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Biomedical subjects

C S Rabkin

Publications and source records attributed to C S Rabkin.

At least 55 records · Page 3Linked to original sources
PubMed1995

Persistence of immunoglobulin heavy chain/c-myc recombination-positive lymphocyte clones in the blood of human immunodeficiency virus-infected homosexual men.

We studied blood lymphocytes of human immunodeficiency virus (HIV)-seropositive and -negative homosexual men for the presence of T(8;14) translocations that recombine c-myc and immunoglobulin heavy-chain (IgH) mu/IgH alpha switch regions. Clones with T(8;14) translocations were detected in 10.5% (12/114) of the HIV-positive and in 2.0% of the 99 uninfected patients. The majority of recombinations were found at a single time point only. Four patients, however, harbored multiple (up to four) and persistent (up to 9 years) translocation-positive cell clones. No correlation between the presence of these aberrant lymphocytes and a later lymphoma could be established. The exon 1/intron 1 region of the recombined c-myc was investigated for the presence of point mutations and these were found in the nonpersistent clones. Additional alterations detected in these clones included duplications and a deletion in the c-myc gene. The pattern of base substitution indicates that they were introduced after the translocation event.

Base Sequence↗
PubMed1995

AIDS-related Kaposi's sarcoma is a clonal neoplasm.

Kaposi's sarcoma is generally believed to be a non-neoplastic hyperproliferation because it may regress spontaneously and its spindle cells lack features of typical tumor cells, such as aneuploidy, nuclear atypia, and permissive growth in cell culture. A fundamental characteristic of neoplasms is clonality, in that they arise from clonal replication of a single cell whereas reactive processes are derived from polyclonal proliferation. We used an X chromosome inactivation assay to determine the clonality of Kaposi's sarcoma nodules from patients with AIDS-related disease. The assay is based on a methyl-sensitive restriction digest followed by PCR amplification of the highly polymorphic androgen receptor gene. Two of three evaluable cases had a monoclonal pattern of inactivation, and the third case had a clonal expansion of cells with an altered microsatellite repeat sequence. These data suggest that Kaposi's sarcoma (at least in the AIDS setting) is a clonal neoplasm.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Cancer incidence in a population with a high prevalence of infection with human immunodeficiency virus type 1.

BACKGROUND: Human immunodeficiency virus type 1 (HIV-1) infection is known to increase the incidence of Kaposi's sarcoma and non-Hodgkin's lymphoma. Parallels with other causes of immunodeficiency suggest a possible effect of HIV-1 on additional cancers. PURPOSE: This study was designed to determine the types and rates of cancers occurring in excess in the presence of HIV-1 infection. METHODS: We examined cancer incidence in a population-based open cohort with a high prevalence of HIV-1 infection. The study population was never-married men aged 25-54 years who resided in San Francisco, Calif., of whom an estimated 20,000 (24%) were HIV-1 seropositive as of late 1984. Cancer registration data covering 1,390,000 person-years of observation of these men from 1973 through 1990 were obtained from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program. Standardized incidence rates and ratios of observed to expected cases (based on rates in the pre-acquired immunodeficiency syndrome [pre-AIDS] period [i.e., 1973-1979]) were calculated for cancers classified by site and by cell type. RESULTS: The incidence of Kaposi's sarcoma in never-married men plateaued in 1988-1990 at 0.5% per year. The incidence of non-Hodgkin's lymphoma increased 20-fold between 1973-1979 and 1988-1990; increases were most pronounced in tumors of higher grade histology and extranodal (especially central nervous system) primary sites. The incidence of Burkitt's and Burkitt-like tumors peaked in 1985-1987, whereas that of large cell diffuse and immunoblastic lymphomas increased throughout the study period. The incidence of Hodgkin's disease was 2.0 (95% confidence interval [CI] = 1.3-3.0) times expected in 1988-1990. The incidence of anal cancer was 9.9 (95% CI = 4.5-18.7) times expected in 1973-1979 and 10.1 (95% CI = 5.0-18.0) times expected in 1988-1990. Ratios of observed to expected cancers of most other sites were 2.0 or less; the ratio of leiomyosarcomas (at any site) was 2.5 (95% CI = 0.5-7.4). CONCLUSIONS: As the HIV-1 epidemic has progressed, the increases in AIDS-related Kaposi's sarcoma, Burkitt's tumor, and other non-Hodgkin's lymphoma have followed different patterns. The effect of HIV-1 on other cancers has been nondetectable. In particular, HIV-1 is not related to the increased risk of anal cancer in homosexual men, which antedated the AIDS epidemic. IMPLICATIONS: These data suggest that the etiologic mechanisms of HIV-1-related malignancy differ for specific cancers and do not globally increase cancer risk. Control of HIV-1-related cancer remains an unsolved challenge in the management of HIV-1 infection.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Risks of immunodeficiency, AIDS, and death related to purity of factor VIII concentrate. Multicenter Hemophilia Cohort Study.

