Check Up: So far, very little flu


CDC Director Gerberding Gives Green Light to G...
CDC Director Gerberding Gives Green Light to Gardasil then Goes to Work for Merck (g1a2d0049c1) (Photo credit: watchingfrogsboil)

Check Up: So far, very little flu

The U.S. Centers for Disease Control and Prevention has confirmed what you already guessed: This has been a remarkably mild flu season.
The influenza virus likes cold weather, so infections normally occur from October through March. But technically, the flu season doesn’t start until labs that test respiratory swabs from sick people find the virus in more than 10 percent of the samples.
This season, that threshold wasn’t reached until the week ended Feb. 11, making this the kindest flu spell in 29 years.
Pennsylvania, for example, had only 80 confirmed cases in all of January – barely more than one achy, feverish, nauseated citizen per county.
What’s going on?
No one really knows.
“With flu, everything is unpredictable,” said immunologist Scott Hensley, a flu expert at the Wistar Institute in Philadelphia. “I don’t think we’re out of the woods; it could just be a delayed season.”
Then again, maybe the flu has been as scarce as snow because snow has been scarce.
“Flu is more easily transmitted in colder temperatures. This has been a mild winter,” Hensley said.
Another theory is that the population has high levels of immunity to the influenza strains now circulating, which include the one that caused the 2009 “swine flu” pandemic. Because the strains have been so stable, people have had time to develop antibodies against them. Vaccination has also boosted immunity.
Although Hensley subscribes to this theory, he adds a caveat: “If that’s true . . . the virus will start mutating” to evade human defenses. “A novel strain might emerge in the next couple of months.”
While there’s no room for complacency, let us celebrate the signs, monitored by the CDC, that the flu has given the nation a respite:
One person per 100,000 has been hospitalized with the flu since October. That’s a 95 percent drop from last season’s rate of 22 people per 100,000.
Only 1 percent to 2 percent of visits to doctors since October have been for flulike illness. The usual rate is 3 percent to 8 percent.
This flu season, there have been three flu-related deaths among children, compared with 122 pediatric deaths last season – and 348 during the 2009 pandemic.
– Marie McCullough

Read more: http://www.philly.com/philly/health/20120227_Check_Up__So_far__very_little_flu.html#ixzz1neP8n4sM Watch sports videos you won’t find anywhere else

Pelvic Examination


Pelvic Examination

A pelvic examination is a complete physical exam of a woman’s pelvic organs camera by a health professional. A pelvic exam helps a health professional evaluate the size and position of the vagina,cervixuterus, and ovaries. It is an important part of preventive health care for all adult women. A pelvic exam is done to help detect certain cancers in their early stages, infectionssexually transmitted infections (STIs), or other reproductive system problems.

Why It Is Done

pelvic exam may be done:

How To Prepare

Before a pelvic exam:
  • Try to schedule the exam when you are not having your period, since blood can interfere with the results of a Pap test. But if you have a new vaginal discharge or new or increasing pelvic pain, a pelvic exam may be done while you are having your period.
  • Do not use douches, tampons, vaginal medications, or vaginal sprays or powders for at least 24 hours.
  • Do not have sex for 24 hours prior to the exam if you have abnormal vaginal discharge.
At the beginning of your visit, tell your health professional:
  • If you are or might be pregnant.
  • If you have any reproductive or urinary tract symptoms such as itching, redness, sores, swelling, or an unusual odor or increased vaginal discharge. If you have been performing regular vaginal self-exams, discuss any changes you have noticed with your health professional. For more information, see the medical testVaginal Self-Examination (VSE).
  • If you are using a method of birth control.
  • If this is your first pelvic exam.
  • The first day of your last menstrual period and how long your period lasted.
  • If you have had surgery or other procedures, such as radiation therapy, involving the vagina, cervix, or uterus.
If you have had problems with pelvic exams in the past or have experienced rape or sexual abuse, talk to your health professional about your concerns or fears before the exam.
No other special preparations are needed before having a pelvic exam. For your own comfort, you may want to empty your bladder before the exam.
Talk to your health professional about any concerns you have regarding the need for the test, its risks, how it will be done, or what the results may mean. To help you understand the importance of this test, fill out the medical test information form.
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Juan Gervas y Vacuna HPV













http://www.equipocesca.org/actividades-preventivas/la-incierta-prevencion-del-cancer-de-cuello-de-utero-con-la-vacuna-contra-el-virus-del-papiloma-humano/

También en:
http://www.equipocesca.org/organizacion-de-servicios/la-vacuna-contra-el-virus-del-papiloma-humano-desde-el-punto-de-vista-de-la-atencion-primaria-en-espana/

http://www.equipocesca.org/actividades-preventivas/vacuna-contra-el-virus-del-papiloma-humano-ciencia-y-ficcion/

Todo ello recogido en:
http://www.equipocesca.org/noticias/razones-para-el-%E2%80%9Cno%E2%80%9D-o-para-la-moratoria-respecto-a-la-vacuna-contra-el-virus-del-papiloma-humano/

Ver también la petición de una moratoria para la vacuna contra el VPH
en España:
http://www.caps.cat/caps/activitats/43-declaracion.html

Es importante:
http://www.cmaj.ca/content/177/5/484.full?sid=8be3cd89-af54-491c-b2ff-9e587acce741

http://www.cmaj.ca/content/177/12/1527.full?sid=2627c0f0-c338-4653-a3c3-7a147b7b9539

http://www.cmaj.ca/content/177/12/1527.full/reply#cmaj_el_19534

He añadido comentarios varios actualizados, de artículos y estudios
publicados en 2010 y 2011.


Juan Gérvas. 


