Search

Background Epidermodysplasia verruciformis (EV) is a rare genodermatosis associated with infections with specific human papillomaviruses (HPVs) belonging to the β genus of HPV. Patients with EV usually have a selective defect in cell-mediated immunity. Although skin cancer frequently develops in the sun-exposed cutaneous lesions of patients with EV, the anogenital area is usually not affected by squamous cell carcinomas related to mucosal HPV types. Observations We report the case of a patient with clinical similarities to EV who also presented with primary lymphedema, anogenital dysplasias, and depressed cell-mediated immunity. Swab samples and biopsy specimens from various body sites collected over a 28-month period were screened by different protocols for DNA of the HPV groups alpha, beta, and mu/nu. Seventeen α-HPV types could be demonstrated. Interestingly, β-HPVs (HPV-22 and HPV-23) were detectable only in plucked eyebrows and in 1 skin swab sample. None of the specimens from lesional biopsies carried β-HPV. Consistently found α-HPV types included HPV types 6, 51, 52, 61, and 84 in the genitoanal region and HPV-57 in skin lesions. Histological and cytological evaluation revealed multifocal anogenital dysplasia and benign genital and cutaneous warts. Conclusions To our knowledge, only 1 other similar case of an EV-like syndrome with impaired, cell-mediated immunity and primary lymphedema has been described in the literature. Based on the characteristic clinical and virological findings in the present case and the previously published case, we speculate that both patients could have a previously unknown syndrome that has clinical similarities to EV but notably differs in the associated HPV types. We suggest the acronym WILD (warts, immunodeficiency, lymphedema, dysplasia) to characterize this syndrome.

Objective To evaluate the treatment of anal intraepithelial neoplasia (AIN) with the local immune response modifier imiquimod in human immunodeficiency virus (HIV)-positive men who have sex with men (MSM). Design Prospective, nonrandomized, open-label pilot study, with a mean follow-up time of 9½ months. Setting Dermatology department of a university hospital. Patients Twenty-eight consecutive HIV-positive MSM with histologically confirmed perianal (n = 23) or intra-anal (n = 5) AIN. Intervention Overnight treatment with self-applied imiquimod cream (perianal AIN) or suppositories (intra-anal AIN) 3 times a week for 16 weeks. Main Outcome Measures Response to treatment was documented using clinical, cytologic, and histologic criteria. Human papillomavirus (HPV) typing and HPV DNA load determination for the high-risk HPV types 16, 18, 31, and 33 were performed. Results Seventeen (61%) of all 28 patients included in the study and 17 (77%) of the 22 patients with AIN, who applied imiquimod as instructed, showed clinical and histologic clearance at the end of therapy. Four patients had residual AIN and 1 patient did not improve. Clinical response was accompanied by a sharp decline in HPV DNA loads and by a reduction in the number of HPV types, but long-term HPV clearance was rarely achieved. In the follow-up period, AIN cleared in 3 patients with residual AIN. Fourteen (78%) of 18 imiquimod responders with at least 5 five months of follow-up had a normal cytologic and clinical picture at the end of the follow-up period. Three primary responders developed a recurrence. In 6 noncompliant patients, there was no clinical or morphological improvement and the HPV DNA loads remained high. Conclusions Imiquimod appears to be a safe and effective treatment option for AIN in HIV-positive MSM. Clinical response is accompanied by a significant decrease in high-risk HPV DNA load. These results should encourage controlled randomized studies of imiquimod treatment of AIN. Trial Registration clinicaltrials.gov Identifier:NCT00365729