In HIV-infected subjects with haemophilia, CD4 counts seem to fall more slowly in those on high-purity factor VIII (FVIII) than on intermediate-purity product. We evaluated whether risks for AIDS or death were associated with either product among 411 HIV-infected individuals. The relative hazard of AIDS was slightly elevated for both current (1.34) [corrected] and cumulative (1.01 per month) use of high-purity products (neither significant). The corresponding hazards for death were 1.49 and 1.03 (neither significant). Thus we found no evidence that high-purity FVIII concentrates retard the development of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Risk of other cancers following Kaposi's sarcoma: relation to acquired immunodeficiency syndrome.

To evaluate the risk of another cancer among persons who initially developed Kaposi's sarcoma, the authors used data from the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute for the years 1973-1990. In persons under 70 years of age, 4,946 cases of Kaposi's sarcoma were observed during the period 1980-1990 (6,217 person-years of follow-up). On the basis of rates seen during the period prior to the epidemic of acquired immunodeficiency syndrome (AIDS), 169 cases were expected. Therefore, cases of Kaposi's sarcoma in this group were assumed to be AIDS-related, while cases occurring in older persons or during the 1970s were assumed to be non-AIDS-related. Rates were compared with the numbers of cases expected overall and by site on the basis of age-, sex-, and calendar year-specific rates from the SEER data. Among the 4,946 persons with AIDS-related Kaposi's sarcoma, the risk of developing non-Hodgkin's lymphoma through 1990 was increased 198-fold (95% confidence interval 169-232). However, the risk of all other cancers was only marginally increased (1.5-fold; 95% confidence interval 0.95-2.3), a risk that was probably biased upward because of ascertainment and misclassification. Among 491 persons with non-AIDS-related Kaposi's sarcoma, the relative risk of all cancers, including non-Hodgkin's lymphoma, was 0.9 (upper 95% confidence limit 1.2), and the risk of non-Hodgkin's lymphoma alone was 0.6 (upper 95% confidence limit 3.3). As of 1990, the risk of having another cancer following Kaposi's sarcoma was increased only in persons infected with human immunodeficiency virus, who were at high risk of non-Hodgkin's lymphoma but probably not of other cancers as a whole.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Epidemiology of AIDS-related malignancies.

HIV infection is known to increase the incidence of Kaposi's sarcoma and non-Hodgkin's lymphoma. Kaposi's sarcoma preferentially affects homosexual men and risk varies by geographic area, suggesting there is an environmental cofactor for Kaposi's sarcoma in addition to HIV. Despite intensive investigation, the responsible cofactor has not been conclusively identified. HIV-associated non-Hodgkin's lymphoma affects all HIV transmission groups, and non-Hodgkin's lymphoma risk increases with duration of HIV infection and age. Epstein-Barr virus has been implicated in the pathogenesis of this tumor, but the precise mechanisms have not been worked out. Cervical cancer and anal cancer have a less certain association with HIV infection and immunodeficiency, although epithelial dysplasia at these sites does seem to be HIV-related. Children with HIV infection are additionally affected by increased incidence of leiomyosarcoma and benign leiomyoma, whereas adults with HIV infection do not seem particularly susceptible to this tumor, perhaps because of hormonal or growth-promoting factors. Apart from these specific disease associations, HIV infection and related immunodeficiency do not result in a generalized tumor diathesis. Prevention and management of HIV-associated cancers are becoming increasingly important as the HIV epidemic continues to grow.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Cancer incidence trends in women at high risk of human immunodeficiency virus (HIV) infection.

