[Histo-cytologic study on the development of moderate cervical dysplasia (cervical intraepithelial neoplasm 2) followed in 267 cases].
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Adolescent↗
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Results for “cervical dysplasia”
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Demonstration and characterization of the angiogenic properties of cervical dysplasia.
Cervical dysplasia, or cervical intraepithelial neoplasia (CIN), is a premalignant precursor to cervical cancer. This study was designed to determine whether dysplastic lesions are angiogenic. Tissue sections from 23 surgical specimens were immunohistochemically stained for factor VIII antigen, a marker for endothelial cells. The results demonstrate that a region of neovascularization develops along the basement membrane subtending dysplastic epithelium when compared to adjacent normal epithelium. Comparison of microvessel counts underlying low grade lesions (condyloma and CIN I) with microvessel counts of CIN III lesions shows a statistically significant increase in the more advanced lesions. In a subset of the high grade lesions, large vascular structures are also noted in the upper layers of the epithelium, suggesting that a second stage of neovascularization consists of extension of stromal vascular papillae into the dysplastic lesions toward the surface of the epithelium. There is no statistical correlation between the amount of inflammation and the angiogenic ratio for each lesion, implying that angiogenesis is not secondary to the inflammatory response evoked by the lesion. The human papillomavirus type present in four CIN III lesions was determined by in situ hybridization; the amount of angiogenesis appears to be independent of the human papillomavirus type.
Epithelium↗
Serological and T-helper cell responses to human papillomavirus type 16 L1 in women with cervical dysplasia or cervical carcinoma and in healthy controls.
In a cross-sectional study we have investigated serological and T-helper (Th) cell responses to human papillomavirus type 16 (HPV-16) L1 in women with HPV-16 related diseases and related them to cervical histology and HPV DNA status. Using a virus-like particle (VLP) based ELISA to detect antibodies to the HPV-16 L1 capsid protein, 45% (33/73) of women with cervical dysplasia, 40% (2/5) of women with cervical cancer, 36% (4/11) of healthy adult female controls and 6% (2/35) of healthy children were found to be seropositive. Amongst women with cervical dysplasia, the highest levels of seropositivity were found in those who were HPV-16 DNA positive (60%, 15/25) or positive for any of the "high-risk' HPV types, 16/18/33 (58%, 18/31), when compared with those with HPV type "X' (25%, 5/20) or with healthy children (6%, 2/35; P < 0.05 for all comparisons). There was a trend for women with cervical dysplasia to show an increased level of seropositivity with increasing grade of lesion. There was no direct correlation found between seropositivity and Th cell responses in all groups studied. However, a combined analysis of each individual's Th and B cell responses suggests that a Th1 pattern of response is predominant amongst healthy adult controls (80% of responders) but reduced in women with cervical dysplasia (55% of responders). A trend towards a decrease in Th1 type responses was also noted with increasing grade of dysplastic lesion. These findings provide further evidence for the importance of the Th response in the control of genital HPV infections.
Adult↗
Proliferative T cell responses to the human papillomavirus type 16 E7 protein in women with cervical dysplasia and cervical carcinoma and in healthy individuals.
