Male Genital Warts Research Articles

Relation of p53 tumor suppressor protein expression to human papillomavirus (HPV) DNA and to cellular atypia in male genital warts and in premalignant lesions.

Functional disturbance of p53 tumor suppressor protein contributes to uncontrolled cell growth. Human papillomavirus (HPV) E6 oncoproteins bind to wild-type p53 and abrogate its function. Our objective was to elucidate the relation of aberrant p53 protein expression to HPV DNA and cellular atypia in male genital warts and premalignant lesions. Immunohistochemically detectable p53 protein expression was studied in 35 male anogenital warts with low-level or no keratinocyte atypia (histologically confirmed condylomata acuminata), in 25 lesions with bowenoid papulosis (BP; carcinoma in situ) histology, and in 10 non-condyloma lesions using immunostaining with three established antibodies recognizing full-length wild-type accumulated p53 protein, or its conformational mutants. HPV DNA specific for HPV 6/11, 16/18, or 31/33/35 was identified by in situ hybridization or by polymerase chain reaction (PCR) - based amplification. Both nuclear and cytoplasmic keratinocyte immunostaining for p53 protein was detected in 41% of condylomata with no keratinocyte atypia and in 42% of condylomata with slight nuclear atypia or with bowenoid papulosis histology. No association of aberrant p53 expression with any specific HPV type or with HPV DNA was observed. Normal skin and some other penile dermatoses were negative for p53 immunostaining. In the follow-up biopsies of 16 BP patients, treated with CO2 laser, recurrence of atypia was seen exclusively in lesions initially positive for both HPV DNA and p53 protein. Our results show that a few cells in male genital warts even with no cellular atypia may express abnormally sequestered or loss-of-function p53 protein, and that concomitant presence of any type of HPV DNA is associated with recurrencies or progression of premalignant changes.

A study of the prevalence of male intrameatal warts using meatoscopy in a genitourinary medicine department.

A cross-sectional study is undertaken to determine the prevalence of male intrameatal and distal urethral warts, using meatoscopy. A group of 169 patients presenting for anogenital warts and a group of 74 unselected patients attending the Department for a variety of reasons during the study period, were examined. Twenty-one patients (13.5%) out of 155 patients with anogenital or related warts had external warts at the meatus. Of these 21 cases, 12 (57.1%) had further extension of their warts into the distal urethra. Fifteen other cases of intrameatal and distal urethral warts were detected in the absence of external warts at the meatus. Twenty-three cases out of 107 males with genital warts (21.5%) were found to have intrameatal or distal urethral warts, thus reflecting the common occurrence of these lesions. A highly significant association between the presence of intrameatal/distal urethral warts and the presence of male genital warts was found (P = 0.003). One hundred and fifty-three repeat meatoscopic examinations were carried out, 6 weeks after their first examination. Three new cases of intrameatal/distal urethral warts were found. Intrameatal and distal urethral warts occurred from a depth of 5 mm to 25 mm. One hundred and eighty-three female partners of the study patients were examined. An association between the presence of intrameatal/distal urethral warts and female anogenital warts was found (P = 0.028). No corroborating association between the presence of male and female anogenital warts was found (P = 0.47). This observation may have a bearing on disease transmission and control. The detection of intrameatal/distal urethral warts will be important in achieving successful treatment of male anogenital warts.

Topical idoxuridine for treatment of genital warts in males. A double-blind comparative study of 0.25% and 0.5% cream.

Fifty heterosexual male patients with histologically verified genital warts of short duration (less than 3 months) were randomly allocated to treatment with either 0.25% or 0.5% idoxuridine cream. The application of the cream to the warts was performed twice daily for an initial period of 14 days, whereafter patients with partial improvement or no response were retreated in the same way for another period of 14 days. Patients not completely healed after 28 days were regarded as treatment failures and withdrawn from the study. After the initial treatment period of 14 days, 19 of 25 patients (76%) treated with 0.5% idoxuridine cream, and 9 of 25 patients (36%) treated with 0.25% idoxuridine cream were completely healed. This difference is significant (p less than 0.01). The corresponding figures at the second follow-up examination (28 days after start of the study) were 19 of 25 (76%) and 13 of 25 (52%), respectively. At the last follow-up examination three months after start of treatment, four patients treated with 0.5% idoxuridine cream and five patients treated with 0.25% idoxuridine cream had a relapse. Thus, the overall rate of complete healing was 15 of 25 (60%) for the patients treated with 0.5% idoxuridine cream and 8 of 25 (32%) for those treated with 0.25% idoxuridine cream. The difference is significant (p less than 0.01). No adverse reactions were observed or reported by the patients.