal serologic testing and endoscopic biopsy of the symptoms, virtually all patients with DH show evi- small intestine further substantiated the diagnosis. dence of the same gluten-sensitive enteropathy of the In the serum, the presence of immunoglobulin G small bowel. antigliadin (42.3 U/mL; reference, ,10), IgA anti– Gluten is a grain protein found in wheat, barley, tissue transglutaminase (anti-tTGase)(.100 U/mL; and rye, but not in oats. Gliadin, the alcohol-soluble reference, ,4), and IgA antiendomysial (positive; fraction of gluten, is believed to be the inciting reference, negative) antibodies were detected. stimulus.1 In addition to antigliadin antibodies, The intestinal biopsy revealed villous atrophy patients with DH have circulating antiendomysial accompanied by duodenitis consistent with celiac and antitransglutaminase antibodies with uncertain 474 CUTIS® Childhood Dermatitis Herpetiformis roles in pathogenesis. The prevailing theory cost-effectiveness of enzyme-linked immunosorbent suggests that gluten sensitivity leads to the forma- assay tTGase testing and proposed that serologic tion of IgA antibodies to gluten-transglutaminase testing be used primarily in the diagnosis of DH. complexes. These antibodies cross-react with other Once patients remove gluten from their diet, the transglutaminases, specifically epidermal transgluta- skin lesions and enteropathy resolve. Furthermore, minase, which is highly homologous. Deposition of tTGase antibodies decrease to levels within refer- IgA–transglutaminase 3 complexes within the papil- ence range in the absence of gluten; thus, serologic lary dermis cause skin lesions of DH.2,3 testing can be used to monitor dietary compliance. Childhood DH is rare, with an uncertain inci- Patients with DH are at higher risk for autoim- dence and prevalence. Cases have been reported in mune diseases, particularly Hashimoto thyroiditis, children as young as 8 months,4 but most children pernicious anemia, and type 1 diabetes mellitus, receive the diagnosis between the ages of 2 and among others.18-20 The association between DH 7 years.5 DH is most prevalent in individuals of and lymphoma, mostly T-cell lymphoma, is well- Northern European descent. In adults, men with documented, with 78% of lymphomas arising from DH outnumber women by a ratio of nearly 2:16; the small bowel, thus warranting vigilant surveil- however, among childhood cases, there is a female lance and regular follow-up with a gastroenter- predominance.5,7 A genetic predisposition for gluten ologist.21 Lewis et al,22 in a retrospective study of sensitivity is supported by the high prevalence of DH 487 patients with DH, found that lymphoma only and CD among first-degree relatives of known occurred in patients not on gluten-free diets or in patients with DH and CD as well as a documented patients who had followed the gluten-free diet for HLA association. The DQ2 and DQ8 alleles are less than 5 years. Moreover, patients in this study most closely linked with DH and CD.8 who did adhere to the gluten-free diet had no The clinical presentation of DH is characterized increased risk for developing lymphoma over the by symmetrically distributed papulovesicular lesions general population.22 and urticarial plaques, often favoring the back, The primary treatment of DH is a gluten-free buttocks, and extensor surfaces of the extremities. diet that is protective against the development of Because the lesions are intensely pruritic, intact lymphoma. Dietary compliance is challenging, espe- vesicles are rarely observed by the clinician. Chil- cially for children; therefore, referral to a dietician dren, by most accounts, present similarly to adults; familiar with this area is helpful. Because months however, uncommon skin findings may be present of dietary restriction are needed before a response is and include isolated involvement of the palms,9 noted, many patients require pharmacologic treat- hemorrhagic lesions of the palms and soles,10 deep ment with dapsone. The recommended starting dose dermal papules and nodules,11 and facial lesions.5,11 for children is 2 mg/kg daily with titration based on Powell et al12 described a case with a predominance clinical response.23 Most patients will have a rapid of urticarial lesions. Thus, childhood DH often is response to dapsone within 48 to 72 hours. However, misdiagnosed as atopic dermatitis, papular urticaria, the enteropathy is unaffected by dapsone therapy scabies, linear IgA dermatosis, or
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