ANÁLISIS DE LOS RESULTADOS DE LA ENCUESTA

Epidemiology 177 Pathology 178 Etiology 178 Natural history 179

Invasive cervical carcinoma 179 Screening and diagnosis 180 Management of abnormal smears and

preinvasive lesions 180 Staging 181 Prognosis 181 Treatment 182 Uterine cancer 188 Diagnosis 189 Clinical presentation 189 Staging and prognosis 189 Treatment 190

Yet there is mystery here and it is not one I under- stand.

Without this sting of otherness, of – even – the vicious,

without the terrible energies of the underside of health, sanity,

sense, then nothing works or can work. I tell you that goodness:

the ordinary, the decent –

these are nothing without the hidden powers that pour forth continually from their shadow sides.

by Doris Lessing, The Marriages Between Zones Three, Four and Five.

CERVICAL CANCER

EPIDEMIOLOGY

The incidence and mortality rates of cervical cancer have decreased in the US by as much as 75% in the last 40 years.1_{This change is the largest}

seen in any cancer site and is attributed to cyto- logical screening in the form of the Papanicolaou smear.2_{The Pap smear allows for the detection of}

early disease at the preinvasive stage. About 65 000 cases of carcinoma in situ are found in this way annually.3_{However, cervical cancer remains}

the most common female cancer in developing countries.4 _{In the US it is the seventh most}

common cancer in women. In 1995, 15 800 cases were diagnosed and there were 4800 deaths.3

PATHOLOGY

Most cervical cancers are squamous-cell carcino- mas.5 _{Adenocarcinomas of the cervix arise from}

endocervical cells and account for 14% of these cancers.6 _{The percentage of adenocarcinomas has}

risen over the years. This is possibly due to the fact that they are more difficult to detect than squa- mous-cell carcinomas at the preinvasive stage. The long-term survival for both types is not signifi- cantly different.

Adenosquamous carcinomas are a mixed type and are associated with a higher risk of pelvic lymph node metastasis.7_{Glassy-cell carcinoma is}

a poorly-differentiated form of adenosquamous carcinoma that responds poorly to surgery and radiation therapy.8 _{Verrucous carcinoma is an}

extremely well-differentiated form of squamous- cell carcinoma. This tumor may invade the vagina and the endometrium but does not usually metas- tasise to lymph nodes. Small-cell carcinomas are distinctive and usually have a very poor prognosis. The most aggressive tumors are those with neuroendocrine differentiation. Other cervical malignancies include sarcomas, malig- nant melanomas, lymphomas, mixed mullerian tumors, germ-cell tumors, and trophoblastic tumors.

ETIOLOGY

There is a well-established association between sexual activity and cervical neoplasia.9 _Human

papilloma virus (HPV) is the most important factor in this association. Factors that were thought to be responsible for cervical intraepithe- lial neoplasia (CIN) include increased number of sex partners, earlier age at first intercourse, lower level of education, and lower income, which can be translate into poorer screening, and smoking. These factors have all now been reduced to one factor; HPV.10

Many types of HPV have been isolated in the human genital tract; types 16, 18, 45, and 56 all have a high correlation with cervical cancer.11

These high-risk types of HPV have been found in 74% of cases of invasive cervical cancer and in 53% of those with moderate to severe dysplasia. HPV- 16 is the most prevalent. HPV 16 and 18 can combine with the p53 protein and cause the same functional consequence as a p53 gene mutation.

An increased risk of cervical neoplasia also results from immunosuppression.12_{This immuno-}

suppression is associated with an increased rate of HPV infection. Women with HIV infection have an increased incidence and recurrence rates of CIN. Also women who are HIV positive who devel- oped invasive cervical cancer were found to have more advanced disease at the time of presenta- tion.13 _{A direct molecular relationship exists}

between HIV, herpes simplex virus (HSV), and HPV. HIV gene products cause a transactivation of HPV proteins.14 _{(This relationship also exists in}

men with HIV infection and manifests as anal condyloma.)

Smoking has also been reported to increase HPV infection.15 _{Conflicting data have been}

reported regarding the implication of oral contra- ceptives but estrogen exposure seems to have a direct relationship with many reproductive cancers, male and female. Women who use the oral contraceptive pill have dryer and more deli- cate vaginal tissues. This makes them more sus- ceptible to abrasion during sexual activity and, therefore, more susceptible to sexually transmit- ted diseases, including HPV. Estrogen exposure can also increase through xenoestrogenic expo- sures. Xenoestrogenic exposures are most highly implicated coming through the food chain and via water. Xenoestrogens activate and also increase the number of certain estrogen receptors in all responsive tissues, including the transition zone of the cervix. It is probable that the combination of many factors, including increased estrogen expo- sure from many sources can contribute to carcino- genicity. Prenatal exposure to DES is also implicated.

Talc is a substance used as a delivery mecha- nism for fragrance in many feminine hygiene products including powders, sanitary pads, and tampons. Talc is a known carcinogen; it occurs nat- urally in the presence of asbestos, which is often found in cosmetic talc. It has not been studied as a causative factor in cervical cancer. The political lobby to keep talc on the market has made access- ing this information difficult and, as a result, most of the population is unaware of the carcinogenic effects of talc, whether or not it contains asbestos. Using pure cotton tampons and other feminine products is essential. Talc is also found in facial cosmetics and should be eliminated from use.

Chinese medicine

Cervical cancer is almost always associated with a latent pathogenic factor (LPF): HPV and possibly HSV infection. HPV is considered a damp phlegm pathogen, which can occur as a result of sexually transmitted disease exposure. This exposure can occur in an internal environment of sinking spleen qi, which is especially common in women who are HIV positive. Any chronic pathogen that has a local hold on tissue will cause several levels of per- sistent and ongoing stasis. Women with spleen deficiency, yin deficiency, a damp constitution, or liver qi constraint are more susceptible to LPFs. See Chapter 11 on leukemias, which goes more deeply into the concept of latent pathogens.

If HPV is left untreated it will move from a damp phlegm stasis to blood level stasis and then blood heat with toxin. This progression is appar- ent when looking at the progression of asympto- matic presentations with an early abnormal Pap result to later presentations with abnormal bleed- ing and then obstructive symptoms and pain.

The procedures utilised by conventional medi- cine in diagnosis, that is cone biopsy and other surgical procedures, also cause blood stasis. This is not a recommendation to avoid those proce- dures, which can be curative. But it is important to treat the underlying environment and to prevent recurrence of the LPF after these proce- dures, whether they are considered curative or not.