The levels of proliferative T cell responses to peptides representing the human papillomavirus type 16 (HPV-16) E7 protein have been measured using short-term T cell lines derived from peripheral blood of healthy women and those with cervical dysplasias and carcinoma of the cervix. In healthy individuals 47 percent (7/15) responded predominantly to the N- and C-terminal regions of the protein and 6/7 responders were to a single peptide between amino acids 80-94. In comparison 29 percent (9/31) of women with cervical dysplasia responded to HPV-16 E7, with a significantly reduced response to both the N- and C-terminal regions (P = 0.03 and 0.038, respectively). A higher proportion of responders was found in patients with high grade lesions (56 percent, 5/9) versus those with atypical or low grade histology (20 percent, 4/20) and the response to a single peptide between amino acids 75-94 was also increased in this patient group (P = 0.044). This may be a reflection of higher levels of current or previous exposure to HPV-16 in patients with high grade lesions. Correlation of T cell responses with HPV DNA type (detected by PCR of cervical biopsy tissue) showed that 3/9 (33 percent) HPV-16 DNA-positive individuals responded. This suggests that E7 may not be the dominant target of the immune response or that the response to E7 is down-regulated in these patients. In addition 4/18 (22 percent) HPV-16 DNA-negative individuals responded, suggesting that their T cells may have been primed by previous exposure to HPV-16 or that a cross-reactive response was detected. Proliferative T cell responses to both HPV-16 E7 and L1 were reduced in women with cervical carcinoma in comparison to those with cervical dysplasia and healthy controls. The observed down-regulation of responses to HPV-16 E7 in women with cervical dysplasia and cervical carcinoma may reflect an altered functional balance between subsets of T helper cells in HPV-16 infections.
Adult↗
Reduced expression of multiple gap junction proteins is a feature of cervical dysplasia.
Cervical dysplasia is a premalignant lesion associated with human papillomavirus (HPV) infection which, over time, can turn cancerous. Previous studies have indicated that loss of gap junctions may be a feature of cervical cancer and premalignant dysplasia. Loss of the gap junction protein connexin43 has been demonstrated in dysplastic cervix, but other connexins have not been investigated. In contrast we previously showed that HPV-associated cutaneous warts--and other hyperproliferative skin conditions--display a dramatic upregulation of certain connexins, in particular connexin26. By performing immunofluorescence staining after antigen retrieval of paraffin-embedded cervical tissue samples, this study reports for the first time that connexin26 and connexin30, in addition to connexin43, are expressed in differentiating cells of normal human cervical epithelia. Moreover, in dysplastic ectocervix, all connexins studied display a dramatic loss of expression compared to adjacent normal epithelia. The role of connexins in keratinocyte differentiation and carcinogenesis is discussed.
Connexin 26↗
Determinants of hospital length of stay for cervical dysplasia and cervical cancer: does managed care matter?
OBJECTIVE: To examine whether type of health insurance plan, among other variables, affects the length of stay for cervical cancer-related hospitalizations. STUDY DESIGN, PATIENTS, AND METHODS: Inpatient admission claims records for cervical dysplasia and cervical cancer were selected for 1994-1997 from the MarketScan private health insurance claims database. After identifying records by stage of disease and deleting records for pregnant women, 1145 unique patient records were used in a truncated count regression model to analyze the predictors of hospital length of stay. RESULTS: All later stages of disease were associated with a longer hospital stay. After controlling for other variables, the coefficients showed an increase in predicted length of admission ranging from 2.5 days for stage I to 6.3 days for stage IV cervical cancer compared with dysplasia/carcinoma in situ (all stages, P < .01). There was no significant statistical difference in the lengths of stay for patients covered under comprehensive fee-for-service plans vs other types of health insurance plans, including managed care. CONCLUSIONS: Managed care plans are often thought to contain healthcare costs by shortening the hospital length of stay. Our findings show no association between managed care plans and hospital length of stay for women with cervical cancer or its precursors.
Aged↗
Overexpression of placental tissue protein 17b/TIP47 in cervical dysplasias and cervical carcinoma.
In our previous Western- and Northern-blot investigations, high over-expression of placental protein 17b/TIP47 was detected in extracts of human cervical carcinoma tissues compared to normal conditions of the cervical tissue. PP17b serum levels were also elevated in untreated cervical carcinoma patients compared to healthy controls. In the present study, the expression pattern of PP17 proteins was investigated in various cervical dysplasias and in cervical carcinoma tissue specimens by the streptavidin-biotin immunoperoxidase technique using PP17-specific antiserum. In normal third-trimester human placentas, which served as positive controls, mainly cytoplasmic PP17 immunostaining of syncytiotrophoblasts and chorionic trophoblasts was observed. Normal human uterine cervical squamous and glandular epithelia were negative or weakly positive, while in low grade dysplasias (CIN I-II) only the cytoplasms of dysplastic cells were weakly positive or positive; in high grade dysplasias (CIN III/ISC) cytoplasms of the dysplastic cells were strongly positive. Normal and superficial cells in the differentiated zones were negative in all tissue specimens. In cases of invasive epithelial cervical carcinomas, small basal-type tumour cells were mostly negative whilst cells with squamous differentiation were strongly positive for PP17. Our hypotheses for this newly detected phenomenon are briefly discussed.