OBJECIONES EN RELACION CON AMBAS VACUNAS DISPONIBLES CONTRA EL VIRUS DEL PAPILOMA HUMANO


Notable HPV types and associated diseasesImage via Wikipedia

OBJECIONES EN RELACION CON AMBAS VACUNAS DISPONIBLES CONTRA EL VIRUS DEL PAPILOMA HUMANO
(especial para SIIC © Derechos reservados)
Se presenta un análisis del diseño, evaluación, aplicación y seguimiento de las 2 vacunas disponibles contra el HPV llevado a cabo por ambos laboratorios fabricantes para comentar sobre su aplicación. Se incluye una breve revisión bibliográfica sobre la historia natural del HPV, el comportamiento del sistema inmune y otros factores en el desarrollo del cáncer cervical uterino.
audisio9_o0510.jpg Autor:
Teresita Audisio
Columnista Experto de SIIC
Institución:
Hospital Materno-Neonatal
 Artículos publicados por Teresita Audisio
Coautores
Vainer Osvaldo*** Ramallo Rogelio* Vásquez Federico** Ringelheim Claudia**** Pelliza Palmes Maria Nuria**** 
Doctor, Clínica del Niño, Córdoba, Argentina*
Doctor, Clínica del Noreste, Córdoba, Argentina**
Doctor, Hospital Materno-Neonatal, Córdoba, Argentina***
Doctora, Hospital Materno-Neonatal, Córdoba, Argentina****
Recepción del artículo
10 de marzo, 2010
Aprobación
26 de junio, 2010
Primera edición
26 de agosto, 2011
Segunda edición, ampliada y corregida
21 de septiembre, 2011

 Resumen
Las infecciones genitales por el virus papiloma humano (HPV) son altamente frecuentes tanto en adultos como en niños; varios estudios demuestran la relativa frecuencia en esta población de los serotipos oncogénicos del HPV (16 y 18), como sus proteínas tempranas (early proteins); por lo que se objeta que la vía de transmisión sexual sea la única. El comportamiento biológico de las neoplasias intraepiteliales cervicales (CIN) I y II en las adolescentes y adultos jóvenes es similar y presenta una alta tasa de regresión espontánea. Por lo tanto, la indicación de las dos vacunas para el HPV disponibles actualmente en el comercio no condice con la historia natural del HPV y las CIN. Los estudios realizados con ambas vacunas han demostrado la baja efectividad y el efecto contraproducente cuando los sujetos eran ADN-HPV positivos a los tipos de HPV que contiene la vacuna, por lo que sería peligroso vacunar si no está asegurado el control de los sitios donde se ubican los tipos de HPV, como el aparato genital. Además, el corto seguimiento de los estudios realizados con ambas vacunas no permitió observar la repercusión en el estado inmunitario, como también el remplazo por los serotipos de HPV que no contiene la vacuna. La rápida autorización de la US Food and Drug Administration (FDA) y de la European Medicines Agency (EMEA) llevó a la introducción de la vacuna en muchos países, sin tener en cuenta las indicaciones y las repercusiones mencionadas.


Clasificación en siicsalud
Artículos originales > Expertos de Iberoamérica >
página  www.siicsalud.com/des/expertocompleto.php/

Especialidades
 Principal: Infectología,  Obstetricia y Ginecología 
  Relacionadas: Atención Primaria,  Educación Médica,  Epidemiología,  Farmacología,  Medicina Farmacéutica,  Inmunología,  Medicina FamiliarMedicina Interna,  Medicina Reproductiva,  Pediatría 

 Enviar correspondencia a:
Teresita Audisio, 5000, Córdoba, Argentina


Artículo completo

(castellano)
Extensión:  +/-4.8 páginas impresas en papel A4
Exclusivo para suscriptores/assinantes
 Abstract
Genitals infection through human papilloma-virus (HPV) is frequently found in both adults and children, and several studies show the relative frequency of oncogenic HPV (16 and 18) in this population as well as their early proteins. This is why we object to the claim that this virus is exclusively sexually transmitted. The biological behavior of cervical intraepithelial neoplasia (CIN) I and II in teenagers and young adults is similar, presenting high spontaneous regression. Therefore, the indications for the two HPV vaccines do not match the natural history of HPV and CIN. The studies performed with both these vaccines have shown their low rate of efficacy and their counterproductive effect when the vaccinated subjects were HPV DNA positive to the HPV types in the vaccine, on account of this, vaccination without control of possible HPV type locations such as the genital apparatus would be dangerous. Besides, the short follow-up that has been made of the studies carried out with both vaccines has not allowed us to see their effects on immune system status nor on possible replacement by other types of HPV not contained in the vaccine. The fact of its rapid authorization by the U S Food and Drug Administration (FDA) and the European Medicines Agency (EMEA) led to the introduction of the vaccine in many countries without considering its indications and the repercussions mentioned above.

