Correspondence
cutaneous lesions of sarcoidosis in areas injected with cosmetic fillers could be more common in IFN-induced sarcoidosis than in sarcoidosis not triggered by IFN. Although foreign bodies or filler substances are not the cause of systemic sarcoidosis, the filler particles did influence the distribution of the lesions when our patient developed sarcoidosis. In patients with granulomatous reactions to cosmetic fillers, sarcoidosis must be excluded, particularly in IFN-treated patients. We treated our patient with potassium iodide, and the EN lesions healed in a few weeks. The facial nodular lesions later slowly disappeared without any treatment. To date, the patient remains asymptomatic. ,2 R. M. Penın,3 I. Figueras,1 J Marcoval,1 J. Ma~ na M. Labori2 and R. Llatjos3 Departments of 1Dermatology, 2Internal Medicine and 3Pathology, Bellvitge Hospital, C/Feixa Llarga s/n, L’Hospitalet de Llobregat, 08907 Barcelona, Spain E-mail: [email protected] Conflict of interest: the authors declare that they have no conflicts of interest. Accepted for publication 21 October 2013
AA is an autoimmune-mediated disease, making it one of the most common autoimmune diseases.1 Infection with human immunodeficiency virus (HIV) has been associated with autoimmune diseases, and several reports describe induction of AA by HIV infection.2 We report a case of AU that resolved spontaneously after HIV infection. This is, to our knowledge, the first report of HIV-induced remission of AA. A 46-year-old patient had sustained recurrent attacks of patchy AA on his scalp since the age of 6 years, progressing to AT at the age of 20 years. When he was 26 years old, he developed AU, which was recalcitrant to treatment. He had tattoos applied to compensate for eyebrow loss.
(a)
References J, Moreno A et al. Foreign bodies in 1 Marcoval J, Ma~ na granulomatous cutaneous lesions of patients with systemic sarcoidosis. Arch. Dermatol 2001; 137: 427–30. 2 Descamps V, Landry J, Frances C et al. Facial cosmetic filler injections as possible target for systemic sarcoidosis in patients treated with interferon for chronic hepatitis C: two cases. Dermatology 2008; 217: 81–4. 3 Sidwell RU, Johnson McL, Francis N et al. Cutaneous sarcoidal granulomas developing after Artecoll facial cosmetic filler in a patient with newly diagnosed systemic sarcoidosis. Clin Exp Dermatol 2006; 31: 208–11. 4 Fischer J, Metzler G, Schaller M. Cosmetic permanent fillers for soft tissue augmentation: a new contraindication for interferon therapies. Arch Dermatol 2007; 143: 507–10. 5 Dal Sacco D, Cozzani E, Parodi A, Rebora A. Scar sarcoidosis after hyaluronic acid injection. Int J Dermatol 2005; 44: 411–12. (b)
Remission of long-standing alopecia universalis after human immunodeficiency virus infection doi: 10.1111/ced.12260
Alopecia areata (AA) is a common disorder, which usually presents as patches of hair loss on the scalp or beard. However, in 5% of the patients,1 the disease may progress to alopecia totalis (AT), affecting all scalp hair, or even alopecia universalis (AU), affecting all scalp and body hair. AU is highly resistant to treatment, and spontaneous remission occurs only rarely.1
2014 British Association of Dermatologists
Figure 1 (a) Almost complete regrowth of hair on the scalp after
human immunodeficiency virus infection with decreased CD4 counts in a patient with alopecia universalis. (b) Regrowth of eyebrow hair, covering the black tattoo used to compensate for the long-standing eyebrow loss caused by the patient’s disease. Picture was taken when the patient was 46 years old, 40 years after alopecia areata had started.
Clinical and Experimental Dermatology (2014) 39, pp395–399
399
Correspondence
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.
400
Clinical and Experimental Dermatology (2014) 39, pp395–400
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.