Adult↗
[Cervical dysplasia and cervical carcinoma in pregnant women].
UNLABELLED: Cytological and histopathological examinations performed in pregnant women allow quick for diagnosis of these pathological states. MATERIAL AND METHODS: 35 pregnant women with cervical dysplasia or carcinoma treated in Department of High Risk Pregnancy from 1996 to 2001 were included in the study. Diagnosis was based on the cytological and histological tests. RESULTS: We observed 10 cases of low-grade dysplasia and 8 cases of medium grade dysplasia. Both groups were qualified for vaginal delivery and treatment was started after delivery. In 12 pregnant women high-grade dysplasia was diagnosed (in 6 of them cervical conization between 16 and 26 week of pregnancy was performed). In 5 women cervical carcinoma in pregnancy was diagnosed. In 3 of them we performed cesarean section with radical operation between 34 and 40 week of gestation. CONCLUSION: Cytological and histological examination in pregnant women with cervical abnormalities should be obligatory because of high rate of dysplasia and cancer in pregnant women.
Adult↗
Significance of smoking and detection of serum antibodies to cytomegalovirus in cervical dysplasia.
Cervical biopsy specimens from 422 women attending a colposcopy clinic showed various grades of dysplasia in 387 and no evidence of dysplasia in 35. Of the women with dysplasia (CIN I, II or III) 67% were smokers and 33% were non-smokers compared with 43% smokers and 57% non-smokers in those without evidence of dysplasia. Of the women with CIN I 56% were smokers and 44% were non-smokers; 66% of those with CIN II were smokers and 34% were non-smokers (P less than 0.02), and 71% of those with CIN III were smokers (P less than 0.01). There were no significant differences between the smokers and non-smokers in the proportion of women who had had either a miscarriage or an abortion, in the prevalence of condylomata acuminata, and the use of oral contraception or barrier methods. Neither were there any significant differences in numbers of patients seropositive for cytomegalovirus or in CMV antibody titres among the groups. The detection of koilocytic cells in cervical biopsies showed a significant difference between smoking and non-smoking groups which reflected a significant increase in koilocytosis in smokers with CIN III.
Adult↗
Cytobrush in evaluation of cervical dysplasia. Is cervical curettage necessary?
203 patients suspected of having dysplasia were evaluated by colposcopy, cytologic smear including cytobrush, endocervical curettage, biopsy and conization. The results obtained on the basis of the final cone suggested that directed biopsies and cytological smear by spatula and cytobrush more accurately define the dysplastic lesion than do biopsies and endocervical curettage. Conization seemed necessary for the evaluation of the cervical lesion in patients revealing non-classified dysplasia at successive examinations.
Adult↗
Comparison of human leukocyte antigen DR-DQ disease associations found with cervical dysplasia and invasive cervical carcinoma.
