Wed Apr 1 02:02:57 SGT 2015  
SINGAPORE
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    Genital Warts
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Genital Warts | SINGAPORE STD ™

Summary

Genital Warts | SINGAPORE STD ™ @singaporestd_com: Genital warts, Singapore. Private & confidential service.

Advertisement: Come to sunny Singapore to have your testing and treatment. Singapore Ministry of Health registered general practice (GP) clinic:
SHIM CLINIC
SINGAPORE STD ™
168 Bedok South Avenue 3 #01-473
Singapore 460168
Tel: (+65) 6446 7446
Fax: (+65) 6449 7446
24hr Answering Tel: (+65) 6333 5550
Web: Genital Warts | SINGAPORE STD ™
Opening Hours
Monday to Friday: 9 am to 3 pm, 7 pm to 11 pm
Saturday & Sunday: 7 pm to 11 pm
Public Holidays: Closed
Last registration: one hour before closing time.
Walk-in clinic. Appointments not required.
Bring NRIC, Work Pass or Passport for registration.

Description

Table of Contents

Genital warts: penile warts / vaginal warts / anal warts / anogenital warts / venereal warts / condyloma / condylomata acuminata / "cauliflower" sex disease.

References

Warts - on male sex organ Genital warts appear within 3 months after sexual contact with an infected person.

Genital warts:

  • are usually soft, pink cauliflower-like growths or flesh-coloured bumps on the sex organs
  • may also be hard and smooth
  • occur alone or in groups
  • tend to recur after treatment
  • increase the risk of cervical cancer in women.


Warts - on female sex organ An infected woman may infect her newborn during childbirth.

A person with genital warts can infect others through sexual contact.



Genital warts treatment / HPV treatment

HPV / human papillomavirus.

  • 120 known human papillomavirus (HPV)
  • 51 HPV types, and 3 subtypes are genital HPV as they infect the genital mucosa.
  • 31 genital HPV types are low risk
  • 6 genital HPV types are intermediate risk
  • 17 genital HPV types are high risk
They cause Genital HPV types, cancer risk, vaccine and test coverage
Type
Species
Risk
Cervarix
Gardasil
Gardasil-9
DigeneHR
DigenePS
CobasHPV
Digene
HybriBio
PapilloCheck
InnoLiPA
LinearArray
61 3 L ----------+-
72 3 L ----------+-
81 3 L -------+--+-
83 3 L ----------+-
84 3 L ----------+-
62 3 L ----------+-
CP6108 3 L ----------+-
71 15 L ---------++-
26 5 H ---------++-
51 5 H ---+-++++++-
69 5 H ---------++-
82 5 H --------+++-
IS39 5 H ----------+-
18 7 H +++++++++++-
39 7 H ---+-++++++-
45 7 H --+++++++++-
59 7 H ---+-++++++-
68 7 H ---+-++++++-
70 7 H --------+++-
53 6 H -------++++-
56 6 H ---+-++++++-
66 6 H -----+-++++-
54 13 L ---------++-
42 1 L ------+++-+-
40 8 L --------+++-
43 8 L ------++++--
6 10 L -++---+++++-
11 10 L -++---+++++-
44 10 L ------++++--
74 10 L ---------+--
16 9 H +++++++++++-
31 9 H --++-++++++-
33 9 H --++-++++++-
35 9 H ---+-++++++-
52 9 H --++-++++++-
58 9 H --++-++++++-
67 9 H ----------+-
73 11 H --------+++-

Legend: 71 (CP 8061), 73/MM9, 81 (CP 8304), 82 (MM4), 82 (IS 39), 83 (MM7), 84 (MM8), 89 (CP 6108)