2014 British Association of Dermatologists
cutaneous lesions of sarcoidosis in areas injected with cosmetic fillers could be more common in IFN-induced sarcoidosis than in sarcoidosis not triggered by IFN. Although foreign bodies or filler substances are not the cause of systemic sarcoidosis, the filler particles did influence the distribution of the lesions when our patient developed sarcoidosis. In patients with granulomatous reactions to cosmetic fillers, sarcoidosis must be excluded, particularly in IFN-treated patients. We treated our patient with potassium iodide, and the EN lesions healed in a few weeks. The facial nodular lesions later slowly disappeared without any treatment. To date, the patient remains asymptomatic. ,2 R. M. Penın,3 I. Figueras,1 J Marcoval,1 J. Ma~ na M. Labori2 and R. Llatjos3 Departments of 1Dermatology, 2Internal Medicine and 3Pathology, Bellvitge Hospital, C/Feixa Llarga s/n, L’Hospitalet de Llobregat, 08907 Barcelona, Spain E-mail: [email protected] Conflict of interest: the authors declare that they have no conflicts of interest. Accepted for publication 21 October 2013
AA is an autoimmune-mediated disease, making it one of the most common autoimmune diseases.1 Infection with human immunodeficiency virus (HIV) has been associated with autoimmune diseases, and several reports describe induction of AA by HIV infection.2 We report a case of AU that resolved spontaneously after HIV infection. This is, to our knowledge, the first report of HIV-induced remission of AA. A 46-year-old patient had sustained recurrent attacks of patchy AA on his scalp since the age of 6 years, progressing to AT at the age of 20 years. When he was 26 years old, he developed AU, which was recalcitrant to treatment. He had tattoos applied to compensate for eyebrow loss.
(a)
References J, Moreno A et al. Foreign bodies in 1 Marcoval J, Ma~ na granulomatous cutaneous lesions of patients with systemic sarcoidosis. Arch. Dermatol 2001; 137: 427–30. 2 Descamps V, Landry J, Frances C et al. Facial cosmetic filler injections as possible target for systemic sarcoidosis in patients treated with interferon for chronic hepatitis C: two cases. Dermatology 2008; 217: 81–4. 3 Sidwell RU, Johnson McL, Francis N et al. Cutaneous sarcoidal granulomas developing after Artecoll facial cosmetic filler in a patient with newly diagnosed systemic sarcoidosis. Clin Exp Dermatol 2006; 31: 208–11. 4 Fischer J, Metzler G, Schaller M. Cosmetic permanent fillers for soft tissue augmentation: a new contraindication for interferon therapies. Arch Dermatol 2007; 143: 507–10. 5 Dal Sacco D, Cozzani E, Parodi A, Rebora A. Scar sarcoidosis after hyaluronic acid injection. Int J Dermatol 2005; 44: 411–12. (b)
Remission of long-standing alopecia universalis after human immunodeficiency virus infection doi: 10.1111/ced.12260
Alopecia areata (AA) is a common disorder, which usually presents as patches of hair loss on the scalp or beard. However, in 5% of the patients,1 the disease may progress to alopecia totalis (AT), affecting all scalp hair, or even alopecia universalis (AU), affecting all scalp and body hair. AU is highly resistant to treatment, and spontaneous remission occurs only rarely.1
2014 British Association of Dermatologists
Figure 1 (a) Almost complete regrowth of hair on the scalp after
human immunodeficiency virus infection with decreased CD4 counts in a patient with alopecia universalis. (b) Regrowth of eyebrow hair, covering the black tattoo used to compensate for the long-standing eyebrow loss caused by the patient’s disease. Picture was taken when the patient was 46 years old, 40 years after alopecia areata had started.
Clinical and Experimental Dermatology (2014) 39, pp395–399
399
Correspondence
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.
400
Clinical and Experimental Dermatology (2014) 39, pp395–400
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.
2014 British Association of Dermatologists