BACKGROUND: Human leukocyte antigen (HLA) molecules, whose biological role is in the regulation of immune responses to foreign antigens and in discrimination of self from non-self antigens, are encoded by a series of closely linked genetic loci found on chromosome 6. Although the evidence for a link between HLA and cervical cancer has been controversial, it has been recently reported that certain HLA class II haplotypes (linked class II alleles) are positively associated with invasive cervical cancer, while other class II haplotypes are negatively associated or protective. Since HLA associations between human papillomavirus type 16 (HPV16)-mediated cancer cases and non-HPV16-mediated cancer cases have been found to be different, this suggests that specific HLA class II haplotypes may influence the immune response to HPV infection and may affect the risk of acquiring invasive cervical carcinoma. PURPOSE: This study was conducted to determine if the same HLA class II haplotypes that are associated with invasive cervical carcinoma are also associated with cervical dysplasia (presumed precursors of invasive cervical cancer). METHODS: We have examined HLA DR-DQ haplotypes among 128 Hispanic women from New Mexico with biopsy-confirmed cervical dysplasia in a case-control study using sensitive DNA-based polymerase chain reaction amplification and sequence-specific oligonucleotide probe hybridization methods to detect the presence and type of HPV and to detect allelic polymorphism in the HLA DRB1 and DQB1 loci. RESULTS: Dysplasia cases were divided into two groups for comparison to controls: severe dysplasia/carcinoma in situ (CIS), and slight/moderate dysplasia. The frequency distribution of HLA class II haplotypes among the HPV16-positive severe dysplasia/CIS cases had a statistically significant (two-tailed P < .005) difference compared with controls, whereas haplotypes among the severe dysplasia/CIS cases containing HPV types other than HPV16 did not show statistically significant frequency differences. DR-DQ haplotypes previously found to be associated with HPV16-invasive cervical carcinomas were also associated with HPV16-positive severe dysplasia/CIS. However, no statistically significant haplotype frequency difference was observed between slight/moderate dysplasia cases and controls. In addition, we noted a DQA1-DQB1 haplotype negatively associated with severe dysplasia/CIS but not with invasive cervical cancers. CONCLUSIONS: Our results strongly suggest that certain HLA haplotypes confer an increased risk for severe cervical dysplasia and invasive cervical carcinoma following HPV16 infection. IMPLICATIONS: Further molecular studies are needed to identify HLA alleles or haplotypes that may provide increased susceptibility to HPV-associated cervical disease.
Adult↗
The clinical significance of the poor correlation of cervical dysplasia and cervical malignancy with referral cytologic results.
OBJECTIVE: We prospectively studied the diagnostic utility of our Bethesda system-based cervical cytology screening program with colposcopy and biopsy as the criterion standard. STUDY DESIGN: We prospectively collected and studied the correlation of cytologic, colposcopic, and histologic data in women referred for colposcopic examination because of "nonnormal" cytologic results or other risk factors. RESULTS: We found that 771 of 5585 initial colposcopic visits yielded high-grade (cervical intraepithelial neoplasia II or worse) biopsies (13.8% prevalence); 13 showed invasive cancer (0.23% prevalence). Only 132 of 771 cases of high-grade dysplasia (17%) and 5 of 13 cases of invasive cancer (38%) followed Papanicolaou smears suggesting high-grade intraepithelial lesions or cancer, with 77% being discovered after "minor" Papanicolaou smear abnormalities. High-grade disease or cancer was confirmed in 1 of 2 high-grade or cancer Papanicolaou referrals and in 1 of 11 referrals with atypical squamous cells of undetermined significance. CONCLUSION: Papanicolaou smears, especially those that are low grade, should not be equated with histologic sampling in association with poor cytohistopathologic correlation. Most high-grade dysplasias and cancers occur in women with either minor Papanicolaou smear abnormalities or visible lower genital tract lesions or both. Colposcopy for women with any "nonnormal" screening result is feasible.
Adenocarcinoma↗
Persistent genital human papillomavirus infection as a risk factor for persistent cervical dysplasia.