References

Cervical cancer HPV vaccine (previously known as cervical cancer vaccine) types:
  • Gardasil® [HPV (Human Papillomavirus) Quadrivalent (Types 6, 11, 16, and 18) Vaccine, Recombinant]
  • Cervarix® [HPV (Human Papillomavirus) Bivalent (Types 16 and 18) Vaccine, Recombinant]
  • V503 [HPV (Human Papillomavirus) Nonavalent (Types 6, 11, 16, 18, 31, 33, 45, 52, and 58) Vaccine, Recombinant]
References Gardasil® [HPV (Human Papillomavirus) Quadrivalent (Types 6, 11, 16, and 18) Vaccine, Recombinant] References Cervarix® [HPV (Human Papillomavirus) Bivalent (Types 16 and 18) Vaccine, Recombinant] References V503 [HPV (Human Papillomavirus) Nonavalent (Types 6, 11, 16, 18, 31, 33, 45, 52, and 58) Vaccine, Recombinant] - to be released in 2013 STD vaccine / hepatitis vaccine shot/jab/injection to prevent some STDs

Vaccine Against Disease Age D
o
s
e
s
Dose schedule Price
per
dose
(SG$)
Havrix™ 1440 Adult Hepatitis A virus Hepatitis A ≥19y 2 m 0 & 6-12 $90/=
Twinrix® Hepatitis A virus
Hepatitis B virus
Hepatitis A
Hepatitis B
1-15y 2 m 0, 6-12 $135/=
≥16y 3 m 0, 1, 6
4 d 0, 7, 21 & m 12
Inactivated / Fractional / Protein / Subunit / Recombinant
Engerix™-B 20 μg Hepatitis B virus Hepatitis B 11-15y 2 m 0, & 6 $50/=
≥20y 3 m 0, 1, & 6
4 m 0, 1, 2, & 12 or
d 0, 7, 21 & m 12
Gardasil® HPV
types 6, 11, 16, & 18
Genital warts
Cervical cancer
9-26y 3 m 0, 2, & 6 or
m 0, 1, & 4
$195/=
Cervarix® HPV
types 16, & 18
(31, 33, & 45)
10-25y 3 m 0, 1, & 6
m 0, 1, & 5
m 0, 2½, 12
$195/=
V503 HPV
types 6, 11, 16, 18,
31, 33, 45,
52, & 58
3 m 0, 2, & 6 or
m 0, 1, & 4
$???/=

HPV test for men/women.

  • Digene® High-Risk HPV DNA Test
  • Digene® HPV DNA Test
  • Digene® HPV Genotyping PS Test
  • Hybribio®
    • HPV GenoArray Test Kit
    • Detects 15 high-risk HPV types: 16, 18, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, and 68. And 6 low-risk HPV types: 6, 11, 42, 43, 44, CP8304
    • Able to differentiate which types are positive.
    • May be available in Singapore soon.
  • Cobas® HPV Test
    • Cobas® HPV Test
    • Detects 14 high-risk HPV types: 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68
    • The test specifically identifies (types) HPV 16 and HPV 18, while concurrently detecting the rest of the high risk types (31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68)
    • Cost is SG$200/=
  • LINEAR ARRAY® HPV Genotyping Test
    • LINEAR ARRAY® HPV Genotyping Test
    • Identifies 37 high-risk HPV genotypes 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68, 73 (MM9), 82 (MM4) low-risk HPV genotypes 6, 11, 26, 40, 42, 53, 54, 55, 61, 62, 64, 67, 69, 70, 71, 72, 81, 83 (MM7), 84 (MM8), IS39, and CP6108
  • INNO-LiPA HPV Genotyping Extra
    • INNO-LiPA HPV Genotyping Extra
    • Identifies 15 high-risk HPV genotypes (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, 82) 3 probable high-risk HPV genotypes (26, 53, 66) 7 low-risk HPV genotypes (6, 11, 40, 43, 44, 54, 70) and some additional types (69, 71, 74).
  • PapilloCheck®
    • PapilloCheck®
    • Identifies 24 hiv-risk HPV types 16 18 31 33 35 39 45 51 52 53 56 58 59 66 68 70 73 82 and low-risk HPV types 6 11 40 42 43 44

Sexual risk (of HIV/STD/pregnancy), and what you can do before and after exposure.