 Key words
HPV, vaccine, pre-teenage

 Bibliografía del artículo 1. VRBPAC. VRBPAC background document. Gardasil HPV quadrivalent vaccine. Vaccine and Related Biological Products Advisory Committee Meeting. Washington, DC, USA; May 18, 2006 http://www.fda.gov/ohrms/dockets/ac/06/briefi ng/2006-4222B3.pdf (accessed may 20, 2008).
2. Paavonen J, Jenkins D, Bosch FX, et al. Effi cacy of a prophylactic adjuvanted bivalent L1 virus-like-particle vaccine against infection with human papillomavirus types 16 and 18 in young women: an interim analysis of a phase III double-blind, randomized controlled
trial. Lancet. 2007; 369: 2161-70.
3. Paavonen J, Naud P, Salmerón J, et al. Efficacy of human papillomavirus (HPV)-16/18 ASO4-adjuvanted vaccine against cervical infection and precancer caused by oncogenic HPV types(PATRICIA):final analysis of a double-blind, randomized study in young women. Lancet. 2009; 374:301-14.
4. Syrjanen K, Kataja V, Yliskoski M, et al. Natural history of cervical human papillomavirus
Lesions do not substantiate the biologic relevance of the Bethesda System. Obstet Gynecol.
1992; 79:675-82.
5. Mount SL, Papillo JL. A study of 10,296 pediatric and adolescent Papanicolaou smear diagnoses in northern New England. Pediatrics.1999; 103(3):539-46.
6. Nasiell K, Nasiell M, Vaclavinkova V. Behavior of moderate cervical dysplasia during long term follow-up. Obstet Gynecol.1983; 61:609-14.
7. Sadeghi SB, Hsieh EW, Gunn SW. Prevalence of cervical intraepithelial neoplasia in sexually active teenagers and young adults. Am J Obstet Gynecol.1984;148:726-9.
8. Moscicki AB. Human Papilloma Virus, Papanicolaou Smears and the College Female. Pediatr Clin N Am. 2005; 52:163-77.
9. Wright TCJ, Cox JH, Massad LS, Carlson J, Twiggs LB, Wilkinson EJ. 2001 Consensus
Guidelines for the Management of Women with Cervical Intraepithelial Neoplasia. Am J Obstet
Gynecol. 2003;189(1):295-304.
10. Rando RF, Lindheim S, Hasty L, Sedlacek TV, Woodland M, Eder C: Increased frequency of
detection of human papillomavirus DNA in exfoliated cervical cells during pregnancy. Am
J Obstet Gynecol.1989;161:50-9.
11. Cason J, Kaye JN, Jewers RJ, et al . Perinatal infection and persistence of human papillomavirus types 16 and 18 in infants. J Med Virol.1995;47:209-18.
12. Powell J , Strauss S, Gray J, Wojnarowska F. Genital Carriage of Human Papilloma Virus (HPV) DNA in Prepubertal Girls with and without Vulval Disease – Pediatric Dermatology. 2003. 20(3):191-4.
13. Rintala M, Grénman S, Puranen M, et al . Transmission of High-Risk Human Papillomavirus (HPV) between Parents and Infant: a Prospective Study of HPV in Families in Finland. Journal of Clinical Microbiology.2005; 43(1): 376-81,
14. Jenison S, Yu X,Valentine J, et al .Evidence of prevalent Genital-Type Human Papillomavirus Infections in Adults and Children.The Journal of Infections Diseases.1990;162:60-9
15. Cason J , Rice P , Best J.Transmission of Cervical Cancer-Associated Human
Papilloma Viruses from Mother to Child. Intervirology.1998; 41:213-18
16. De Palo Bergeron C., Ferenczy A., Richart R.: Underwear: contamination by human papillomavirus. Am. J. Obstet. Gynecol. 1990;162: 25.
17. Müller M, Viscidi R, Ulken V, et al .Antibodies to the E4, E6 and E7 proteins of Human Papillomavirus (HPV) type 16 in patients with HPV-associated diseases and the normal population.J Invest Dermatol.1995;104:138-41.
18. Hildesheim A, Herrero R, Wacholder S, et al. for the Costa Rican HPV Vaccine.Effect of Human Papillomavirus 16/18 L1Viruslike Particle Vaccine Among Young Women With Preexisting Infection- A Randomized Trial. JAMA. 2007; 298(7):743-53.
19. Pasqualini C.D. La etiología del cáncer .Vigencia de cinco paradigmas sucesivos. Medicina. 2003;63:757-60.
20. Pasqualini CD.Papel bivalente del sistema inmune en el crecimiento tumoral. Medicina. 2004; 64:277-80.
21. Pasqualini CD,Ruggiero RA,Bustuoabad OD, Nepomnaschy I,Piazzon I. Experimental Oncoinmunology Revisited. Current Cancer Therapy Reviews CCTR. 2005; I:289-98.
22. Broca KE, Nerry et al Nutrients in diet and plasma and risk of in situ cervical cancer. J Natl Cancer Inst.1988; 80:580-5.
23. Slattery ML; Abbott TM; Overall JC et al. Dietary vitamins A,C and E and selenium as risk factors for cervical cancer. Epidemiology.1990;1:8-15.
24. Van Eenwick, Davis FG, Bowen PE. Dietary and serum carotenoids and cervical Intraepithelial neoplasia. Int J Cancer.1991; 48: 34-8,
25. Meyskens FL;Surwit E; Moon TE et al. Enhancement of regression of cervical intraepithelial neoplasia II with topically applied all -trans-retinoic acid: a randomized trial. Journal of the National Cancer Institute.1994; 86(7): 539-43.
26. Buckley DI, Mc Pherson RS, North CQ; Becker TM. Dietry micronutrients and cervical dysplasia en Southwestern American Indian women. Nutr and cancer.1992; 9: 179-85.
27. Amburgey CF, Van Eenwyck J, Davis FG; Bowen PE .Undernutricion as a risk factor for cervical intraepithelial neoplasia: a case-control analysis. Nutr.Cancer.1993; 20:51-60.
28. Piyathilake CJ, Henao OL, Macaluso M, Cornwell PE, Meleth S, Heimburger DC, Partridge EE. Folate is associated with the natural history of high-risk human papillomavirus. Cancer Res. 2004; 64(23):8788-93.
29. Botella J. Contraceptivos, carencia de folatos y displasia cervical uterine; Acta Gin. 1987; 44: 343-8.
30. Whitehead N; Reyner F; Lindenbaum J: Megaloblastic changes in the cervical epithelium: Association with oral contraceptive therapy and reversal by folic acid. JAMA, 1973; 226:1421-4.

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Intrauterine device use, cervical infection with human papillomavirus, and risk of cervical cancer: a pooled analysis of 26 epidemiological studies


Mirena IntraUterine SystemImage via Wikipedia

The Lancet Oncology, Early Online Publication, 13 September 2011
doi:10.1016/S1470-2045(11)70223-6Cite or Link Using DOI

Intrauterine device use, cervical infection with human papillomavirus, and risk of cervical cancer: a pooled analysis of 26 epidemiological studies

Summary

Background

Intrauterine device (IUD) use has been shown to reduce the risk of endometrial cancer, but little is known about its association with cervical cancer risk. We assessed whether IUD use affects cervical human papillomavirus (HPV) infection and the risk of developing cervical cancer.