To determine the types and rates of tumors which may be associated with HIV infection in women, we used cancer incidence data from New York and northern New Jersey. We examined changes in incidence of selected cancers in women aged 20-49 years and compared groups differing in incidence of AIDS. Black women were compared to white women in New York City and in the remainder of New York State; for cervical cancer, rates were also compared for Blacks and Whites in northern New Jersey. The incidence of Kaposi's sarcoma in women increased in New York City, beginning in 1982 for Blacks and in 1984 for Whites, but remained stable in the remainder of New York State. The incidence of non-Hodgkin's lymphoma in New York women doubled in Blacks after 1982 whereas incidence trends in Whites were unchanged. No consistent variation was seen in the incidence of Hodgkin's disease. Cervical cancer in New York and northern New Jersey Blacks declined over the same period by approximately 40% for invasive tumors and 50% for in situ lesions. The HIV epidemic is associated with substantial excesses of Kaposi's sarcoma and non-Hodgkin's lymphoma in women. The absence of Kaposi's sarcoma in upstate New York women suggests the existence of a geographically restricted co-factor(s) for Kaposi's sarcoma in addition to HIV. If HIV affected cervical cancer incidence through 1988, its impact was small compared to the striking decreases which followed widespread adoption of Papanicolaou screening.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Trends in death with tuberculosis during the AIDS era.

OBJECTIVE: To describe and analyze recent changes in tuberculosis mortality in the United States during the acquired immunodeficiency syndrome (AIDS) epidemic. DESIGN: We used National Center for Health Statistics multiple-cause mortality data and analyzed deaths with tuberculosis (1980 through 1990) and/or AIDS (1987 through 1990) as an underlying or associated cause. We also categorized the 50 states and the District of Columbia into high (five states), medium (23 states), and low (23 states) AIDS incidence groups and then compared the groups' rates of death with tuberculosis during the period 1980 through 1990. STUDY POPULATION: Residents of the United States who died in the period 1980 through 1990. MAIN OUTCOME MEASURES: Death certificates indicating AIDS and/or tuberculosis. RESULTS: A bimodal age distribution of persons dying with tuberculosis has emerged concurrent with the AIDS epidemic. A new peak spanning the ages 20 to 49 years accompanies the preexisting peak in the elderly. In 1990, 54.2% (729/1344) of the deaths with tuberculosis in persons 20 to 49 years of age occurred in persons who also had AIDS listed on their death certificates. During the period 1987 through 1990, there was an increasing trend in the proportion of AIDS deaths that also had tuberculosis: 2.3% (353/15,075) in 1987, 2.5% (460/18,649) in 1988, 3.0% (738/24,607) in 1989, and 3.0% (836/27,975) in 1990 (P < .001). Of AIDS deaths in 1990, 1.6% (253/15,565) of whites died with tuberculosis, compared with 4.7% (400/8533) of blacks (P < .001) and 4.7% (172/3666) of Hispanics (P < .001). In the high AIDS incidence states, the rate of death with tuberculosis in persons aged 20 to 49 years rose from 0.61 to 2.82 per 100,000 population in the period 1982 through 1990, an increase of 362%. For this age group in the states with medium and low AIDS incidence, the rates of death with tuberculosis during this period rose 52% and 47% (from 0.44 to 0.67 and from 0.19 to 0.28 per 100,000 population), respectively. The increases in the rate of death with tuberculosis within all three groups and the differences among the groups were all highly statistically significant (P < .001). CONCLUSION: The AIDS epidemic has significantly increased the number and rate of tuberculosis deaths in younger adults through 1990, although in this study discrimination of deaths due to tuberculosis from deaths with tuberculosis was not possible. Vigorous efforts to prevent and treat tuberculosis and AIDS are indicated to reverse the trends we have described.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Human immunodeficiency virus-related conditions in children and adults with hemophilia: rates, relationship to CD4 counts, and predictive value.