BACKGROUND: Cervical dysplasia, also referred to as squamous intraepithelial lesion (SIL) in cytology or cervical intraepithelial neoplasia in histopathology, is thought to have the potential to advance in progressive stages to cervical cancer. However, not all cases of SIL progress, and most of the mild lesions spontaneously regress. Factors that govern regression, persistence, and progression of SIL are poorly understood. PURPOSE: Our analysis sought to identify factors that determined persistence or regression of SIL. METHODS: Seventy subjects with histopathologically confirmed cervical dysplasia were followed at 3-month intervals for 15 months. At each visit, the cervix was evaluated by Pap smear and colposcopy, and exfoliated cervicovaginal cells were analyzed for human papillomavirus (HPV) DNA. For each subject, data from every two consecutive visits were grouped as a pair. Persistent SIL was considered present if a lesion was detected at a visit (t) as well as at the next visit (t + 1) and absent if a lesion was detected at visit t but not at visit t + 1. A statistical model for time-dependent data correlated persistent SIL with various risk factors. RESULTS: Age, ethnicity, education, sexual behavior, smoking, and the use of oral contraceptives did not correlate with persistent SIL. The risk of persistent SIL was associated with continual HPV infection in visits t and t + 1 (HPV positive by Southern blot analysis: odds ratio [OR] = 3.91, and 95% confidence interval [CI] = 1.58-9.65; HPV positive by polymerase chain reaction [PCR]: OR = 2.42, and 95% CI = 1.03-5.67) and a persistent high viral load (OR = 4.07, and 95% CI = 1.35-12.30). When typed by PCR, individuals with type-specific persistent infection in visits t and t + 1, and particularly those with a continual high viral load (OR = 4.97; 95% CI = 1.45-17.02), had the highest risk for persistent SIL compared with those with a low level of type-specific persistent infection or non-type-specific persistent infection. The presence of persistent HPV infection in visits t-1 (the preceding time interval) was also predictive of persistent SIL in visits t and t + 1, although the strength of association was weaker, suggesting that persistent HPV and SIL occur synchronously. CONCLUSION: HPV infection and its associated cervical lesions tend to occur concurrently, and type-specific persistent HPV infection, particularly with a high viral load, produces chronic cervical dysplasia. IMPLICATIONS: The natural history of genital HPV infection directly influences the prognosis of cervical dysplasia as measured by persistence of the lesion. Testing for HPV infection may be valuable in the clinical management of women with cervical dysplasia.
Adult↗
Human papillomavirus infection, cervical dysplasia and invasive cervical cancer in Honduras: a case-control study.
A substantial body of evidence has confirmed human papillomavirus (HPV) infection as the central etiological agent in human cervical carcinogenesis. In Honduras, cervical cancer is the most common cancer among women, with a high annual incidence. We conducted a population-based, case-control study of 229 patients with different grades of CIN and invasive cervical cancer and 438 matched controls. A structured questionnaire was used to investigate known and probable risk factors for cervical cancer. Cervical scrapes were tested for the presence of different HPV types using a general primer-mediated PCR followed by PCR-based sequencing. HPV DNA was detected in 87% of all cancer in situ and invasive cancer cases, and 95% of invasive cases could be attributed to high-risk types. In control women, 39% were positive for HPV DNA sequences. HPV 16 prevalence ranked highest in all stages of cervical dysplasias, invasive cancers and controls. A statistically significant association with HPV was observed for CIN II, CIN III and invasive cancer, showing an upward trend to more severe lesions and being more pronounced for HPV 16 and related types. The OR for HPV 16- and 18-related invasive cancer cases was 14.88 (95% CI 5.12-43.25) and 74.66 (95% CI 7.77-717.62), respectively. Our results confirm a central role of HPV as the cause of cervical cancer in Honduras and provide information as to the type distribution of HPVs in the country.
Adolescent↗
Herpes simplex virus type 2 and human papillomavirus type 16 in cervicitis, dysplasia and invasive cervical carcinoma.