Methods

We did a pooled analysis of individual data from two large studies by the International Agency for Research on Cancer and Institut Català d’Oncologia research programme on HPV and cervical cancer; one study included data from ten case—control studies of cervical cancer done in eight countries, and the other included data from 16 HPV prevalence surveys of women from the general population in 14 countries. 2205 women with cervical cancer and 2214 matched control women without cervical cancer were included from the case—control studies, and 15 272 healthy women from the HPV surveys. Information on IUD use was obtained by personal interview. HPV DNA was tested by PCR-based assays. Odds ratios and 95% CIs were estimated using multivariate unconditional logistic regression for the associations between IUD use, cervical HPV DNA, and cervical cancer.

Findings

After adjusting for relevant covariates, including cervical HPV DNA and number of previous Papanicolaou smears, a strong inverse association was found between ever use of IUDs and cervical cancer (odds ratio 0·55, 95% CI 0·42—0·70; p<0·0001). A protective association was noted for squamous-cell carcinoma (0·56, 0·43—0·72; p<0·0001), adenocarcinoma and adenosquamous carcinoma (0·46, 0·22—0·97; p=0·035), but not among HPV-positive women (0·68, 0·44—1·06; p=0·11). No association was found between IUD use and detection of cervical HPV DNA among women without cervical cancer.

Interpretation

Our data suggest that IUD use might act as a protective cofactor in cervical carcinogenesis. Cellular immunity triggered by the device might be one of several mechanisms that could explain our findings.

Funding

Instituto de Salud Carlos III; Agència de Gestió d’Ajuts Universitaris i Recerca; Marató TV3 Foundation; Bill & Melinda Gates Foundation; International Agency for Research on Cancer; European Community; Fondo de Investigaciones Sanitarias, Spain; Preventiefonds, Netherlands; Programa Interministerial de Investigación y Desarrollo, Spain; Conselho Nacional de Desenvolvimiento Cientifico e Tecnologico, Brazil; and Department of Reproductive Health & Research, WHO.

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Ante la incorporación de la vacuna HPV como obligatoria en Argentina


