Key Point Oncogenic HPV types are the core cause of cervical cancer. Background In a meta-analysis, specific oncogenic HPV types have been identified in 63% – 97% of invasive cervical cancer cases worldwide. 1 Among 85 studies measuring HPV prevalence in invasive cervical cancer by polymerase chain reaction (PCR)–based assays (N=10,058), HPV 16 was the predominant type in squamous cell carcinoma cases (46% – 63%), followed by HPV 18 (10% – 14%), 45 (2% – 8%), 31 (2% – 7%), and 33 (3% – 5%), except in Asia, where HPV 58 and 52 were found in 6% and 4% of cases, respectively. In adenocarcinoma and adenosquamous-carcinoma cases, HPV 18 was predominant (37% – 41%), followed by type 16 (26% – 36%) and type 45 (5% – 7%). The overall detection of HPV DNA in invasive cervical cancer was similar in different regions worldwide. 1 Due to sample inadequacy or integration events effecting the HPV L1 gene, the target of the PCR-based assay, some projected prevalences may actually be underestimated. Walboomers and colleagues conducted a study to more accurately assess the prevalence of HPV DNA. 2 A PCR-based test was used; however, in HPV-negative cases, the biopsy was reanalyzed by a sandwich procedure, in which the inner sections of a series of tissue sections were assayed by 3 different HPV PCR assays targeting different open reading frames, while the outer sections were reviewed to verify the presence of malignant cells. Analysis of 932 specimens from women with cervical cancer in 22 countries indicated that worldwide HPV prevalence in cervical carcinomas is 99.7%. 2 References 1. Clifford GM, Smith JS, Plummer M, Mu ñ oz N, Franceschi S. Human papillomavirus types in invasive cervical cancer worldwide: A meta-analysis. Br J Cancer . 2003;88:63 – 73. 2. Walboomers JM, Jacobs MV, Manos MM, et al. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol . 1999;189:12 – 19.
Key Point More than 90% of anogenital warts are associated with HPV types 6 and 11. Anogenital warts are clinically apparent in ~1% of the sexually active US adult population. Background More than 90% of anogenital warts are associated with HPV types 6 and 11. 1 The prevalence of anogenital warts has been reported to be highest in women 20 to 24 years of age (6.2 cases/1000 person years) and men 25 to 29 years of age (5.0 cases/1000 person years). 2 About 1% of sexually active adults have clinically apparent genital warts, and at least 15% have subclinical infection. 3 The estimated lifetime risk of developing genital warts is approximately 10%. 4,5 In UK, the number of new cases has been increased over the past 1-2 decades, 32% increase from 1995 to 2004, about 4% of the population reported having been diagnosed to have genital warts, which is the most common STI. References 1. Jansen KU, Shaw AR. Human papillomavirus vaccines and prevention of cervical cancer. Annu Rev Med. 2004;55:319 –331. 2. Insinga RP, Dasbach EJ, Myers ER. The health and economic burden of genital warts in a set of private health plans in the United States. Clin Infect Dis. 2003;36:1397 –1403. 3. Koutsky L. Epidemiology of genital human papillomavirus infection. Am J Med . 1997;102:3 – 8. 4. Franco EL, Villa LL, Richardson H, Rohan TE, Ferenczy A. Epidemiology of cervical human papillomavirus infection. In: Franco EL, Monsonego J, eds. New Developments in Cervical Cancer Screening and Prevention . Oxford, UK: Blackwell Science; 1997:14–22. 5. Tortolero-Luna G. Epidemiology of genital human papillomavirus. Hematol Oncol Clin North Am . 1999;13:245–257, x.