Sera and biopsies of cervical lesions from 55 women with benign or malignant disease were analyzed for evidence of infection with herpes simplex virus type 2 (HSV-2) or human papillomavirus (HPV). In addition, information regarding known risk factors for cervical cancer was obtained by interview. The sera were tested for HSV-2 antibodies and the biopsies were tested for HPV or HSV DNA sequences by Southern blot hybridization. HSV-2 sequences were detected in 2/13 (15%) invasive neoplasms and in 1/12 (7%) benign lesions. Under non-stringent conditions of hybridization, reactions with HPV DNA were detected in biopsies of 2/17 (12%) inflammatory lesions, 6/12 (50%) intraepithelial neoplasms and 13/20 (65%) invasive neoplasms. All but one of the positive biopsies of invasive cancer, but only 4/11 biopsies of non-invasive lesions, contained HPV-16 DNA as determined by stringent hybridization conditions. Women with cervical cancer possessed the risk factors associated with the disease. Cigarette smoking and the presence of HPV-16 DNA were the most prominent risk factors. No evidence of an interaction between HSV-2 and HPV-16 was found among the cases of invasive cervical cancer.
Adult↗
HLA DOA1 and DOB1 loci in Honduran women with cervical dysplasia and invasive cervical carcinoma and their relationship to human papillomavirus infection.
Molecular and epidemiological studies have demonstrated that certain types of human papillomavirus (HPV), mainly HPV-16 and HPV-18, are the primary causes of cervical cancer and its precursor lesions; there is now evidence for a clear association with specific HLA class I and class II loci contributing independently to the expression of cervical cancer. Among Honduran women carcinoma of the cervix is the most common type of cancer, and infections with high-risk HPV types are highly prevalent. To study the interactive role of viral-host genetics, we performed PCR amplification of DNA and sequence-specific oligonucleotide probe typing on cervical scrapes from 49 women [24 with cervical intraepithelial neoplasia stage III or cervical cancer (severe cases) and 25 with stage I or II cervical intraepithelial neoplasia (mild cases)] and 75 control subjects to look for possible associations between HPV and HLA class II DQA1 and DQB1 alleles in the development of dysplasias and invasive cancer. This analysis revealed a predominance of HLA-DQA1*0301 among severe-case patients [relative risk (RR) = 3.45, p = 0.008), whereas DQA1*0501 was negatively associated (RR = 0.30, p = 0.03), suggesting a protective effect of this allele. HPV typing showed a decreased relative risk among the HPV-16 or HPV-18 carrying patients and other HPV-related positive patients in the presence of DQB1*0602 compared with positive control subjects (p = 0.04). No statistically significant allele frequency difference was observed between mild dysplasia cases and control subjects. The results suggest that DQA1*03011, which is in linkage desequilibrium with all HLA-DR4 alleles, confers an increased risk for severe cervical dysplasia and invasive cancer, whereas DQA1*0501, which is in several DR52 haplotypes, has a protective effect. Furthermore, specific HLA-DQB1 sequences may be important in determining the immune response to HPV peptides and may affect the risk for cervical cancer after HPV infection in mestizo Honduran women.
Adult↗
An unusual cervical finding. Female genital schistosomiasis with associated cervical severe squamous dysplasia (cervical intraepithelial neoplasia grade III).
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Adult↗
Cervical dysplasia: early intervention.
Cervical cancer is the second-most common cancer in young women and is one of the most common causes of cancer deaths among women, particularly in minorities and in impoverished countries. Cervical dysplasia, a premalignant lesion that can progress to cervical cancer, is caused primarily by a sexually transmitted infection with an oncogenic strain of the human papillomavirus (HPV). Not all women with the virus develop cervical dysplasia or cervical cancer. It has been postulated there are multiple host factors that contribute to progression of disease. Many of these factors, such as nutrient deficiencies, can be reversed, which will result in regression of dysplastic lesions. Studies have shown dietary intervention and nutrient supplementation to be effective in preventing cervical cancer. Additionally, local escharotic treatment combined with systemic treatment shows significant potential in reducing dysplasia. Recent advances in vaccination technology demonstrate the effectiveness of an HPV vaccine. The vaccine, however, may have many social and cost-prohibiting limitations, as well as health side effects.
Antioxidants↗