Juan GérvasImage via Wikipedia

Ante la incorporación de la vacuna HPV como obligatoria en Argentina
Gérvas J. La incierta prevención del cáncer de cuello de útero con la vacuna contra el virus del papiloma humano. Rev Port Clín Geral. 2007;23: 547-55
Gérvas, J. Prevention of cervical cancer by the HPV vaccine is not definitive. Rev. Port Clin Geral. 2007; 23: 547-55.
Juan Gérvas
jgervasc@meditex.es
Médico de Canencia de la Sierra, Garganta de los Montes y El Cuadrón (Madrid) España
Equipo CESCA, Madrid, España
Abstract with Eleven Questions & Answers into Spanish and English.
English translation by Juan Gérvas (“nogracias” Spain, http://www.nogracias.eu) and Joana Ramos, (www.healthyskepticism.og )
Resumen
En 2007 se ha comercializado de la vacuna contra el virus del papiloma humano, con la que se propone vacunar a niñas de 11 y 12 años para la prevención primaria del cáncer de cuello de útero, dada la fuerte asociación entre el cáncer y algunos tipos oncogénicos del virus. La vacuna ha sido rápidamente incluida en los calendarios vacunales de la mayoría de los países desarrollados. En este texto se revisa el fundamento científico de dicha decisión. Son puntos clave: la ausencia de cambios en la epidemiología de la infección, la estabilidad o disminución del la incidencia y mortalidad del cáncer de cuello de útero, la falta de correlación entre respuesta inmunitaria serológica y la inmunidad natural, el impacto de la vacuna en la ecología del virus, las evaluaciones coste-efectividad que dependen de la duración desconocida de la inmunización, la dependencia excesiva de la investigación financiada por la industria farmacéutica, y la necesidad de mantener la citología de cribado. Se precisaría más tiempo e información antes de introducir la vacunación en el calendario vacunal.
Palabras clave: Vacunas, Virus del papiloma humano, Evaluación.
Abstract
Sales of the vaccine against human papilloma virus began in 2007, promoted for administration in girls 11 -12 years old, as preventative measure against cervical cancer, due to the strong link between this cancer with the presence of certain oncogenic strains of the papilloma virus. The vaccine was quickly included in the official immunization programs in many developed countries. In this paper I review the scientific basis for that decision. Critical questions for review are: the absence of changes in the epidemiology of the infection; stability or reduction in the incidence and mortality from cervical cancer; lack of correlation between levels of serologic immune response and natural immunity; the effect of the vaccine on virus ecology; evaluation of the cost-effectiveness of immunization in the face of lack of definitive information about the length of its effectiveness; pharmaceutical industry sponsorship of most of the HPV vaccine research; and the need to maintain screening with Papanicolau exams. More time and information are needed before including this vaccine in the official immunization program.
Key words: Vaccines, Human papilloma virus, Evaluation.
Once preguntas básicas (sin respuesta concluyente)
Eleven basic questions (with no definitive answer)
Con un ímpetu frenético, sin parangón en el campo vacunal, la vacuna contra el virus del papiloma humano se ha incluido en los calendarios vacunales de casi todos los países europeos, Alemania, Austria, Bélgica, Dinamarca, España, Grecia, Holanda, Italia, Luxemburgo, Reino Unido, Suecia y Suiza (1) y en otros desarrollados como Australia, Canadá y EEUU.
With a speed never before seen in the field of immunization, the HPV vacccine has been added to the vaccination schedules of almost all the European countries, including Germany, Austria, Belgium, Denmark, Spain, Greece, the Netherlands, Italy, Luxemburg, the UK, and Switzerland (1) and in other developed nations like Australia, Canada, and the USA.
¿Indica la unanimidad lógica y certeza científica? No. La prevención es campo aparte, como se deduce de otros casos; por ejemplo, respecto al cribado de la displasia del desarrollo de caderas en el recién nacido (2-4).
Does this mean that there is complete agreement and solid scientific basis for this action? No.
The field of preventive medicine is a whole different matter as we can learn from other cases; for example, with respect to screening of newborns for hip displasia (2-4).
En el caso de la vacuna contra el virus del papiloma humano existen dudas razonables acerca de la racionalidad de la decisión de su inclusión en el calendario vacunal. Al menos hay once preguntas básicas sin respuesta concluyente, que hacen dudar de la oportunidad de la aprobación del nuevo calendario:
Reasonable doubts exist about the rationale for the decision to include the HPV vaccine in the immunization schedules. At the very least, there are eleven basic unresolved questions, which raise doubts about the appropriateness of its inclusion in the new [vaccination] schedule.
¿Hay cambios recientes en lo que respecta a la infección por virus del papiloma humano? No. De hecho, desconocemos su historia natural. Es la enfermedad de transmisión sexual más frecuente y la más benigna (el 90% de las infecciones curan espontáneamente) (5). Seguimos sin saber porqué algunas infecciones son persistentes y cancerígenas (al cabo de 20-30 años provocan cáncer de cuello de útero).
Have there been any recent changes in our understanding of the papilloma virus infection? No.
In fact we do not know its natural history. It is the most common sexually transmitted disease, but most cases are benign (90% clear spontaneously) (5). We still don’t know why some infections become chronic and cause cancer (it takes about 20-30 years for [the infection] to transform into cervical cancer).
2. ¿Hay cambios en los países desarrollados de la epidemiología del cáncer de cuello de útero que lo justifiquen? Por ejemplo, en España la incidencia se mantiene estable y baja, así como la mortalidad (respectivamente, de 7,11 y de 2,4 casos por 100.000 mujeres y año) (6). En EEUU disminuye, y cada año hay unos 11.100 nuevos casos y unas 3.700 muertes por cáncer de cuello de útero (5).
Are there known changes in the epidemiology of cervical cancer in developed countries that would justify vacciantion? No.
In most developed countries mortality is stable or decreasing.
No. In Spain, for example, the incidence has remained stable to low, as has the monthly rate (some 7. 11 cases and 2.4 deaths yearly per 100,000 women, respectively) (6). In the USA, there has been a decrease, and there are about 11,100 new cases and about 3700 deaths from cervical cancer annually (5).
3. ¿La inmunidad natural, ¿conlleva la presencia de anticuerpos en sangre? No. La cifra de anticuerpos en sangre es muy baja o inexistente (en la mitad de los casos) en las mujeres inmunes naturalmente. La infección no conlleva viremia (la replicación vírica se produce en la superficie epitelial, muy lejos de la células presentadoras de antígeno y de los macrófagos) (7). Desconocemos en detalle la respuesta inmunológica normal, pero es muy efectiva. Además, no se ve afectada por la re-exposición debida a la actividad sexual continuada.
Is natural immunity correlated with levels of antibodies in the blood? No.
In most cases, the quantity of blood antibodies is very low to nonexistent (in half of all cases) among women with natural immunity. Infection does not correlate with viremia (viral replication occurs on the epithelial surface, very far from the antigen-presenting cells and from the macrophages) (7). Viral replication is a cellular phenomenon. We do not understand very well the normal immune response, but it is very effective. Furthermore, it does not seem to be affected by re-exposure resulting from ongoing sexual activity.
4. La vacuna, y re-vacuna, provoca la presencia en sangre de anticuerpos, en dosis de hasta veinte veces las máximas normales, pero ¿existe relación demostrada entre el nivel de anticuerpos y la eficacia de la vacuna? No. No hay correlación inmunológica demostrada. Ignoramos el mecanismo de acción de la vacuna. Se supone que los anticuerpos en sangre ayudan a eliminar los virus en la superficie epitelial, pero no sabemos cómo (5, 8). La inmunidad natural es celular, no serológica.
Vaccination, and re-vaccination, boost the presence of antibodies in the blood, up to twenty times the normal maximum counts, but is there any relationship shown between the antibody levels and the effectiveness of the vaccine? No.
There is no immunological correlation shown at all. The vaccine’s mode of action is unknown. It is theorized that antibodies in blood might help in getting rid of the infection, but we don’t know how (5,8). Natural immunity is cellular, not serological.
5. Si la vacuna elimina los virus, puede tener un doble efecto beneficioso y perjudicial? Por ejemplo, la vacuna disminuye las infecciones persistentes y las lesiones pre-malignas causadas por los virus contra los que se vacuna (beneficioso). Pero si eliminase otros virus del papiloma humano no sabríamos cómo valorarlo. Por ejemplo, la co-infección con los tipos 6 y 11 (bajo riesgo oncológico) disminuye naturalmente la posibilidad de ser infectado por el tipo 16 (alto riesgo oncológico) (9). En general se acepta que la vacuna evita la presencia o actividad de los virus contra los que vacuna. Por ello cambia la “ecología” del cuello uterino y alrededores, y hay datos (10) que sugieren un efecto de “nicho vacío”, que permite la proliferación de otros virus de alto riesgo oncológico, o la transformación de los de bajo riesgo.
If the vaccine eliminates the viruses, is it possible that it might have two effects, both beneficial and harmful? Yes.