Key Point The main predisposing factor for VaIN is likely exposure to HPV. VaIN is often asymptomatic and difficult to treat. VaIN can progress to vaginal cancer. Background The true incidence of vaginal intraepithelial neoplasia (VaIN) is unknown but is far lower than for cervical intraepithelial neoplasia (CIN). 1 The incidence of VaIN is expected to rise because of wider application of cytologic screening and colposcopy as well as increased awareness of this disease. 2 The average age of women with VaIN is 35–50 years, which is older than for those presenting with CIN. 2 The main predisposing factor for VaIN is likely to be exposure to HPV, explaining why VaIN is often found in conjunction with CIN. 1 In vaginal smears of 616 women with a prior hysterectomy, vaginal HPV was found 2.4 times more frequently in women with a history of CIN or cervical cancer than in all other women. 3 In addition, of 110 HPV-positive patients, 5 had VaIN, whereas none of the 506 HPV-negative women had VaIN; this difference was statistically significant; all 5 VaIN cases were positive for HPV 16. 3 HPV types 16 and 18 were more often identified in patients with a history of cervical carcinoma; HPV types 6 and 11 were more often seen in patients with a history of benign uterine disease. 3 While untreated VaIN can spontaneously regress, there is a potential for VaIN to progress to invasive vaginal cancer. 2 VaIN is often asymptomatic and difficult to diagnose. A retrospective chart review of 121 women with confirmed histologic diagnosis of VaIN showed that 94% of the patients were asymptomatic; disease was most often identified via an abnormal Pap smear, followed by colposcopy-directed biopsy. 2 Although VaIN is primarily asymptomatic, approximately 80–90% of women with invasive vaginal cancer have symptoms, which may include abnormal vaginal bleeding, abnormal vaginal discharge, a mass that can be felt, or pain during intercourse. 4 References 1. Winter-Roach B, Monaghan JM, de Lopes A. Colposcopy of the vagina. In: Bosze P, Luesley D, eds. EAGC Course Book on Colposcopy . Budapest: Primed-X Press; 2004:120–123. 2. Dodge JA, Eltabbakh GH, Mount SL, Walker RP, Morgan A. Clinical features and risk of recurrence among patients with vaginal intraepithelial neoplasia. Gynecol Oncol. Nov 2001;83:363–369. 3. Schneider A, de Villiers EM, Schneider V. Multifocal squamous neoplasia of the female genital tract: significance of human papillomavirus infection of the vagina after hysterectomy. Obstet Gynecol. Sep 1987;70:294–298. 4. American Cancer Society. Detailed Guide: Vaginal Cancer. Available at: http://www.cancer.org/docroot/CRI/content/CRI_2_4_1X_What_is_vaginal_cancer_55.asp?rnav=cri. Accessed August 15, 2006.
Key Point The rate of VIN has been increasing worldwide; and the mean age of women with VIN has decreased from >50 to women in their 30s and 40s. Background The incidence of vulvar intraepithelial neoplasia (VIN) is increasing in the United States and worldwide. 1 The rate of VIN 3 (vulvar carcinoma in situ) in the United States nearly doubled from 1973 to 1987 from 1.1 to 2.1 per 100,000 women-years, surpassing the rate of invasive vulvar cancer. 1 The increased frequency of VIN 3 in the United States has particularly been observed in women less than 35 years of age. 2 The rate has also been increasing worldwide; this increase appears to be associated with HPV infection, especially HPV 16. 1 In the United States, the age of peak incidence of VIN 3 has declined over time from >54 years to between 35 and 54 years. 2 Evidence from outside the United States also suggests that the mean age of women with VIN (including high-grade VIN) is decreasing to <40 years. 3,4 Symptoms occur in the majority of patients with VIN, most commonly pruritus (severe itching), and may be present for a long time prior to diagnosis (median of 1 year). Other symptoms include vulvar pain or soreness, warts, swelling, discoloration, vaginal discharge, or bleeding. 4 References 1. Joura EA. Epidemiology, diagnosis and treatment of vulvar intraepithelial neoplasia. Curr Opin Obstet Gynecol. Feb 2002;14:39–43. 2. Sturgeon SR, Brinton LA, Devesa SS, Kurman RJ. In situ and invasive vulvar cancer incidence trends (1973 to 1987). Am J Obstet Gynecol. 1992;166:1482–1485. 3. Jones RW, Rowan DM, Stewart AW. Vulvar intraepithelial neoplasia: aspects of the natural history and outcome in 405 women. Obstet Gynecol. 2005;106:1319–1326. 4. Herod JJ, Shafi MI, Rollason TP, Jordan JA, Luesley DM. Vulvar intraepithelial neoplasia: long term follow up of treated and untreated women. Br J Obstet Gynaecol. 1996;103:446–452.