Patients with psoriasis treated with psoralen-UV-A (PUVA) are at increased risk of skin cancer; however, the exact causes of this increased incidence are not well understood. It has been suggested that PUVA may increase expression of the tumorigenic agent human papillomavirus (HPV) in skin by directly stimulating virus replication, immune suppression, or both, thereby leading to skin cancer formation.To determine whether HPV DNA prevalence in the skin is increased after long-term PUVA treatment.Screening for the presence of HPV sequences in DNA isolated from plucked body hairs of patients with psoriasis with a history of PUVA exposure and a history of skin cancer (group A), PUVA exposure and no history of skin cancer (group B), and no PUVA exposure and no history of skin cancer (group C).University hospital.Hair samples were obtained from 81 patients with psoriasis (56 men and 25 women; mean age, 52 years), including 16 in group A (mean number of PUVA exposures, 702), 35 in group B (mean number of PUVA exposures, 282), and 30 in group C. DNA was isolated from the hair samples and analyzed by polymerase chain reaction with the use of 2 nested primer systems specific for epidermodysplasia verruciformis-associated or related and genital or mucosal virus types, respectively.The rate of HPV DNA positivity was significantly higher in groups A (73% [11/15]) and B (69% [24/35]) than in group C (36% [10/28]) (A + B vs C, P =.009; chi(2) test; age adjusted). Conclusion The prevalence of HPV in the skin (hair follicles) is increased in patients with psoriasis who have a history of PUVA exposure.

Objective To evaluate Merkel cell polyomavirus (MCPyV) DNA prevalence and load among men with human immunodeficiency virus (HIV) (hereafter referred to as HIV-positive men) and among healthy male control subjects. Design Prospective study from February 4, 2009, through April 24, 2010. Setting Dermatology department of a university hospital. Patients A total of 449 male adults were prospectively recruited, including 210 HIV-positive men who have sex with men and 239 healthy controls. Cutaneous swabs were obtained once from the surface of the forehead in all participants. Main Outcome Measures Swabs were evaluated for the presence of MCPyV DNA using single-round and nested polymerase chain reaction. The MCPyV DNA load (the number of MCPyV DNA copies per β-globin gene copy) was determined in MCPyV-positive samples using quantitative real-time polymerase chain reaction. Results Among 449 forehead swabs analyzed, MCPyV DNA was detected in 242 (53.9%). Compared with healthy controls, HIV-positive men more frequently had MCPyV DNA on nested polymerase chain reaction (49.4% vs 59.0%, P = .046) and on single-round polymerase chain reaction (15.9% vs 28.1%, P = .002). The MCPyV DNA loads in HIV-positive men were similar to those in HIV-negative men, but HIV-positive men with poorly controlled HIV infection had significantly higher MCPyV DNA loads than those who had well-controlled HIV infection (median and mean MCPyV DNA loads, 2.48 and 273.04 vs 0.48 and 11.84; P = .046). Conclusions Cutaneous MCPyV prevalence is increased among HIV-positive men who have sex with men. Furthermore, MCPyV DNA loads are significantly higher in HIV-positive men with poorly controlled HIV infection compared with those who have well-controlled HIV infection. This could explain the increased risk of MCPyV-associated Merkel cell carcinoma observed among HIV-positive individuals.

We followed with interest the discussion in several articles that appeared in theArchiveson the controversy about the significance of human papillomaviruses (HPVs) for nonmelanoma skin cancers (NMSCs). 1-3 Despite several reports on the recovery of HPVs from NMSCs, it is still unclear if HPVs are in fact involved in the genesis of these tumors. 1 Also, the types of HPVs that are possibly implicated are a matter of controversy: chiefly mucosal HPVs (types 6, 11, 16, and 18) are reported by Goldberg and Griego, 2 Moy and Eliezri, 3 Euvrard et al, 4 and Soler et al. 5 In sharp contrast, only HPV types of the epidermodysplasia verruciformis group were detected in NMSCs by Berkhout et al 6 and De Jong-Tieben et al, 7 whereas mucosal HPVs, as described by others, were ruled out. The primers used for this study are suitable for the amplification of both the

At least 45 different human papillomavirus (HPV) types are presently known, which induce epithelial tumors of the skin or mucosa. 1 The majority of the warts, papillomas, leukoplakias, or hyperplasias are benign, but some lesions, particularly dysplasias of the cervix uteri, macules of patients with epidermodysplasia verruciformis (EV), and laryngeal papillomas in adults, may progress to squamous cell carcinomas. Infection by HPV elicits humoral and cellular immune mechanisms against virus particles and tumor tissue, 2,3 which trigger tumor regression and leave the host immune to reinfection. The incidence of some HPV types appears rather unaffected by the immune status of the patient, while susceptibility to other types depends more or less on an impaired immune system. Infections by HPV 2, 3, 4, and 10, for example, are considerably favored by a compromised immune system, which is reflected by the frequent occurrence in immunosuppressed allograft recipients. 4-6