For example, the vaccine might reduce chronic infections and pre-malignant lesions caused by the viruses which the vaccine acts against (helpful). But if this eliminated other human papilloma viruses, we wouldn’t know how to assess such a change. For example, co-infection with types 6 and 11 (low cancer risk) naturally decreases the probability of infection by type 16 (high cancer risk) (9). It is generally accepted that the vaccination blocks the appearance or activation of the viruses that it targets. Because of these changes occur in the “ecology” of the uterine cervix and surrounding areas, and there are data (10) to support the existence of an “empty niche” effect, that permits the proliferation of other high cancer risk viruses, or that permits the transformation of low-risk viruses into high-risk ones.
6. ¿Se ha demostrado su efectividad? No; no se tienen datos sobre su resultado en la práctica clínica diaria, ni siquiera ensayos clínicos con resultados en salud en las niñas en que se propone la vacunación. Se tienen datos de eficacia de casi el 100% (resultados de ensayos clínicos para los que cumplen todas las condiciones ideales, muy diferentes de la clínica diaria), para lesiones asociadas a los virus contra los que se vacuna, en mujeres de 16 a 26 años, generalmente blancas, sanas, de países desarrollados y educadas (10-14). Cuando se tiene en cuenta “la intención de tratar” (se incluyen todos los pacientes participantes en los ensayos, aunque no hayan cumplido las condiciones ideales) la eficacia baja al 50% (10-14), y si se incluyen las lesiones no asociadas a los virus contra los que se vacuna, la eficacia baja hasta el 17% (11).
Has the vaccine been shown to be effective? No.
There are no clinical data about its effectiveness, nor have there been clinical trials showing health outcomes for girls in the age group being targeted for vaccination. There is data showing almost 100% effectiveness (results from clinical trials conducted under the most ideal conditions, quite different from real-life clinical practice) for lesions associated with the viruses that the vaccine targets, in women ages 16 to 26, who were mostly white, healthy, well educated and living in developed countries (10-14). When “intention to treat” is taken into account (if all patients who participated in the trials are included, even if not meeting ideal inclusion criteria), the vaccine’s effectiveness decreases to 50% (10-14). And if all those patients whose cervical lesions are not associated with the viruses targeted by the vaccine are included then the rate of effectiveness of the vaccine falls to 17% (11).
7. ¿Se sabe cuánto dura la inmunidad? No, no se sabe. Lo máximo demostrado son cinco años. Si la inmunidad decae, se podría precisar de una re-vacunación cada cierto tiempo. Además del gasto y complicaciones que ello implica, no sabemos si al ceder la inmunidad artificial se debilitaría la inmunidad natural y habría infecciones oncogénicas más graves y agresivas (algo parecido sucede con la vacunación contra la varicela) (7,12).
Do we know how long immunity [from the vaccine] will last? No.
So far, it has been shown to work for five years. If immunity would decrease, then re-vaccination would be necessary after a certain length of time. Besides the expense and logistical complications this would entail, we do not know if inducing artificial immunity would inhibit natural immunity, resulting in serious and more aggressive oncogenic infections. (something similar to what has happened with small pox vaccination) (7,12).
8. ¿Se ha determinado el coste-efectividad de la vacuna? Sí. Pero se asumen condiciones no demostradas. Especialmente respecto a la efectividad y respecto a la duración de la vacuna. De hecho, en condiciones muy probables, si la inmunidad provocada por la vacuna dura menos de treinta años, y si la efectividad es del 70%, en Canadá, el coste-efectividad es nulo. Es decir, habría que vacunar a infinitas niñas para evitar un caso de cáncer de cuello de útero (15).
Has the vaccine’s cost-effectivenes been determined? Yes.
But some unproven assumptions have been made about its effectiveness and duration of immunity it offers. In fact, under ordinary conditions, if the period of immunity from the vaccine lasts less than 30 years, and if its rate of effectiveness is 70%, in the case of Canada, then it is not cost-effective at all. In other words, it would be necessary to vaccinate all girls in order to prevent one case of cervical cancer (15).
9. ¿Sirve en mujeres que ya han iniciado la actividad sexual? No. Las mujeres se contagian al comienzo de la actividad sexual. La eficacia (ensayos clínicos, condiciones ideales) es muy baja en mujeres que ya han iniciado la actividad sexual, de alrededor del 17% (10,16). Es una vacuna profiláctica (que evita el contagio), no terapéutica (que elimine el virus de las células epiteliales) (5, 10).
Is the vaccine effective for women who are already sexually active? No.
Women get the infection when they become sexually active. Clinical trials done under ideal conditions show that the vaccine has very low efficacy in sexually active women, about 17% (10,16). The vaccine is prophylactic (blocks transmission), not therapeutic (which would eliminate virus in the epithelial cells) (5, 10).
10. ¿Hay ensayos clínicos y estudios independientes, no financiados o promovidos por la industria farmacéutica? No, o son irrelevantes. El grueso de la investigación sobre la vacuna contra el virus del papiloma humano ha dependido, depende y dependerá de la industria que fabrica dichas vacunas (10). Se ignora porqué los gobiernos de los países desarrollados han renunciado a tener un papel activo en el conjunto de la salud sexual, y se reservan sólo el papel pasivo de “pagador” de la vacuna.
Are there clinical trials and independent research that have not been financed or sponsored by the pharmaceutical industry? No, or if so, they are irrelevant.
The bulk of the research on the HPV vaccine has been, is, and will continue to be dependent on the manufacturers of the vaccine. It is unclear why the governments of wealthy countries have declined to take an active role in this area of sexual health services, and instead have assumed merely a passive role as “payor” for the vaccine (10).
11. ¿Se precisa mantener el programa actual de detección precoz del cáncer de cuello de útero? Sí. Los actuales programas de cribaje con la citología (Papanicolau) tienen graves problemas de cobertura y fundamento científico, pero la vacuna no los evita, pues combate sólo dos de los quince virus oncogénicos. No sabemos en qué forma se modificará la sensibilidad y especificidad del cribaje (5,7).
Is it still necessary to continue the current early dectection programs for cervical cancer? Yes.
Current screening programs to detect cervical cancer by cytology (Pap smears) have serious problems in terms of patient access as well as scientific basis, the vaccine doesn’t replace them, as the vaccine only acts against 2 of the 15 oncogenic viruses. We do not know how the specificity and sensibility of screening tests should be modified (5,7).
Bibliografía
Bibliography
Vacuna.org. Calendario de vacunación. Europa. http://www.vacunas.org/index.php?option=com_content&task=view&id=2472&Itemid=336. Consultado el 13 de octubre de 2007.
Gervas J, Pérez Fernández M, González de Dios J. Problemas prácticos y éticos de la prevención secundaria. A propósito de dos ejemplos en pediatría. Rev Esp Salud Pública. 2007;81:345-52.
Starfield B, Hyde J, Gérvas J, Heath I. The concept of prevention: a good idea gone astray? J Epidemiol Community Health. 2008 [in press].
Gérvas J, Starfield B, Heath I. Caution in clinical prevention. Lancet. 2008 [in press].
Markowitz LE, Dunne EF, Saraiya M, Lawson HW, Chessm H, Unger E for the ACIP. Quatrivalent human papilloma virus vaccine. MMWR. 2007;56(RR02): 1-24.
Galceran J, Marcos R, Izquierdo A, Borrás J. Carcinoma invasor y lesiones premalignas del cuello uterino en los registros poblacionales: utilidad y limitaciones. En: Sanjosé S, García A (coordinadoras). Madrid: Sociedad Española de Epidemiología (4ª Monografía); 2006. p. 15-29.
Navarro JA, Bernal PJ, Pérez JJ. Interrogantes en la introducción de la vacuna frente al virus del papiloma humano en los calendarios sistemáticos. Med Clín (Barc). 2007;129:55-60.
EMEA. EPARS for authorised medicinal products. Gardasil. http://www.emea.europa.eu/humandocs/Humans/EPAR/gardasil/gardasil.htm. Consultado el 13 de octubre de 2007.
Hughes JP, Garnett GP, Koutsky L. The theoretical population-level impact of a prophylactic human papilloma virus vaccine. Epidemiol. 2002;13: 361-9.
Sawaya GF, Smith K. HPV vaccination. More answers, more questions. N Engl J Med. 2007;356:1991-3.
Kahn JA, Burk RD. Papillomavirus vaccines in perspective. Lancet. 2007;369:2135-7.
Lippman A, Melnychuk R, Shimmin C, Boscope M. Human papillovirus, vaccines and women’s health: questions and cautions. CMAJ. 2007;177:484-7.
Joura EA, Leodoter S, Hernández-Ávila M, Wheeler CM, Pérez G, Loutsky LA et al. Efficacy or quadrivalent prophylactic human papillomavirus (types 6, 11,16, and 18) L1 virus-like-particle vaccine against high-grade vulvar, and vaginal lesions: a combined analysis of three randomised clinical trials. Lancet. 2007;369:1693-702.
Rambout L, Hopkins L, Hutton B, Fergusson D. Prophylactic vaccination against human papillomavirus infection and disease in women: a systematic review of randomized controlled trials. CMAJ. 2007;177:469-79.
Brisson M, Velde N, Wals P, Boily MC. Estimating the number needed to vaccinate to prevent diseases and death related to human papillomavirus infection. CMAJ. 2007;175:464-8.
Future II Study Group. Quatrivalent vaccine against human papillomavirus to prevent high-grade cervical lesions. N Engl J Med. 2007:356:1915-27.
Fuente: Gervas, J. (2008, June 8). June08. Retrieved Sep. 21, 2008, from http://www.healthyskepticism.org/news/2008/June08.htm.

