The results of the present study indicate that most patients with anal SCC was 54.96 years constituting a sample younger than that reported in the literature. According to several researches, the peak incidence of anal cancer is between the ages of 58 and 64 years [6,7,8,9,10]. The mean age of patients with anal cancer may had vary among studies, possibly because of the type of population studied and the presence of risk factors such as sexual orientation, immunosuppression (patients with HIV+ infection and transplant recipients), tobacco smoking, and alcoholism [6,7,8,9,10].
We did not evaluated the social economic status of our population but the study was developed on a very poor area of Brazil, with one of the lowest human development indexes. According to National Cancer Institute, cervical cancer and penile cancer are the second more incident type of cancer among women and men, respectively, in Maranhão [4]. Both cancer, as well as anal SCC, are associated with HPV infection and with poor social-economic status, health conditions and hygiene practices of the population. This condition may explain the younger status of our studied population.
Our samples presented a high prevalence of HPV, which are consistent with those reported in the literature. Alemany and coauthors applied a retrospective approach (1986–2011) to evaluate 496 cases of invasive anal cancer for DNA-HPV presence in a multi-center study involving patients from Europe, North America, Latin America, Africa, and Asia. The prevalence of HPV infection for each continent was 87.6, 95.8, 90.4, 61.9, and 81.1%, respectively [10]. In Brazil, Aguiar and co-authors conducted a study of patients with anal carcinomas in Goiânia-Goiás, and found that 76.3% of the samples collected were positive for HPV [9]. The results of our study also corroborate the findings of Varnai and colleagues [11], Ramamoorthy and colleagues [12], de Vuyst and colleagues [13], and Rodel and colleagues [14], who reported the detection of HPV-DNA presence in 60.6, 80, 73, and 95.8% of anal cancer samples examined, respectively.
Torres Neto and colleagues [15] performed a retrospective study about mains demographics characteristics of anal cancer patients in Sergipe, another city of Northeast State of Brazil. However, they did not performed any HPV analysis.
Infection with oncogenic, or high-risk, HPV-16 was detected in all cases. Other studies also report that HPV-16 was the main HPV type found in over 80% of carcinomas [10,17,, 16–18].
Female patients constituted the majority of the cases on our work. Alemany and co-authors [10] found that female patients constituted the majority of the cases of SCC (66.3%). Ouhoummanea and co-authors [8] found that the majority of incidence of anal cancer (60%) was in women. Aguiar and colleagues found that 62.8% of patients with anal cancer were women [9]. The results of a study of Czech patients with anal cancer by Tachezy et al. [6], in which the same number of patients was analyzed as in our study, revealed that 52.4% of the patients were female. Two other studies, conducted in Brazil, found that the occurrence of anal cancer was 62.8–78.8% among the female patients studied [19, 20].
The prevalence of anal SCC in women may be explained by the anatomical proximity between the vaginal opening and the anus. A study by Giraldo and co-authors [21] of 184 Brazilian women demonstrated a significant association between cervical intraepithelial lesions and anal intraepithelial lesions. Anal lesions were found to be present in 17.4% of patients with genital lesions, but only in 3.2% of patients without genital lesions. HPV infection in women may also be facilitated by non-sexual practices and self-inoculation (via vaginal secretions, transfer of fomites, and digital transfer), in view of the anatomical proximity between the vaginal opening and the anus [11, 22].
In what concerns the pathologic characteristics of the anal SCC samples, the most common morphology type observed on our work was the ulcerative form, presented a size of 2.1–5.0 cm, came from the anal canal region and moderately differentiated. However, the majority did not present invasion, infiltration, metastasis, and lymph node involvement. These clinical pathological characteristics are in accordance with others findings. Salati and Kadi [23] reported that the mean size of anal tumors investigated in their study was 3.9 cm. They report that spread of anal cancer is mainly local and regional. Usually, the tumor spreads into the ischiorectal fossae, the prostatic urethra and bladder in men, and the vagina in women. Anal cancer may spread via the lymphatic vessels (10–15%). Hematogenous spread develops in fewer than 10% of cases [23]. Studies have shown that the incidence of nodal metastasis in anal cancer is low (approximately 10%) [17, 24]. Ouhoummanea and co-authors [8] reported that, of the tumors studied, 43% were moderately differentiated.
No statistically significant association (p < 0.05) was found between HPV infection and clinical and histopathological variables. Other reports have also concluded that anal tumors are highly likely to be positive for infection with HR-HPV, regardless of the morphology of the tumor [6].
The understanding of HPV prevalence and knowledge of the viral subtype distribution constitute important epidemiological information that can assist the development of local or regional public policies to prevent HPV and of new vaccines. The present study, in agreement with other epidemiological and molecular studies, demonstrates that HPV infection is an important etiological agent of anogenital cancer [21, 25].