Timeline HIV STD Pregnancy
Before exposure
Abstain from sex, Be faithful, or Condom use
Circumcision (males only)
Contraception (females only)
HIV PrEP (pre-exposure prophylaxis) STD vaccine:
- Hepatitis vaccine
- HPV vaccine
STD / HIV exposure
Unsafe sex / unprotected sex:
No condom / Condom broke / Condom slip
0-72 hours HIV prevention
HIV PEP (post-exposure prophylaxis) treatment
- Stop HIV infection after exposure.
STD testing.
If STD symptoms appear, then do STD treatment.
- Males: Do not urinate for at least 4 hours before arriving.
- Females: testing is more accurate when you are not menstruating.
Emergency contraception (females only)
2 weeks HIV DNA PCR test
1 month 20 minute HIV rapid test - SD Bioline HIV Ag/Ab Combo:
- Fingerprick blood sampling.
3 months 20 minute HIV rapid test - OraQuick®:
- Oral saliva or
- Fingerprick blood sampling.
Full & comprehensive STD testing
- Males: Do not urinate for at least 4 hours before arriving.
- Females: testing is more accurate when you are not menstruating.

References


Latest News

Detection of human papillomavirus in women attending Pap cervical screening camp at a peripheral hospital of North-Eastern India
Mon, 30 Mar 2015 00:00:00 +0100 | Medical Journal Armed Forces India
Publication date: April 2015 Source:Medical Journal Armed Forces India, Volume 71, Issue 2 Author(s): Sibnarayan Datta , Manisha Agarwal , Soumya Chatterjee , Hemanta Kumar Gogoi , Vijay Veer , Lokendra Singh Human papillomavirus (HPV) associated cervical cancer is the leading cause of deaths in India. However, cytological/HPV screening may result in early detection of cervical cancer, resulting in early treatment and reduced mortality. Although reports related to general population is available, data on HPV prevalence among women attending AFMS health care facilities is scarce. Cervical samples were collected for cytological staining by Pap test and molecular detection by PCR, genotyping by HPV specific primers and sequencing. Apart from finding of atypical cells of undetermined signifi...

Does it matter? Discounting and its role in the cost-effectiveness of preventative interventions. The case of HPV vaccination
Mon, 30 Mar 2015 00:00:00 +0100 | Public Health
Human papillomavirus (HPV) infection is the necessary cause of cervical cancer (CC), which is the fourth most common cancer in women worldwide in 2012.1 In the United Kingdom (UK), a HPV vaccination programme is delivered to girls aged 12–13 years, the primary aim of which is to prevent CC. Secondary aims include prevention of other cancers (including vulvar and vaginal) and protection against genital warts (GW). (Source: Public Health)

12 Invited lecture: High-throughput functional genomics – An emerging field in head and neck cancer research
Sun, 29 Mar 2015 04:16:53 +0100 | Oral Oncology
Head and neck squamous cell carcinomas (HNSCC) belong to the six most frequent tumors worldwide, and the incidence is rising. HNSCCs develop in the mucosal linings of the upper aerodigestive tract, and are preceded by prenoplastic changes, a phenomenon coined as “field cancerization”. Risk factors for HNSCC are smoking and excessive consumption of alcohol. Moreover, there are genetic predisposition syndromes, most particularly Fanconi anemia, associated with a very high risk for HNSCC. In recent years it became evident that also infection with the human papillomavirus (HPV) causes HNSCC, particularly tumors that arise in the oropharynx. (Source: Oral Oncology)

41 Is HPV infection the first genetic hit in head and neck cancer?
Sun, 29 Mar 2015 04:16:47 +0100 | Oral Oncology
Besides smoking and excessive consumption of alcohol, infection with the human papillomavirus (HPV) is an accepted risk factor for head and neck cancer. HPV-positive tumors are molecularly distinct from HPV-negative tumors. Moreover, HPV-positive oropharyngeal squamous cell carcinomas (OPSCC) have a better prognosis than patients HPV-negative OPSCC. Important factors contributing to this better prognosis are relatively low numbers of local/regional recurrences (LRR) and second primary tumors (SPT) in patients with HPV-positive OPSCC. (Source: Oral Oncology)