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A new approach to cervical screening


Age-standardised death rates from Cervix uteri...              Image via Wikipedia

The Lancet Oncology, Volume 12, Issue 7, Pages 612 – 613, July 2011
doi:10.1016/S1470-2045(11)70159-0Cite or Link Using DOI
Published Online: 17 June 2011

A new approach to cervical screening

At present, screening for cervical cancer is done mainly by reading Pap smears for abnormal cells. Although this subjective method has led to a decrease in incidence and mortality attributable to cervical cancer in developed countries, false-positive and false-negative screening results happen regularly. With the insight that infection with high-risk human papillomavirus (HPV) is obligatory for the development of cervical cancer, and the introduction of sensitive HPV testing methods, it was foreseen in 1992 that testing for HPV had implications as a primary technique for cervical screening.1 Despite the overwhelming evidence that testing for HPV results in earlier detection of cervical intraepithelial neoplasia (CIN) grade 3 and cervical cancer, it has not yet been implemented in regular screening programmes. Resistance from cytopathologists against a molecular test and the fear of higher colposcopy referral rates due to the 4—6% lower specificity of the HPV test are among the main reasons.
In The Lancet Oncology, the study by Hormuzd Katki and colleagues2 provides extensive data about the cumulative incidence of CIN2 or worse and CIN3 or worse after HPV and cytology co-testing of more than 300 000 women aged 30 years or older participating in the Kaiser Permanente cervical screening programme. Although similar conclusions from randomised trials have been published earlier, the strength of the report lies in the reliable risk estimates for CIN2 or worse and CIN3 or worse for rare combinations of HPV and cytology results and the routine setting wherein the results have been obtained.
An important conclusion is that the 1-year and 4-year cumulative incidences of CIN3 or worse of sole HPV testing and HPV and cytology co-testing are similar, which questions the value of co-testing, still being recommended in the USA for women aged 30 years or older. Moreover, the CIN3 or worse risk after a negative HPV test is much lower than after a negative cytology test, providing justification for an extension of the screening interval. Another important conclusion is that women positive for HPV but negative by cytology have a substantial risk of CIN3 or worse. This finding, usually underestimated by clinicians, necessitates closer surveillance. A third important conclusion is that testing for HPV detects more adenocarcinomas and precursors than cytology, providing hope that the incidence of adenocarcinoma will decrease in the future.
From these and other data, it becomes clear that guidelines for cervical screening have to be changed in the near future. The expectation is that the primary screening method will be a clinically validated HPV test and the role of cytology will be to triage women positive for HPV to restrict the number of colposcopy referrals. Cytologically negative women can be followed up by HPV testing after 3 years3 or by cytology after 6—12 months.4 HPV16/18 genotyping has also been suggested as a triage method but will lead to many more colposcopy referrals.4
For triage of women positive for HPV, cytology will face growing competition from other methods that detect viral (eg, E6/E7 region mRNA) or non-viral markers. The latter includes an immunocytochemical assay, which relies on dual-staining of cervical cells for p16INK4a and Ki67 antigens and has revealed promising data.5 Another promising candidate triage tool involves measurement of promoter methylation of CADM1 and MAL genes6 that has the advantage that it is a molecular technique and hence not troubled by subjective interpretation.
Finally, it must be remarked that screening refusal is an important problem in several countries, and efforts should be made to maximise the uptake of screening. For women that refuse to respond to a screening invitation, devices for self-collection of cervicovaginal material for HPV testing have been developed and data are accumulating suggesting that the sensitivity for high-grade CIN can be similar to that of testing for HPV on a physician-collected cervical smear. However, unlike the HPV test, cytology on self-sampled vaginal material is not reliably applicable, and triage of women positive for HPV by molecular markers seems indicated. We foresee that in the future, cervical screening will be done by the testing of HPV on either a smear taken by a physician or a self-sampled specimen, dependent on the preference of the woman, followed by triage by a molecular marker, making cervical screening objective and reproducible.
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Full-size image (32K) Russell Kightley/Science Photo Library
CJLMM has served on an advisory board for Qiagen and has received speakers’ fees from Qiagen and Roche. JB has received an unrestricted research grant of GlaxoSmithKline. PJFS has served on advisory boards for Gen-Probe, Roche, and GlaxoSmithKline.