To further elucidate the natural history of human immunodeficiency virus (HIV) infection, we studied intermediate HIV-related conditions occurring before acquired immunodeficiency syndrome (AIDS) in a prospectively observed multicenter cohort of 738 HIV-infected persons with hemophilia. We analyzed the frequency in adults and children of common HIV-related conditions and the relative risk of AIDS after occurrence of these conditions, controlling for age at seroconversion and the percentage of CD4+ lymphocytes. Thrombocytopenia was the most frequently observed condition with cumulative incidences of 43% +/- 7% in adults and 27% +/- 6% in children and adolescents by 10 years after seroconversion. Oral candidiasis, fever, weight loss, and non-AIDS pneumonia were two to four times more common in adults than children, whereas herpes zoster risk was similar in the two age groups. HIV-related conditions were infrequent during the first 4 years of infection, particularly in children. With the exception of thrombocytopenia, mean CD4 counts were less than 350 cells/microL at the onset of the conditions. The relative hazard of AIDS after oral candidiasis was 18 in children and 3.8 in adults. Relative hazard in adults was also increased after persistent fever (10), weight loss (3.2), and non-AIDS pneumonia (2.2). Herpes zoster and thrombocytopenia were not significantly associated with AIDS in either age group. We conclude that intermediate HIV-related conditions occur more frequently in adults than in children with hemophilia. Persistent fever is the strongest predictor of AIDS in adults, whereas oral candidiasis is the strongest predictor in children. These findings should facilitate the design and conduct of clinical trials as well as the management of HIV-infected children and adults.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Cytomegalovirus infection and risk of AIDS in human immunodeficiency virus-infected hemophilia patients. National Cancer Institute Multicenter Hemophilia Cohort Study Group.

The effects of prevalent and incident cytomegalovirus (CMV) infection on human immunodeficiency virus (HIV) disease progression were examined in 393 hemophilia patients with known dates of HIV seroconversion. Of the cases, 191 (49%) had IgG antibody to CMV in their earliest stored sera (median date, November 1983). CMV-seropositive subjects were one and a half times more likely to develop AIDS, and they were also older than CMV-negative subjects. Adjusted for age, CMV seropositivity was not associated with the development of AIDS. In age-adjusted analyses, CMV-seropositive subjects had a small, but statistically insignificant, decrease in survival after HIV seroconversion. Older subjects were more likely to CMV seroconvert by the time of their latest available serum samples (P = .03). CMV seroconverters were five times more likely to develop clinical CMV disease than were subjects initially CMV-positive (P = .02). To avoid this source of serious morbidity, CMV-seronegative hemophiliacs with HIV infection should not be exposed to cellular blood products or body fluids from CMV-seropositive donors.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Second primary cancers following anal and cervical carcinoma: evidence of shared etiologic factors.

The authors examined the incidence of second primary cancers occurring after cervical and anal cancer. Data from the Connecticut Tumor Registry for 1935-1988 and eight other US tumor registries for 1973-1988 were used. Women with primary invasive cervical cancer had a relative risk of 4.6 (95% confidence interval (CI) 2.4-8.1) for subsequent invasive anal cancer. Increased relative risks after cervical cancer were also found for cancers of the oral cavity (relative risk (RR) = 2.2), stomach (RR = 1.5), rectum (RR = 1.4), larynx (RR = 3.4), lung (RR = 3.0), vagina (RR = 5.6), bladder (RR = 2.7), for kidney (RR = 1.9); decreased relative risks were noted for melanoma (RR = 0.5) and breast cancer (RR = 0.8). Patients with a primary diagnosis of anal cancer had relative risks for subsequent invasive and in situ cervical cancer of 1.3 (95% CI 0.2-4.5) and 3.4 (95% CI 0.9-8.8), respectively. Anal cancer was also associated with increased relative risks of subsequent lung (RR = 2.5) and prostate (RR = 1.8) cancers, whereas the relative risk of uterine cancer was 0.2 (95% CI 0.0-0.9). These findings support other evidence for common factors, such as human papillomavirus infection and cigarette smoking, in the etiology of cervical and anal cancer.

Anus Neoplasms↗
PubMed1992

Incidence of lymphomas and other cancers in HIV-infected and HIV-uninfected patients with hemophilia.