HPV Phylogenetic Tree Cancer-Causing HPV Species HPV Phylogenetic Tree
Key Point GARDASIL™ is Merck’s quadrivalent HPV L1 VLP vaccine. It is produced in recombinant yeast, like the hepatitis B vaccine, and adsorbed on a proprietary aluminum adjuvant, like the tetanus vaccine. Background Merck’s quadrivalent vaccine has the advantage that it targets 4 HPV types (6, 11, 16 and 18). 1 Together, HPV Types 16 and 18 account for about 70% of cervical cancer and high-grade lesions, whereas HPV Types 6 and 11 are associated with approximately 90% of anogenital warts. 1 Together, these 4 types are responsible for over 40% of low-grade cervical lesions, 2 and HPV 16 and 18 account for over 50% of high-grade lesions. 3 The active quadrivalent vaccine is a mixture of 4 recombinant HPV type-specific VLPs consisting of the L1 major capsid proteins of HPV 6, 11, 16, and 18 synthesized in Saccharomyces cerevisiae. 1 Expression of the L1 protein in yeast generates noninfectious VLPs that resemble HPV virions. 1 A similar method is used for hepatitis B vaccine. 4 The 4 VLP types were purified and absorbed onto amorphous aluminum hydroxyphosphate sulfate adjuvant. 1 The adjuvant dose was 225 micrograms per dose, and the vaccine injection volume was 0.5 mL, given by intramuscular injection at Day 1, Month 2, and Month 6. 1 GARDASIL is a trademark of Merck & Co., Inc., Whitehouse Station, NJ, USA. References 1. Villa LL, Costa RLR, Petta CA, et al. Prophylactic quadrivalent human papillomavirus (types 6, 11, 16, and 18) L1 virus-like particle vaccine in young women: A randomised double-blind placebo-controlled multicentre phase II efficacy trial. Lancet Oncol . 2005;6:271–278. 2. Clifford GM, Rana RK, Franceschi S, Smith JS, Gough G, Pimenta JM. Human papillomavirus genotype distribution in low-grade cervical lesions: Comparison by geographic region and with cervical cancer. Cancer Epidemiol Biomarkers Prev . 2005;14:1157–1164. 3. Clifford GM, Smith JS, Plummer M, Muñoz N, Franceschi S. Human papillomavirus types in invasive cervical cancer worldwide: A meta-analysis. Br J Cancer . 2003;88:63–73. 4. Recombivax HB ® Hepatitis B Vaccine (Recombinant) prescribing information. Merck & Co, Inc. Whitehouse Station, NJ. 1998. 3/Recombivax HB/p. 1/ ¶1. 1/Villa/p. 271/col 1/ ¶2 . 1/Villa/p. 272/col 1/ ¶3 . 1/Villa/p. 271/col 2/ ¶1 . 1/Villa/p. 271/col 2/ ¶1 . 1/Villa/p. 272/col 1/ ¶3 . 1/Villa/p. 272/col 2/ ¶1,2 . 2/Clifford/ p.1159/col 2/¶3, table 2 3/Clifford/p.65/ col 2/ ¶2 1/Villa/p. 271/abstract. 1/Villa/p. 272 /col 1/ ¶3. 1/Villa/p. 272 /col 1/¶4. 1/Villa/p. 272 /col 2/¶2. 1/Villa/p. 272 /col 2/¶2.
We want to make it available everywhere Approval vs. Launch * Note: Due to importation, distribution and other regulatory requirements as well as price negotiations, a licensed vaccine may not be marketed in a given country. Registration pending in 26 additional GAVI-eligible countries + WHO pre-qualification submitted Potential Q: which GAVI countries have access to GARDASIL? Indonesia, Kenya and Nicaragua
Messages 100% efficacy lasting for 5 years with antibody titres (neutralising, HPV type specific) plateauing at high level will not drop off tomorrow We therefore expect that Gardasil will protect a long time, 20, may be 30, may be 40 years, may be life-long Comments/Additional information Prevention of Human Papillomavirus infection is essentially through antibodies (neutralising, specific) and not through cell mediated immunity The formulation with 225 μ g of Merck’s aluminium phosphate adjuvant has proven to stimulate high antibody response for Gardasil It is very unusual that vaccines show a higher immune response than natural infection. Gardasil shows ~50 times higher immune response (note that the scale on the left is a log scale!) which is extremely high and exceptional already. Given the 100% efficacy this again shows that there is no sense in trying to induce even higher immune response.