References

1 Meijer CJ, van den Brule AJ, Snijders PJ, Helmerhorst T, Kenemans P, Walboomers JM. Detection of human papillomavirus in cervical scrapes by the polymerase chain reaction in relation to cytology: possible implications for cervical cancer screening. IARC Sci Publ 1992; 119: 271-281. PubMed
2 Katki HA, Kinney WK, Fetterman B, et al. Cervical cancer risk for women undergoing concurrent testing for human papillomavirus and cervical cytology: a population-based study in routine clinical practice. Lancet Oncol 201110.1016/S1470-2045(11)70145-0. published online June 17. PubMed
3 Dillner J, Rebolj M, Birembaut P, et al. Long term predictive values of cytology and human papillomavirus testing in cervical cancer screening: joint European cohort study. BMJ 2008; 337: a1754. CrossRef | PubMed
4 Rijkaart DC, Berkhof J, van Kemenade FJ, et al. Evaluation of 14 triage strategies for HPV DNA-positive women in population-based cervical screening. Int J Cancer 201110.1002/ijc.26056. published online Mar 11. PubMed
5 Petry KU, Schmidt D, Scherbring S, et al. Triaging Pap cytology negative, HPV positive cervical cancer screening results with p16/Ki-67 Dual-stained cytology. Gynecol Oncol 2011; 121: 505-509. CrossRef | PubMed
6 Hesselink AT, Heideman DA, Steenbergen RD, et al. Combined promoter methylation analysis of CADM1 and MAL: an objective triage tool for high-risk human papillomavirus DNA-positive women. Clin Cancer Res 2011; 17: 2459-2465. CrossRef | PubMed
a Department of Pathology, VU University Medical Centre, Amsterdam, Netherlands
b Department of Epidemiology and Biostatistics, VU University Medical Centre, Amsterdam, Netherlands

Cervical cancer risk for women undergoing concurrent testing for human papillomavirus and cervical cytology: a population-based study in routine clinical practice


Age-standardised death rates from Cervix uteri...                                           Image via Wikipedia

The Lancet Oncology, Early Online Publication, 17 June 2011
doi:10.1016/S1470-2045(11)70145- 

Cervical cancer risk for women undergoing concurrent testing for human papillomavirus and cervical cytology: a population-based study in routine clinical practice

Summary

Background

Concurrent testing for human papillomavirus (HPV) and cervical cytology (co-testing) is an approved alternative to cytology alone in women aged 30 years and older. We aimed to assess the safety in routine clinical practice of 3-year screening intervals for women testing negative for HPV with normal cytology and to assess if co-testing can identify women at high risk of cervical cancer or cervical intraepithelial neoplasia grade 3 (CIN3) or worse over 5 years.

Methods

We assessed the 5-year cumulative incidence, starting in 2003—05, of cervical cancer and CIN3 or worse for 331 818 women aged 30 years and older who enrolled in co-testing at Kaiser Permanente Northern California (Berkeley, CA, USA) and had adequate enrolment co-test results. Follow-up continued until Dec 31, 2009. We defined cumulative incidence to include prevalence at enrolment and incidence after enrolment. Prevalence at enrolment was defined as the ratio of women diagnosed with each outcome on the biopsy visit immediately after their enrolment screening visit to the total enrolled women. At screening visits only HPV test and Pap smear samples were collected, and at biopsy visits colposcopically directed biopsies were taken. To estimate post-enrolment incidence, we used Weibull survival models.

Findings

In 315 061 women negative by HPV testing, the 5-year cumulative incidence of cancer was 3·8 per 100 000 women per year, slightly higher than for the 306 969 who were both negative by HPV and Pap testing (3·2 per 100 000), and half the cancer risk of the 319 177 who were negative by Pap testing (7·5 per 100 000). 313 465 (99·5%) women negative by HPV testing had either normal cytology or equivocal abnormalities. Abnormal cytology greatly increased cumulative incidence of CIN3 or worse over 5 years for the 16 757 positive by HPV testing (12·1% vs 5·9%; p<0·0001). By contrast, although statistically significant, abnormal cytology did not increase 5-year risk of CIN3 or worse for women negative by HPV testing to a substantial level (0·86% vs 0·16%; p=0·004). 12 208 (73%) of the women positive by HPV testing had no cytological abnormality, and these women had 258 (35%) of 747 CIN3 or worse, 25 (29%) of 87 cancers, and 17 (63%) of 27 adenocarcinomas.

Interpretation

For women aged 30 years and older in routine clinical practice who are negative by co-testing (both HPV and cytology), 3-year screening intervals were safe because a single negative test for HPV was sufficient to reassure against cervical cancer over 5 years. Incorporating HPV testing with cytology also resulted in earlier identification of women at high risk of cervical cancer, especially adenocarcinoma. Testing for HPV without adjunctive cytology might be sufficiently sensitive for primary screening for cervical cancer.

Funding

Intramural Research Program of the US National Cancer Institute/NIH/DHHS, and the American Cancer Society.