Pruritic eosinophilic papular eruption revealing HIV infection

ARTICLE

Case report

A 30-year-old black woman from Ethiopia had an 8-month history of pruritic follicular papular rash over the face and trunk. On examination, the forehead, cheeks, nose, shoulders and upper back showed isolated small pruritic follicular papules with a central pinpoint vesicle and occasional pustules (Fig. 1). Cultures for bacteria and fungi were negative. The rash was unaffected by a course of minocycline (100 mg daily for 4 weeks) and oral antihistamines failed to provide relief against itching. Topical preparations including 1% salicylic acid lotion and 1% clindamycin in an acqueous gel base were ineffective. Under laboratory examination, the leukocyte count was 4.57 x 10⁹/l, with high relative eosinophilia (15.1%; 0.690 x 10⁹/l) and the erythrocyte sedimentation rate (ESR) 68 mm/hr. The CD4⁺ T cell count was 101/mul. The levels of serum IgE and IgG were increased at 971 IU/ml and 2,440 mg/dl, respectively. Chest X-ray was normal.

Skin punch-biopsies obtained from papular lesions on the face and back revealed an upper dermal perivascular and perifollicular inflammatory infiltrate, consisting of lymphocytes, histiocytes and a large number of eosinophils invading the follicular epithelium (Fig. 2A, B). No bacteria, yeast or Demodex mites were observed in the specimens examined. Human immunodeficiency virus (HIV) antibody tests (immunoenzymatic assay and radioimmunoblotting assay) were then performed; the positive results led us to make diagnosis of HIV-associated eosinophilic folliculitis (HIV-EF).

Discussion

Eosinophilic folliculitis (EF) occurring in HIV-infected individuals is a papular pruritic eruption usually involving the face, neck, upper trunk and arms, characterized by a folliculocentric mixed inflammatory infiltrate mostly composed of eosinophils [1]. Identical histologic findings are present in eosinophilic pustular folliculitis (EPF), a cutaneous eosinophilic disease first described by Ofuji et al. in 1970, consisting of recurrent crops of pruritic follicular papulopustules localized on the face, trunk and extremities, mainly affecting Japanese men [4, 5]. Several cases of eosinophilic folliculitis of the scalp have also been described in children [6-8]. Some authors suggest a distinction between EPF in classical, pediatric and HIV-associated variants [8]. The diagnostic criteria of HIV-EF include culture-negative follicular and nonfollicular pruritic papules spreading over the head, neck, upper trunk and arms with microscopic evidence of folliculocentric inflammation showing lymphocytes and histiocytes and a large number of eosinophils [9, 10]. Spongiosis of follicular and isthmic epithelium is documented and eosinophilic aggregates are a common feature along with the so called "flame figures" resulting from the alteration of collagen by eosinophil degranulation [9]. Laboratory data include HIV positive test and CD4⁺ T cell count usually less than 200/mul. Elevated serum IgE and peripheral eosinophilia may be present [2, 9]. Our case fullfils the criteria for HIV-EF but is unusual in that the occurrence of this folliculitis in women is extremely rare [11, 12]. Furthermore, the onset of this type of dermatosis in patients unaware of their HIV-infection is equally rare. Given that our patient was not an intravenous drug user and had received no blood transfusions, it is likely that the mode of transmission of the HIV was by heterosexual contact.

Although HIV-EF produces clinical and histological features similar to those observed in Ofuji's disease, they are currently considered as two distinct entities [9]. The clinical aspects of EF in HIV-infected adults differ slightly from EPF as described by Ofuji. In HIV-associated EF, papules have an urticarial appearance whereas lesions observed in Ofuji's disease are usually papules and pustules which coalesce into arciform plaques with a tendency to peripheral extension and central healing, with possible subsequent hyperpigmentation [13, 14].

HIV-EF patients are regarded as a subset of the AIDS population presenting the so called pruritic papular eruption [9]. EF would account for 25-50% of pruritic papular eruption that actually is not a specific diagnosis but rather a group of different conditions revealing the predisposition to develop hypersensitivity reactions including those directed against drugs, microorganisms such as Demodex and Pityrosporum, sebocyte or some constituent of sebum acting as the autoantigen [15, 16].

It is well known that late-stage HIV infection is characterized by a shift from a Th1- to a Th2-dominant profile immune response with increased secretion of interleukin-4 and interleukin-5, both cytokines capable of stimulating eosinophilia [3]. Eotaxin, a member of the beta-chemokine family, recently reported to play a pivotal role in inducing tissue eosinophil recruitment and Th2 immunoinflammatory response, has been shown to be expressed by perifollicular infiltrate in HIV-EF patients [17, 18]. Evaluating the therapeutic approach to this condition [9], medications such as permethrin - active against Demodex - may induce prolonged remission of skin eruption and both metronidazole and itraconazole have been shown to improve HIV-EF, without evidence of working through eliminating specific organisms [19]. Some patients respond to several months of oral isotretinoin or to phototherapy under ultraviolet light B (UVB). Alternative treatments include short term application of potent topical steroids and low dose prednisone (10-20 mg/daily). Our patient could not be treated since she moved to another country and she did not show up at the follow-up visit. In conclusion, EF appears to be a clinical marker of HIV infected subjects and seems to occur in a stage of HIV disease with a CD4⁺ cell count < 200/mul with a higher risk of opportunistic infections and characterized by a shift in the Th1/Th2 cytokine profile. A peculiar aspect of our case is the occurrence of HIV-EF in a black female unaware of the underlying pathologic condition and without clinical signs of HIV infection despite the low CD4⁺ T cell count (101/mul), so that the pruritic papular outbreak could be considered the onset of a HIV-associated disease.

Article accepted on 16/7/02

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