In figure 1, the proportion of new clients with a GW diagnosis was calculated by dividing the number of GW diagnoses by the number of new clients seen in the relevant risk group in 6-month periods. ORs and 95% CIs for a diagnosis of warts in each additional 12-month period after 1 July 2007 were calculated using logistic regression and adjusted for the number of sexual partners in the previous 12 months. The same analysis was also undertaken for the 3-year period from 1 July 2004. These analyses were stratified by different age groups and risk groups. All calculations were performed in Stata V.11 (StataCorp). From 1 July 2004 to 30 June 2011, 52 454 new patients were seen at MSHC and 5021 (9.6%, 95% CI 9.3% to 9.8%) were diagnosed with GWs. The proportion of individuals diagnosed each year with GWs by age and risk group is shown in table 1. The largest declines between the 2007/2008 and 2010/2011 periods occurred in women under 21 years of age (a reduction from 18.6% to 1.9%) and in heterosexual men under 21 years of age (reduction from 22.9% to 2.9%). From 1 July 2010 to 30 June 2011, only four cases of warts occurred in heterosexual women <21 years of age compared with between 46 and 66 cases per annum before July 2007. Figure 1 shows these data in six monthly intervals. Before July 2007, GW diagnoses in women increased significantly with each year (OR 1.16, 95% CI 1.05 to 1.28) and were unchanged in all other groups (table 2). After July 2007, wart diagnoses decreased significantly in women <21 years of age or 22e29 years of age but not older women. Similarly, wart diagnoses decreased in heterosexual men aged <21 years and in those aged 22e29 years but not in older heterosexual men. After July 2007, wart diagnoses did not change in men who have sex with men (MSM) or non-residents. Among women who reported receiving the HPV vaccine, the adjusted OR for a diagnosis of warts was 0.29 (95% CI 0.13 to 0.65) in 2010/2011 compared with 2009/2010.
3.the cost effectiveness & real world impact of quadrivalent
The Cost Effectiveness & Real World Impact ofQuadrivalent HPV vaccine Endy M. Moegni KOGI XV Bali Nusa Dua Convention Center 29 Juni- 5 Juli 2012
Quadrivalent HPV Vaccine (4 in 1 HPV vaccine) Diphtheria antitoxin discovered Measles (live)* Human Papillomavirus* Mumps* Zoster (live)* Measles (live attenuated virus)* Rotavirus* Measles, mumps, rubella (MMR)* Pneumococcal (14-valent polysaccharide)*1895 1963 1967 1968 1971 1977 1978 1981 1983 1986 1989 1995 1996 1996 1996 2005 2006 2006 2006 Measles, mumps, rubella, varicella* The First Cancer Vaccine Haemophilus influenzae type b / Hepatitis B* Haemophilus influenzae type b (liquid)* of the World Hepatitis A (inactivated)* Varicella (chicken pox) virus* Haemophilus influenzae type b (conjugated)* Hepatitis B (recombinant)* Pneumococcal (23-valent polysaccharide)* Hepatitis B (plasma derived)* Measles, mumps, rubella virus vaccine live (new rubella strain: RA 27/3)* Tam Kar Fai
Cervical Cancer Is Essentially Caused by Oncogenic HPV HPV is a main cause of cervical cancer Analysis of 932 specimens from women in 22 countries indicated prevalence of HPV DNA in cervical cancers worldwide = 99.7%.1. Muñoz N, Bosch FX, de Sanjosé, et al. N Engl J Med. 2003;348:518–527. 2. Walboomers JM, Jacobs MV, ManosMM, et al. J Pathol. 1999;189:12–19.
HPV and Anogenital Warts HPV 6 and 11 responsible for >90% of anogenital warts1 Clinically apparent in ~1% of sexually active US adult population2 Estimated lifetime risk of developing genital warts ~10%3,4Images top left and top right: Reprinted with permission fromNZ DermNet (www.dermnetnz.org)1. Jansen KU, Shaw AR. Annu Rev Med. 2004;55:319–331. 2. Koutsky L. Am J Med. 1997;102:3–8. 3. Franco EL,Villa LL, Richardson H, Rohan TE, Ferenczy A. In: Franco EL, Monsonego J, eds. Oxford, UK: Blackwell Science;1997:14–22. 4. Tortolero-Luna G. Hematol Oncol Clin North Am. 1999;13:245–257, x.
