Hiperplasia epitelial focal

Vera-Iglesias, E.; Sánchez-Caminero, P.; Romero-Aguilera, G.; Calle, P. Cortina de la

doi:10.1016/s0001-7310(07)70148-5

Cited by 17 publications

(6 citation statements)

References 11 publications

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“…The risk of co-infection was higher for types 6,11,16,18,31,33,51,52,56. Co-infection by types 31-35-56, 16-51-52, 16-18 and 51-52 was more numerous than expected.…”

Section: Multiple Infectionsmentioning

confidence: 95%

“…It have not been enough studies to establish the existing prevalence of Human Papillomavirus (HPV) infection in our population [1,2]. Mostly collected samples arising from private medical offices, and two of them studied immigrant women on specific sexual groups outside of Ecuador [3,4], while others researchers focused HPV infection in different pathologies, always using Ecuadorian samples [5,6]. Some authors pointed out the threat of certain HPV types being more widespread in women in Latin-American Countries than elsewhere [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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HPV genotyping in anogenital abnormal samples of Ecuadorian women

González-Andrade

Sánchez

2009

CBM

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We found 23 different genotypes. 84/104 cases were positive for HPV (67.7%); 32/124 cases were negative (25.8%); and, in 8/124 cases (6.5%) we were unable to ascertain the existence or lack of HPV. The most common viral genotype was 6 (8.8%) followed by the 66 (4.8%) and 16, 31, 44 types (2.4% each one). Types 11, 34, 35, 54, 59, 62 and 67 showed a frequency equivalent to 1.6% each one. The remaining types showed a 0.8% frequency. Most common high-risk genotypes were 16 and 31, low-risk 6 and 41 and, the third most common group HPV type detected in this cohort was HPV 66. HPV 6 showed the highest prevalence. HPV 66 was associated with atypical cytology and was found in women with borderline cytology, low-grade lesions and high-grade lesions, but was most frequent in the threshold group. We examine a case of coexistence of 2 genotypes together 51 and 58. We found very low prevalence of HPV18 alone or HPV16/18. In 25 samples, 20.16% (25/124) we found HPV presence but we were unable to identify the genotype. We need more studies with a broad sampling to complete our geographic pattern of HPV distribution.

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“…The risk of co-infection was higher for types 6,11,16,18,31,33,51,52,56. Co-infection by types 31-35-56, 16-51-52, 16-18 and 51-52 was more numerous than expected.…”

Section: Multiple Infectionsmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

HPV genotyping in anogenital abnormal samples of Ecuadorian women

González-Andrade

Sánchez

2009

CBM

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“…However, other factors play a role, as the zones where the disease is most frequently observed (the oral mucosa) are contact areas with dental prostheses [47]. There are also family and ethnic associations (the disease was first described in Inuits and is not common in Caucasians), thus supporting a possible genetic component associated with HLA-DR4 [48]. Sexual transmission is not considered common, as the disease is most common in patients before the second decade of life.…”

Section: Focal Epithelial Hyperplasia or Heck's Diseasementioning

confidence: 99%

“…Its maximum diameter is usually 5 mm, although it can be confluent; therefore, the sizes reported in the literature vary between 1 and 10 mm, and the lesion may even have a cobbled aspect. It is asymptomatic [47,48] Heck's disease lesions have been described almost exclusively in the oral mucosa. The most common location is the lower lip, followed by the jugal mucosa, the upper lip and the tongue.…”

Section: Focal Epithelial Hyperplasia or Heck's Diseasementioning

confidence: 99%

“…Mucosal neuroma, white sponge nevus, florid oral papillomatosis and diffuse epithelial hyperplasia in tobacco chewers are considered in the differential diagnosis. Neurofibromas on the mucosal affectation of the neurofibromatosis and the papule or labial papillomas of Cowden's syndrome are usually located in similar zones, thus indicating these systemic diseases [47,48]. Treatment deserves a brief mention.…”

Section: Focal Epithelial Hyperplasia or Heck's Diseasementioning

confidence: 99%

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Clinical Manifestations of the Human Papillomavirus

Arrabal-Polo¹,

Girón-Prieto²,

JacintoOrgaz-Molina³

et al. 2013

Human Papillomavirus and Related Diseases From Bench to Bedside a Diagnostic and Preventive Perspective

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Human papillomavirus molecular biology and disease association

Doorbar

Egawa

Griffin

et al. 2015

Reviews in Medical Virology

709

624

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SummaryHuman papillomaviruses (HPVs) have evolved over millions of years to propagate themselves in a range of different animal species including humans. Viruses that have co‐evolved slowly in this way typically cause chronic inapparent infections, with virion production in the absence of apparent disease. This is the case for many Beta and Gamma HPV types. The Alpha papillomavirus types have however evolved immunoevasion strategies that allow them to cause persistent visible papillomas. These viruses activate the cell cycle as the infected epithelial cell differentiates in order to create a replication competent environment that allows viral genome amplification and packaging into infectious particles. This is mediated by the viral E6, E7, and E5 proteins. High‐risk E6 and E7 proteins differ from their low‐risk counterparts however in being able to drive cell cycle entry in the upper epithelial layers and also to stimulate cell proliferation in the basal and parabasal layers. Deregulated expression of these cell cycle regulators underlies neoplasia and the eventual progression to cancer in individuals who cannot resolve high‐risk HPV infection. Most work to date has focused on the study of high‐risk HPV types such as HPV 16 and 18, which has led to an understanding of the molecular pathways subverted by these viruses. Such approaches will lead to the development of better strategies for disease treatment, including targeted antivirals and immunotherapeutics. Priorities are now focused toward understanding HPV neoplasias at sites other than the cervix (e.g. tonsils, other transformation zones) and toward understanding the mechanisms by which low‐risk HPV types can sometimes give rise to papillomatosis and under certain situations even cancers. Copyright © 2015 John Wiley & Sons, Ltd.

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Hiperplasia epitelial focal

Cited by 17 publications

References 11 publications

HPV genotyping in anogenital abnormal samples of Ecuadorian women

HPV genotyping in anogenital abnormal samples of Ecuadorian women

Clinical Manifestations of the Human Papillomavirus

Human papillomavirus molecular biology and disease association

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