OBJECTIVE: To determine the types and rates of cancers occurring in excess in the presence of infection with the human immunodeficiency virus type 1 (HIV-1). DESIGN: Cohort analytic study of HIV-infected and HIV-uninfected subjects followed for up to 12 years. SETTING: Fifteen hemophilia treatment centers. PATIENTS: A total of 1701 patients with hemophilia, of whom 1065 (63%) were HIV-1 seropositive. MAIN OUTCOME MEASURES: Morphologic classification and incidence rates of cancers. MAIN RESULTS: The incidence of non-Hodgkin's lymphoma after HIV seroconversion averaged 0.15 case per 100 person-years (95% confidence interval [CI], 0.08 to 0.25) and rose exponentially with increasing duration of HIV infection. Although the greatest absolute risk of lymphoma was in the oldest age group, the relative increase compared with general population rates was 38-fold in subjects 10 to 39 years old and 12-fold in older subjects (P less than .05). The CD4+ T-lymphocyte levels for lymphoma cases were similar to HIV-positive subjects without the acquired immunodeficiency syndrome (AIDS) who had been infected for the same length of time. The incidence of Kaposi's sarcoma was increased 200-fold (95% CI, 20 to 700). The incidence of cancers other than non-Hodgkin's lymphoma and Kaposi's sarcoma were not increased in the HIV-positive subjects (ratio of observed to expected cases, 0.9 [95% CI, 0.4 to 1.9]). The HIV-negative subjects had no significant increase in cancer incidence. CONCLUSIONS: HIV infection has restricted effects on cancer incidence that are only partly explained by immunosuppression. Paradoxically, improvements in therapy of HIV infection that prolong survival may lead to further increases in HIV-associated lymphoma.

Acquired Immunodeficiency Syndrome↗
PubMed1992

The epidemiology of acquired immunodeficiency syndrome-related lymphomas.

Approximately 3% of acquired immunodeficiency syndrome cases present with non-Hodgkin's lymphoma. By 6 to 8 years after human immunodeficiency virus infection, lymphoma risk is elevated 100-fold, and the risk approaches 1% per year following acquired immunodeficiency syndrome diagnosis. The proportions presenting as lymphoma differ by age, sex, and race, with relative rates being higher in older persons, males, and whites. The differences are similar in magnitude and direction to those seen in non-human immunodeficiency virus-infected persons and account for the variation by risk group. The relative risk of high-grade lymphoma is greatest, but significant increases are also seen for some intermediate-grade tumors. At diagnosis, persons with Burkitt's lymphoma, more common in children, have significantly higher average CD4 counts than those with immunoblastic tumors. Human immunodeficiency virus-associated lymphoma risk is probably related to dysregulation of the immune system leading to uncontrolled proliferation of transformed cell clones and subsequent genetic accidents. Environmental factors are unlikely to be important. By 1994, 10% of all lymphomas will be human immunodeficiency virus related, but this proportion will increase in the future. New approaches to the therapy of lymphoma are needed for this tumor, which we can neither prevent nor adequately treat.

Adolescent↗
PubMed1991

Projections of the incidence of non-Hodgkin's lymphoma related to acquired immunodeficiency syndrome.

Advances in antiretroviral therapy and treatment or prophylaxis against opportunistic infection have resulted in prolongation of the survival of patients with acquired immunodeficiency syndrome (AIDS). Previous research has demonstrated an association between AIDS and risk of non-Hodgkin's lymphoma (NHL). In addition to the approximately 3% of individuals found to have NHL at the time of AIDS onset, others continue to develop NHL following AIDS diagnosis. Data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute demonstrated a sharply increasing incidence of NHL among men in the age range 20-49 years since 1983 in the United States. Based on new data on the risk of NHL following AIDS diagnosis, on estimates of improved survival following AIDS diagnosis, and on projections of future AIDS incidence, we considered four sets of assumptions and estimated the number of AIDS-related NHL cases in 1992 to be between 2900 and 9800. Three of these projections were higher than the estimate of 4700 cases obtained by linear extrapolation of SEER incidence trends. These projections of AIDS-related NHL incidence suggest that between 8% and 27% of all NHL cases that occur in the United States in 1992 will arise as a consequence of infection with the human immunodeficiency virus (HIV), imposing a substantial health care burden. More research into the pathogenesis of lymphoma and new approaches to antiretroviral and antilymphoma therapy will be necessary to prevent and treat this formidable complication of infection with HIV.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Increasing incidence of cancers associated with the human immunodeficiency virus epidemic.