Vaginal Intraepithelial Neoplasia (VaIN) Main predisposing factor for VaIN is likely exposure to HPV.1 – VaIN is often found in conjunction with cervical intraepithelial neoplasia (CIN). 1. Winter-Roach B, Monaghan JM, de Lopes A. Colposcopy of the vagina. In: Bosze P, Luesley D, eds. EAGC Course Book on Colposcopy.
Vulval Intraepithelial Neoplasia (VIN) HPV 16 appears to be the dominant HPV type associated with high-grade VIN (up to 81% in VIN 3)3 – Majority of VIN 1 cases are associated with HPV types 6 and 11 3 – HPV 6, 11, 16, or 18 can be found in VIN 2 or 3 4 Photo courtesy of Dr. J. Monsonego Photos courtesy of Dr. E.J. Mayeaux. 3. Buscema J, Naghashfar Z, Sawada E, et al. Obstet Gynecol. 1988;71:601–606. 4. Koutsky L. Am J Med.1997;102:3–8..
VaIN and VIN are of concern because they are considered as precancerous lesions with about 40 - 50% associated with HPV infection In UK, vulval cancer is 6 times and vaginal cancer 20 times less common than cervical cancer1 No screening programme exists1. Gonzalez Inchaurraga MA et al. HPV and carcinogenesis. Acta Dermatovenerol. 2002;1:1-8.2. Parkins DM et al. International Agency for Research on Cancer, 2002;8.
Phylogenetic Tree of HPV Family HPV 16 RelatedHPV18Related
Infection From Time of First 12 16 20 24 28 32 36 40 44 48 52 56 Sexual Intercourse Study of female college students (N=603) Months Since First Intercourse 8 4 0 1.0 0.8 0.6 0.4 0.2 0.0From Winer RL, Lee S-K, Hughes JP, Adam DE, Kiviat NB, Koutsky LA. Genital human papillomavirus infection:Incidence and risk factors in a cohort of female university students. Am J Epidemiol. 2003;157:218–226, by HPV Infectionpermission of Oxford University Press. Cumulative Incidence of
Quadrivalent HPV L1 VLP Vaccine1 Quadrivalent HPV L1 VLP vaccine – (Types 6, 11, 16, 18) VLPs manufactured in: – Yeast – Recombinant VLPs (empty shell protein L1) – Do not contain Virus DNA (not infectious) Amorphous Aluminum Hydroxyphosphate Sulfate Adjuvant (225 μg per dose) No Mercury preservative (thimerosal) Storage: 2 to 8 OCGARDASIL is a trademark of Merck & Co., Inc., Whitehouse Station, NJ, USA.*VLP = Virus-like particle. 1. Villa LL, Costa RL, Petta CA, et al. Lancet Oncol. 2005;6:271–278.
Dosage & Administration3 doses within 6 months – (0, 2, 6 months) 0.5mL volume IM injection Package: – Prefilled syringe – Shake well before use Injection Site: – Upper arm (Deltoid region) – Thigh (higher anterolateral area)
Gardasil / Silgard ApprovalsGARDASIL approved in 127 countries (includes 24 GAVI-eligible) Europe:Caribbean & Central America: North America: Germany Cyprus Ireland France Czech Republic LatviaCosta Rica Trinidad/Tobago USA UK Denmark LithuaniaPuerto Rico El Salvador Canada Spain Estonia LuxembourgGuatemala Honduras Italy Finland Malta Asia Pacific & Japan: MexicoCuraçao Nicaragua Austria Greece Netherlands KyrgyzstanBermuda Panama Belgium Hungary Norway UzbekistanBahamas Cayman Islands Bulgaria Iceland Poland KazakhstanBarbados Aruba Portugal Romania Slovakia AustraliaJamaica Dominican Republic Slovenia Sweden Serbia Indonesia Korea 42 Montenegro Bosnia Switzerland Russia Liechtenstein Belarus Taiwan Croatia Turkey Ukraine Hong KongSouth America:Brazil Bolivia 3 Herzogovina Macedonia Albania Singapore New ZealandArgentina Uruguay MacauPeruColombia Ecuador Chile 16 35 22 Malaysia Philippines ThailandParaguay 9 India VietnamMiddle East & Africa: Fiji BhutanGabon NamibiaIsrael C.A.R. GeorgiaMorocco Mauritius JAPANKenya Kuwait Sri LankaMauritania UAE BruneiGuinea Eq. EthiopiaUganda TogoMalawi Congo Brazzaville GAVI – Eligible Registration Approvals (24): Burkina Faso, Cameroon, CentralJordan Egypt African Republic, Chad, Congo (DR), Cote d’Ivoire, Ethiopia, Guinea (Conakry),Cote d’Ivoire Burkina Faso India, Kenya, Kyrgyzstan, Malawi, Mali, Mauritania, Nicaragua, Nigeria, Pakistan,Chad Bahrain Botswana Rwanda, Tanzania, Togo, Uganda, Uzbekistan, Vietnam, ZambiaLebanon Tanzania ZambiaSouth Africa Cameroon NigeriaPakistan Tunisia MaliGuinea Conakry Saudi Arabia Rwanda as of 8 June 2012
