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Urticarial Vasculitis in an Infant

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Urticarial Vasculitis in an Infant Urticarial Vasculitis in an Infant Phoebe E. Koch, BA; Rossitza Lazova, MD; James P. Rosen, MD; Richard J. Antaya, MD Urticarial vasculitis (UV), a subtype of leukocy- referred to dermatology. Physical examination toclastic vasculitis, is a small vessel necrotizing revealed a healthy 9-month-old infant of normal vasculitis characterized by urticarial lesions and length and weight, having attained the expected decreased serum complement. Primarily a dis- developmental milestones. He was a term infant ease of adult women, this immune complex dis- born to nonconsanguineous parents. In addition order is seldom reported in children. Pathologic to his skin lesions, his medical history included examination of skin lesions in patients with UV gastroesophageal reflux disease for which he was reveals leukocytoclastic vasculitis. UV is a fre- taking famotidine. Family history included a mater- quent finding, particularly involving early compo- nal grandfather who died suddenly at 31 years of nents of the classical complement cascade C1q age from an autoimmune membranoproliferative and C2 to C4. We report a 9-month-old male infant glomerulonephritis (as determined by postmortem who presented with chronic urticaria of 7 months’ renal biopsy), a maternal great-aunt with Berger duration that was unresponsive to conventional disease, and another maternal great-aunt with dis- therapies for urticaria. His lesions appeared as coid lupus erythematosus. Also, the patient’s mother erythematous wheals followed by the develop- had a history of childhood alopecia areata. Recent ment of purpuric papules and resolving with laboratory analysis of the mother’s blood revealed ecchymoses and postinflammatory hyperpigmen- the following elevated liver function tests of unclear tation. Laboratory studies and skin biopsy results etiology: aspartate aminotransferase, 106 U/L (refer- were consistent with UV. ence range, 3–35 U/L); alanine aminotransferase, Cutis. 2008;81:49-52. 175 U/L (reference range, 3–40 U/L); lactate dehy- drogenase, 392 U/L (reference range, 100–250 U/L), with negative hepatitis A and B serologies. Screen- ing for cardiolipin antibody and antinuclear antibody Case Report was negative, and complement levels (including An otherwise healthy 9-month-old male infant pre- C3 and C4) were within reference range. sented with a 7-month history of chronic recurrent Cutaneous examination of the infant revealed urticaria. The patient’s symptoms began at 2 months multiple dusky, erythematous to violaceous, urti- of age with the acute onset of fever (39.98C), malaise, carial wheals concentrated on the back (Figure 1) diarrhea, and a rash. During the following months, his and extending to involve the extremities, some rash appeared intermittently, beginning on the trunk scattered purpuric papules, ecchymotic plaques, and and often extending to involve the entire body. The mild dermatographism. The parents reported that exacerbations continued despite chronic treatment these flares lasted from 72 to 96 hours on average. with H1 blockers (ie, hydroxyzine, diphenhydramine Gastrointestinal and constitutional symptoms were hydrochloride, cetirizine), occasional courses of oral absent. Examination of the eyes, mucosa, and joints glucocorticosteroids for less than 1 week, and brief was unremarkable. improvement following epinephrine injection. Initial laboratory evaluations included a normal After months of evaluation and treatment, his complete blood count, liver function tests, urinaly- condition failed to improve and the patient was sis, creatinine, and thyroid-stimulating hormone. Further analysis revealed low serum complement Accepted for publication January 2, 2007. levels including a C2 less than 1.3 mg/dL (refer- Ms. Koch and Drs. Lazova and Antaya are from Yale University ence range, 1.6–3.5 mg/dL), C3 of 30 mg/dL School of Medicine, New Haven, Connecticut. Dr. Rosen is from (reference range, 90–180 mg/dL), C4 of 6 mg/dL (ref- the Connecticut Asthma and Allergy Center, LLC, West Hartford. erence range, 16–47 mg/dL), CH50 of 13 U/mL (ref- The authors report no conflict of interest. Correspondence: Richard J. Antaya, MD, Director of Pediatric erence range, 26–58 U/mL), and C1q of 4.1 mg/dL Dermatology, Yale University School of Medicine, 333 Cedar St, (reference range, 5.0–8.6 mg/dL). Immunoglob- Box 208059, New Haven, CT 06520-8059 ([email protected]). ulin (Ig) G antibody against C1q was negative as VOLUME 81, JANUARY 2008 49 Urticarial Vasculitis glucocorticosteroids. His mother recalls that her son’s initial flares seemed to coincide with his immu- nization schedule; however, recent immunizations have been uneventful. According to the patient’s allergist, skin flares often