We examined data from San Francisco and other areas participating in the Surveillance, Epidemiology, and End Results (SEER) Program to determine the effect of the human immunodeficiency virus (HIV) epidemic on cancer incidence between 1973 and 1987. In this period, non-Hodgkin's lymphoma incidence has increased over 10-fold and Kaposi's sarcoma incidence has increased over 5000-fold in single San Francisco men 20 to 49 years of age. Increases in non-Hodgkin's lymphoma have been restricted to high-grade and diffuse large-cell (intermediate-grade) histological types. With the exceptions of non-Hodgkin's lymphoma and Kaposi's sarcoma, no other tumor has significantly increased in incidence. During 1987, we estimate that HIV-seropositive men in San Francisco had a 0.47% risk of developing non-Hodgkin's lymphoma and a 1.6% risk of developing Kaposi's sarcoma. The relative risks for non-Hodgkin's lymphoma and Kaposi's sarcoma associated with HIV infection were 104 and 40,000, respectively. For 1987, HIV was associated with 14% of all reported cancers (except non-melanoma skin cancer) in men aged 20 to 49. We expect that 1,890 to 2,730 excess cases of non-Hodgkin's lymphoma and 6,490 to 8,320 excess cases of Kaposi's sarcoma will occur in the United States in 1990.

Adult↗
PubMed1991

HIV infection and cancers other than non-Hodgkin lymphoma and Kaposi's sarcoma.

In populations with non-HIV immunodeficiency, non-Hodgkin lymphoma and soft tissue sarcoma, especially Kaposi's sarcoma, are the most prominent tumours, but Hodgkin's disease, gastric carcinoma, squamous cell skin cancer, malignant melanoma, hepatoma, myeloid leukaemia and/or colorectal carcinoma have been linked in various studies. Population based cancer registries and cohort studies of HIV infected persons have generally failed to detect HIV related increases in total cancer incidence or in specific tumours other than non-Hodgkin lymphoma and Kaposi's sarcoma; however, associations with anal carcinoma, hepatoma and Hodgkin's disease have been suggested by some studies. Although not indicating increased risk, HIV induced immunosuppression has been linked to an acceleration of cervical and anal neoplasia and to increased aggressiveness of Hodgkin's disease with a relative excess of the mixed cellularity type. Advances in treatment for HIV infection will delay progression to AIDS and may allow an altered natural history to emerge, including the occurrence of excesses of additional cancer types.

Epidemiologic Methods↗
PubMed1990

Interaction of human immunodeficiency and papilloma viruses: association with anal epithelial abnormality in homosexual men.

During the 7th annual follow-up of our cohort of homosexual men in 1989, we tested the hypotheses that infection with human immunodeficiency virus (HIV) may enhance the expression of human papilloma virus (HPV) and that the development of anal epithelial abnormality is related to a biologic interaction between these two viruses. Overall, 41 (39%) of the 105 men had anal swabs positive for one or more genotypes of HPV 6/11, 16/18 or 31/33/35. Twenty-three (53%) of the 43 HIV-positive subjects harbored HPV compared to 18 (29%) of the 64 HIV-negative subjects (p = 0.012), including higher prevalence rates for HPV genotypes 16/18 (p = 0.01), 6/11 (p = 0.007), and 31/33/35 (p = 0.07). Multivariate logistic regression analysis of the HIV-positive subjects showed low CD4+ cell counts to be an independent risk factor for detection of HPV (p = 0.04) and in particular for HPV genotypes 31/33/35 (p = 0.02) and 6/11 (p = 0.07). In contrast, similar analysis of the HIV-negative subset showed that a positive antibody test for syphilis was associated with HPV (p = 0.03). Anal epithelial abnormalities were found in 13 (14%) of 92 technically adequate cytologic smears and were strongly associated with detection of any HPV genotypes by the dot-blot method (p = 0.01), and in particular with HPV genotypes 6/11 (p = 0.001). None of 15 subjects with HPV detected only by PCR had anal epithelial abnormality. We propose a viral interaction model, in which HIV-related immune deficiency allows reactivation of HPV, with a subsequent or concomitant appearance of epithelial abnormality.

Anal Canal↗