38 Immune evasion of HPV-associated HNSCC
Sun, 29 Mar 2015 04:16:47 +0100 | Oral Oncology
The immune system is recognized as an important player during development and progression of human papillomavirus (HPV)-induced cancers. While on the one hand a sufficient effector immune response is discussed to represent an important contributor to regression, immune evasion is suggested to contribute to progression. Previously we characterized the tumor tissue of oropharyngeal cancers (OPSCC) for characteristics potentially contributing to either an effective immune response or to immune evasion, including alterations in antigen presentation (HLA class I heavy chain and 2-microglobulin) and infiltration with T cells of effector or suppressor phenotype. (Source: Oral Oncology)

42 CD56-positive lymphocyte infiltration in correlation with outcome and human papilloma virus association of oropharyngeal squamous cell carcinoma
Sun, 29 Mar 2015 04:16:46 +0100 | Oral Oncology
Tumor infiltrating lymphocytes and immune factors within the tumor microenvironment are critically related to cancer patient’s prognosis. Human papillomavirus (HPV)-related oropharyngeal tumors are clinical and biological distinct from their HPV unrelated counterparts and patients with HPV relates oropharyngeal tumors display improved prognosis. We investigated possible immune cell infiltrations associated with this tumor phenotype. (Source: Oral Oncology)

P31 Prevalence of human papillomavirus in laryngeal and hypopharyngeal squamous cell carcinomas
Sun, 29 Mar 2015 04:16:39 +0100 | Oral Oncology
Recent studies support a role for human papillomavirus (HPV) in oropharyngeal squamous cell carcinomas (SCCs); however, the significance of HPV in non-oropharyngeal head and neck cancers is uncertain. In addition, the incidence varies widely depending on the geographic location and time period studied. The aim of this study was to determine the prevalence of HPV in a large cohort of oropharyngeal, laryngeal and hypopharyngeal SCCs in northern Spain. (Source: Oral Oncology)

P29 The role of HPV in cervical lymph node metastases from squamous cell carcinoma
Sun, 29 Mar 2015 04:16:39 +0100 | Oral Oncology
Human papillomavirus (HPV) infection is a risk factor for various cancer types, including head and neck squamous cell carcinoma (HNSCC). HPV-positive HNSCC show better survival compared to HPV-negative HNSCC despite their frequent early metastatic spread to cervical lymph nodes. Patients initially presenting only with a cervical lymph node metastasis (CLNM) during work-up are frequently diagnosed with HNSCC. In a few CLNM cases no primary tumor is detected. Aggressive multimodal treatment of these cancers of unknown primary site (CUP) often leads to substantial side effects and loss of quality of life. (Source: Oral Oncology)

P33 HPV16-dependent promoter methylation in HNSCC
Sun, 29 Mar 2015 04:16:38 +0100 | Oral Oncology
Aberrant promoter methylation of specific genes and infection with Human Papillomavirus 16 (HPV16) are known risk factors for the development of Head and Neck Squamous Cell Carcinoma (HNSCC). In previous studies we were able to show a significantly higher methylation frequency of Cyclin A1 (CCNA1) in tumors arising from the oropharynx (OSCC). Moreover we found an elevated methylation frequency for HPV-positive OSCC compared to HPV-negative OSCC. The protein expression of CCNA1, however, also showed an increased level in HPV-positive OSCC. (Source: Oral Oncology)

P32 Prospective study on human papillomavirus significance in oral dysplasias in association with clinical parameters and P16INK4a expression
Sun, 29 Mar 2015 04:16:38 +0100 | Oral Oncology
Human papillomavirus (HPV) DNA and RNA is found in a subset of oral cavity squamous cell carcinomas (OSCC), indicating a transforming role of the virus in a proportion of those cancers. HPV DNA has also been detected in some oral premalignant lesions (OPL). However, the significance of HPV DNA detection in those lesions is currently unclear. In particular, the association with clinical parameters, p16INK4a and progression risk has not been analyzed in a prospective cohort yet. (Source: Oral Oncology)