HPV Recommendations by National Expert Advisory Bodies on Immunization: 40 Countries National Funding by 38 Countries 23 Europe Austria3 Belgium Bulgaria North America Czech Republic Denmark USA France Canada Germany Mexico Greece Iceland Ireland Italy Latvia Luxemburg Macedonia Netherlands2 Norway Portugal Caribbean & Central America Romania Slovenia Puerto Rico Spain Panama Sweden Switzerland United Kingdom3 Cayman Is.South AmericaArgentinaPeruGuyana FUNDING 6 Asia Pacific GARDASIL only Australia Bivalent Only 3 New Zealand Malaysia Both vaccines Middle East & Africa India No funding Singapore Kuwait Japan UAEUpdate: June 8, 2012 Lesotho
HPV Vaccine: National Immunization Program 15 countriesEleven European countries (Germany, France, Italy, Belgium, Austria, Norway, Sweden, Greece, Denmark, Luxemburgand Switzerland), as well as the United States, Canada, Australia and UK have already reviewed the positive public health impact and recommended the quadrivalent HPV vaccine for universal human papillomavirus vaccinationwith accelerated reviews.
Sustained clinical efficacy and antibody titer for at least 5 years GMT (mMU/mL) GARDASIL 100% 10 000Neutralising antibodies GARDASIL Clinical efficacy* 1 000 (HPV type 16) 100 10 Natural infection 0 7 12 18 24 30 36 54 60 months 5 years 1st 2nd 3rd Dose * against infection, CIN (Cervical intraepithelial neoplasia) and genital warts due to HPV types 6,11,18; 5 yrs follow up (after dose 1) of a subset (241 women, Villa L High Sust Eff Proph Quad HPV Vacc 5 Year Followup Br J vaccine Can 2006 95 1459 & placebo) from a phase II efficacy study
Long Term Response Modified power law model Conventional power law modelThe conventional power law model estimated a median duration of detectableantibody of 32 years.The modified power law model predicted a long-term plateau of antibodyduration with a near life-long persistence above the level of detection.Model-based prediction of GMTs and proportions above different thresholds following HPV-16 L1 VLP vaccination predicted from the models.GMTs predicted from the power-law(- - -) and modified power law(—) models, using antibody data measured during 48 months followingHPV-16L1 VLP vaccination are shown for 30 yrs. 1. C. Fraser et al. / Vaccine 25 (2007) 4324–4333
CDC 2010 Mar – Gardasil Q&A for publicAccessed 10 Jul 2010http://www.cdc.gov/vaccines/pubs/vis/downloads/vis-hpv-gardasil.pdf
Australia Free NationalHPV vaccination Program Malaysia Free NationalHPV vaccination Program
The near disappearance of genital warts in young women 4 years after commencing a national human papillomavirus (HPV) vaccination programmeTim R H Read,1 Jane S Hocking,2 Marcus Y Chen,1 Basil Donovan,3Catriona S Bradshaw,4 Christopher K Fairley1
• From July 2004 to June 2011, • 52 454 new patients were seen at Melbourne Sexual Health Centre and 5021 (9.6%, 95% CI 9.3% to 9.8%) were diagnosed with GW. • From July 2004 to June 2007, the proportions with GW either increased or did not change in all groups.Tim R H Read,1 Jane S Hocking,2 Marcus Y Chen,1 Basil Donovan,3Catriona S Bradshaw,4 Christopher K Fairley1
• The two 12-month periods of 2007/2008 and 2010/2011, GW declined in women under 21 years from 18.6% to 1.9% and in heterosexual men under 21 years from 22.9% to 2.9%. • There was no significant change in GW in women $30 years (OR 0.97, 95% CI 0.84 to 1.12), heterosexual men $30 years (OR 0.97, 95% CI 0.89 to 1.06) or in homosexual men (OR 0.95, 95% CI 0.85 to 1.07).Tim R H Read,1 Jane S Hocking,2 Marcus Y Chen,1 Basil Donovan,3Catriona S Bradshaw,4 Christopher K Fairley1
Conclusions• The dramatic decline and near disappearance of GW in women and men under 21 years of age, 4 years after commencing this programme, suggest that the basic reproductive rate has fallen below one.
