In January 2010, at the age of 43 years, the patient was diagnosed with HIV infection, with a CD4 count of 819 cells/mm3 (CD4 percentage = 39%). In February 2011, when his CD4 count was 562 cells/mm3 (37%), the patient started to experience dramatic regrowth of scalp and body hair (Fig. 1), which increased as his CD4 count reduced, reaching a maximum of 90% regrowth in March 2013, when his CD4 count was 469 cells/mm3 (27%). The patient started anti-retroviral treatment (tenofovir disoproxil/emtricitabine, atazanavir and ritonavir) in May 2013, and did not have recurrence of hair loss when his CD4 counts increased to 623 cells/mm3 (33%) a month later, or after starting treatment for associated syphilis. To our knowledge, this is the first report of induction of hair growth in a patient with AA after HIV infection, and the first report of remission of a long-standing autoimmune disease after acquisition of HIV. This finding is especially noteworthy given that remission occurred in longstanding AU. This report raises interesting questions about the pathogenesis of AA, and emphasizes that changes in the systemic immune system can lead to disease regression. Previous reports have suggested that HIV infection may be associated with AA induction.2,3 One of these studies also reported that the CD4/CD8 ratio decreased when AA commenced, but paradoxically, this immune dysregulation was associated with an influx of CD4+ cells to the follicular bulb.3 Nevertheless, all preceding reports described the initiation of acute AA with HIV infection, whereas our patient experienced remission of a chronic case of AU. This may suggest that different sub-populations of T cells are involved in the acute and chronic phases of AA, a fact that has also recently been shown experimentally.4 It was previously shown that a high CD4/CD8 ratio of perifollicular infiltrate is associated with active AA, and that a decreased ratio accompanies hair regrowth.5 This may explain why decreased CD4 counts accompanied AA remission in our patient. Further insight into the pathogenesis of AA remission in patietns with HIV may help elucidate the underlying mechanism of AA in the general population.
2 Cho M, Cohen PR, Duvic M. Vitiligo and alopecia areata in patients with human immunodeficiency virus infection. South Med J 1995; 88: 489–91. 3 Stewart MI, Smoller BR. Alopecia universalis in an HIV-positive patient: possible insight into pathogenesis. J Cutan Pathol 1993; 20: 180–3. 4 Ito T, Hashizume H, Shimauchi T et al. CXCL10 produced from hair follicles induces Th1 and Tc1 cell infiltration in the acute phase of alopecia areata followed by sustained Tc1 accumulation in the chronic phase. J Dermatol Sci 2013; 69: 140–7. 5 Gregoriou S, Papafragkaki D, Kontochristopoulos G et al. Cytokines and other mediators in alopecia areata. Mediators Inflamm 2010; 2010: 928030.
Bullous acral lichen sclerosus with milia doi: 10.1111/ced.12278 A 79-year-old woman presented with a 5-year history of painful lesions on the sole of her right foot. The patient reported that the lesions had been present for 5 years,
Y. Ramot,1 T. Tetro,1 I. Levi,2 and A. Zlotogorski1 1 Department of Dermatology, Hadassah–Hebrew University Medical Center, PO BOX 12000, Jerusalem 9112001, Israel; and 2Sheba Medical Center, Tel-Hashomer, Israel E-mail: [email protected]
Conflict of interest: the authors declare that they have no conflicts of interest. Accepted for publication 13 October 2013
References 1 Price VH. Therapy of alopecia areata: on the cusp and in the future. J Investig Dermatol Symp Proc 2003; 8: 207–11.
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Figure 1 Sole of the right foot, showing a well-demarcated,
slightly erythematous, sclerotic plaque with some pale areas and yellowish translucent papules (arrows) on the lateral foot edge.
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and she believed they had appeared after a herpes zoster infection. Initially, the lesions had the appearance of blisters, which resolved spontaneously. The patient had previously been treated by her family doctor with betamethasone dipropionate ointment without improvement. At presentation, pain was the main symptom. On physical examination of the sole of the patient’s right foot, a well-demarcated, slightly erythematous, sclerotic plaque was seen, which had some pale areas suggestive of blister formation. On the lateral foot edge, approximately 15 yellowish translucent papules were visible (Fig. 1). Genital lesions were absent. On histological examination of a biopsy taken from the sole of the right foot, there was marked hyperkeratosis, thinning of the Malpigian layer, vacuolar alteration of the basal layer, and a broad zone of subepidermal oedema with homogenization of collagen. A biopsy taken from one of the translucent yellowish papules showed similar features, along with focal subepidermal blisters and a small dermal cyst, which was lined by squamous epithelium with keratinous material in its core (Fig. 2). The patient was diagnosed as having acral bullous lichen sclerosus (LS) with secondary milia formation.
LS is rarely seen on the palms or soles, and only a few cases of LS at these locations have been described. In our patient, the formation of milia was a prominent finding. Although clinically, the blisters were no longer apparent, a skin biopsy did show marked dermal oedema with subepidermal blister formation, which apparently resulted in the formation of milia. Mechanical forces have been described as possible contributors to LS. Considering that the feet are subject to shear forces from the wearing of shoes and pressure from walking, in addition to the papillary oedema typical of LS, blister formation can occur easily.1,2 This possibly accounts for the large number of secondary milia found on our patient’s foot, which would have arisen as a result of previous blister formation. None of the other six reported cases of LS involving the palms and/or soles described milia formation.3–5 However, most of these cases had been present for a shorter time (mean duration 2 years), which may indicates that the time of clinical and histological evaluation may be of importance in finding milia, as these are the residual lesions of previous subepidermal blister formation. L. Vink, and T. M. Starink Department of Dermatology, VU University Medical Center, Amsterdam, the Netherlands E-mail: [email protected]
Conflict of interest: the authors declare that they have no conflicts of interest. Accepted for publication 1 October 2013
References 1 Ballester I, Banuls J, Perez-Crespo M, Lucas A. Extragenital bullous lichen sclerosus atrophicus. Dermatol Online J 2009; 15: 6. 2 Tudino ME, Wong AK. Bullous lichen sclerosus et atrophicus on the palms and wrists. Cutis 1984; 33: 475–6. 3 Steff M, Toulemonde A, Croue A et al. [Acral lichen sclerosus et atrophicus]. Ann Dermatol Venereol 2008; 135: 201–4. 4 Petrozzi JW, Wood MG, Tisa V. Palmar-plantar lichen sclerosus et atrophicus. Arch Dermatol 1979; 115: 884. 5 Hammar H. Plantar lesions of lichen sclerosus et atrophicus accompanied by erythermalgia. Acta Derm Venereol 1978; 58: 91–2.
Are dermatoscopes a potential source of nosocomial infection in dermatology clinics? doi: 10.1111/ced.12277 Figure 2 Biopsy from the foot showing oedema and homogeniza-
tion of collagen with milia formation in the centre. Note focal subepidermal blister formation (arrow) (haematoxylin and eosin, original magnification 9 25).
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Dermatoscopes are often directly applied on patients’ skin during dermatology examinations and could therefore act as potential vectors of infection. Nosocomial or hospital-
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