coincided with a missed dose of montelukast sodium. We recently referred the patient to a nephrologist for consultation after his mother noted blood in his urine. Repeat urinalysis showed a pH of 5.5, specific gravity of 1.010, trace protein, and small hemolyzed occult hematuria. Microscopic evaluation revealed 3 to 4 eumorphic red blood cells per high-power field, without evidence of casts or white blood cells. A subsequent urinalysis was normal. Aside from his cutaneous flares, the patient is otherwise healthy and thriving. We will continue to closely monitor him for the development of renal or other systemic complications in the future. Figure 1. Patient’s back at 10 months of age with raised erythematous wheals. Comment This case of hypocomplementemic UV is notable measured by enzyme-linked immunosorbent assay. for its presentation in a male infant beginning at Tryptase, erythrocyte sedimentation rate, antinu- 2 months of age, which is considerably younger clear antibody (titer ,1:40), and thyroglobulin than any patient with UV previously described in antibody all were within reference range, while thy- the literature. Children are seldom affected by this roid peroxidase antibody was elevated at 47 IU/mL syndrome; a review of the literature found one report (reference, ,35 IU/mL). Because our patient’s ini- of normocomplementemic UV in an infant1 and few tial presentation suggested a viral infection, hepa- reports of UV in children.2-7 Among patients with titis B and C serologies were obtained; both were chronic urticaria, the prevalence of UV has been negative. Antibodies for dsDNA, c-ANCA (anti- estimated at 5% to 10%8-11; of those patients with UV, neutrophil cytoplasmic antibody), p-ANCA, rapid the majority are women, with onset typically occur- plasma reagin, anti-Sm (Smith), and Sjögren syn- ring at a median age of 43 years.12,13 drome antigens SS-A and SS-B also were negative. Although our patient showed no signs of renal C1 esterase inhibitor levels were within reference disease, several previously reported cases of children range, and a test for cryoglobulins was negative. A with UV describe the development of renal disease chest radiograph was unremarkable. years after initial presentation. Cadnapaphornchai A 4-mm punch biopsy specimen from the mid- et al2 described a 12-year-old girl originally line lower back was examined histologically. There diagnosed with juvenile rheumatoid arthritis at was a superficial and deep perivascular and inter- 3 years of age. At 4 years of age, she developed stitial infiltrate containing prominent neutrophils, an intermittent purpuric rash and was diagnosed eosinophils, and lymphocytes (Figures 2 and 3), as with Henoch-Schönlein purpura (HSP). It was not well as fibrinoid degeneration of small blood vessel until 8 years later while being evaluated for the walls. Leukocytoclasis was present but to a lesser development of hematuria and proteinuria that degree than is usually observed in classic leuko- she was found to have UV. Renal biopsy revealed cytoclastic vasculitis. A punch biopsy taken from membranoproliferative glomerulonephritis and perilesional skin was submitted for direct immu- the patient was started on oral dapsone 100 mg nofluorescence and revealed deposits of C3, IgM, daily, with good results. Waldo et al3 described a IgA, and, focally, fibrinogen around vessels of the 16-year-old boy with a less fortunate outcome. His superficial plexus. These results are consistent with UV developed at 2 years of age, with the onset of urticarial vasculitis (UV). hematuria and proteinuria 10 years later. Renal The patient currently is being maintained on biopsy revealed mesangial proliferation with mem- 4-mL hydroxyzine hydrochloride syrup twice daily branoproliferative features. Unfortunately, he did and 4-mg montelukast sodium once daily. He not respond to steroid and cytotoxic therapy and continues to experience flares that are temporar- ultimately progressed to end-stage renal disease.3 ily relieved by short 4- to 5-day courses of oral Martini et al4 reported 2 pediatric patients with UV. 50 CUTIS® Urticarial Vasculitis Figure 2. Superficial and deep perivascular and intersti- Figure 3. Perivascular infiltrate with eosinophils and tial infiltrate (H&E, original magnification 3100). extravasated fibrin (arrows). A hint of leukocytoclasis also was present (H&E, original magnification 3400). One patient ultimately developed pulmonary hem- 4 weeks of onset of symptoms.17 This pattern is not orrhage, presumably due to UV, in the absence of seen in pediatric patients with UV. renal disease. The other patient, who presented at Patients with idiopathic UV often are stratified 6 years of age with urticarial lesions, eventually on the basis of serum complement results. Those developed proteinuria and hematuria at 10 years with
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