Comparative Cost-Effectiveness of HPV Vaccines in the Prevention of Cervical Cancer in Malaysia • Cost effectivenes options were compared for three programs i.e. screening via Pap smear; modeling of HPV vaccination (QV and BV) and combined strategy (screening plus vaccination).Sharifa WP Ezat1*, Syed Aljunid2
Methods Forthis cross sectional study in 2006-2009 respondents were interviewed from six public Gynecology-Oncology hospitals. (502 cervical cancer patients participated). Methods included expert panel discussions to estimate treatment costs by severity and direct interviews with respondents using costing and quality of life questionnaires. Sharifa WP Ezat 1*, Syed Aljunid2
Results A total of 502 cervical cancer patients participated with a mean age at 53.3±11.2 years and a mean marriage length of 27.7±12.1 years, Malays accounting for 44.2%. Cost/quality adjusted life year (QALY) for Pap smear Cost/quality adjusted life year (QALY) for strategy with HPV vaccination only Cost/quality adjusted life year (QALY) for strategy with combined strategy (screening + HPV vaccination)
Results(Incremental Cost Effectiveness Ratio (ICER))
Conclusions QV is more cost effective than BV. The QV combined strategy was more cost effective than any method except Pap smear screening with high population coverage. Sharifa WP Ezat 1*, Syed Aljunid2
Comparing Bivalent and Quadrivalent Human Papillomavirus Vaccines: Economic Evaluation Based on Transmission Model Author: Jit et al
Results Effect on disease: – Use of either vaccine is expected to substantially decrease the incidence of HPV related cancers regardless of which scenario is assumed – By 2109, HPV vaccine may prevent: Cervical cancer cases vulval, vaginal, reduction and anal cancers cases reduction QHPV 700 (630–800) to 430 (380–490) to 1000 (940–1100) 630 (950–670) BHPV 730 (650–830) to 1100 (990–1200) – Use of the qHPV is expected to decrease the incidence of vaccine type warts and recurrent respiratory papillomatoses by up to 95% if duration of protection is lifelong.Jit et al. 2011. BMJ 2011;343:d5775
Conclusions• The quadrivalent vaccine may have an advantage over the bivalent vaccine in reducing healthcare costs and QALYs lost .
UK switched to QV from Sept 2012 United Kingdom (UK) Department of Health announced that from next September 2012, UK will use QV for HPV vaccination program in UK QV protects against the two types of HPV virus that cause more than 70 percent of cervical cancer in England and two types of HPV virus that cause 90 percent of genital warts.
Eradication of Cervical Cancer and HPV Related Diseases Not a Dream Anymore…
References• Donovan et al. 2010. Quadrivalent human papillomavirus vaccination and trends in genital warts in Australia: analysis of national sentinel surveillance data. DOI:10.1016/S1473- 3099(10)70225-5• Read et al. The near disappearance of genital warts in young women 4 years after commencing a national human papillomavirus (HPV) vaccination programme. Sex Transm Infect. doi:10.1136/sextrans-2011-050234• Ezat et al. 2011. Comparative Cost-Effectiveness of HPV Vaccines in the Prevention of Cervical Cancer in Malaysia. Asian Pacific J Cancer Prev, 11, 1-6.• Jit et al, Comparing bivalent and quadrivalent human papillomavirus vaccines: economic evaluation based on