The incidence of prostate cancer is a disease of old age in men, and rarely develops before the age of 50.
The incidence of prostate cancer varies greatly from country to country. 1988 to 1992, the incidence of prostate cancer was 2 in Shanghai, China, and 137 in black America, a difference of 68.5 per 100,000 men. In Beijing, the incidence rate was 2.14 in 1985~1987 and 3.43 in 1991, with a significant increase in incidence worldwide. The expansion of the aging population, serum PSA, biopsy, and ultrasonography have improved diagnostic techniques and detected more and earlier prostate cancers. Prostate cancer is higher in developed countries than in developing countries. In the United States, prostate cancer incidence is the first and mortality rate is second only to lung cancer, and in Europe prostate cancer incidence is second only to lung cancer. The incidence of prostate cancer in China is much lower than that in western countries, but in recent years there has been a significant increase in the trend. I remember that from 1993 to 1994, an epidemiological survey of prostate cancer was conducted in Shanghai, and it was found that there were about 100 new cases of prostate cancer each year.
The incidence of prostate cancer should include latent cancer and incidental cancer in addition to the clinical incidence of the population. The former is clinically asymptomatic and is discovered during autopsy or other examination of the prostate gland, while the latter is found incidentally during surgery in patients with benign prostatic hyperplasia.
The latter is found incidentally during surgery in patients with BPH. The natural history of latent prostate cancer found at autopsy: 10% at age 40-50, 25% at age 65, and 40% at age 75. It takes 11-12 years for these cancers to develop into clinical prostate cancer, of which 50-75% do not develop into clinical cancer. The incidence of latent stage cancer in China is similar, but it may take longer for patients to develop into clinical cancer.
Second, the etiological analysis of prostate cancer.
1, food and nutrition Chinese or Japanese immigrants to the United States in San Francisco have a 3-7 times higher incidence of prostate cancer than their natives, and Japanese immigrants to Los Angeles have a 4-9 times higher incidence than their natives. Although this is related to many environmental factors, the important thing is nutrition, especially fat intake. Many reports suggest that excessive fat intake is the key to prostate cancer, and that red meat is a major source of fat. (e.g. pork, beef, lamb, etc.)
①Difference in food structure between East and West Western has less fiber and more fat. The East has more fiber and less fat. Now it is considered that the proportion of fat in total calories 30% is too high, not more than 20% is reasonable, 10% is a healthy level.
②Soy protein has a low incidence of prostate cancer in many countries along the Pacific coast, food with more soy contains phytoestrogens, the structure of which is similar to that of estrogenic steroids, typical Western food without soy products, estimated at <1mg/day. When someone compared typical western food for Finns and typical Japanese food for Japanese, it was found that isoflavones in urine and blood were 30 times higher and 7-110 times higher in Japanese.
③Green tea may reduce the incidence of cancer, Chinese and Japanese people often drink green tea, the incidence of prostate cancer is low, the flavonol in tea called catechuic acid, in animal experiments can inhibit planted in nude mice on human prostate cancer to make it smaller.
④Vitamin A can come from liver, eggs and milk, but also from fruits and vegetables. The body turns carotenoids into VitA. There are hundreds of carotenoids, about 50 of which can be turned into VitA. The more studied are beta carotene and lycopene. There are reports of 47,000 healthy men with 7 years of follow-up, 812 cases of prostate cancer diet analysis, only lycopene is associated with the reduction of prostate cancer, food tomatoes, ketchup, pizza in high lycopene. However, there are also negative results of the relationship between beta carotene and prostate cancer development.
⑤ Selenium Some people studied the effect of selenium on non-melanoma skin cancer after giving selenium in 1996 and unexpectedly found that the incidence of prostate cancer was low in people who gave selenium. 33,000 people had selenium in their toenails which could represent the selenium level in several months and after 7 years of follow-up, it was found that advanced prostate cancer was negatively correlated with selenium level, but some people opposed it.
(6) Vitamin Finland 29000 smoking men were divided into 4 groups, beta carotene group lung cancer increased by 18%, while VitE group prostate cancer decreased by 32%, animal experiments also proved that VitE can inhibit the occurrence of prostate cancer.
2, sexual activity prostate is androgen-dependent, controlled by serum testosterone, 90-95% of testosterone produced by the testes, testosterone in the prostate into dihydrotestosterone, is extremely important for the growth and development of the prostate. The sexual activity of prostate cancer patients is higher than that of the control group.
3. Body Mass Index (BMI) Body Mass Index = Weight (Kg) / Height (M) The American Cancer Society found that overweight men have a 30% increased risk of prostate cancer than those within 10% of their ideal weight. Italy found that the risk of prostate cancer can rise to 2.2~4.4 for high BMI group (normal BMI value is 20~25).
4. Occupation and economic income have statistics that farmers have a higher chance of prostate cancer for unknown reasons, but some believe it is related to the application of insecticides. In Canada, 1148 cases died of prostate cancer (out of 2.2 million people), prostate cancer deaths are related to pigeon farming, livestock, insecticides, and fuel.
5. Estrogen metabolism decreases and ethylene estradiol rises in hepatic sclerosis. Because ethylene estradiol can treat prostate cancer, it can reduce the risk of prostate cancer patients during hepatic stearosis, but it has not been confirmed yet.
6. Genetic factors prostate cancer genetic factors are important. The incidence of prostate cancer is high in blacks worldwide, and the incidence is also high in those with family history. Brothers have 3 times higher chance of prostate cancer than others, especially in early age. (Before the age of 60) 7. Relationship between prostate cancer and prostate enlargement The two should be unrelated and independent diseases. It is only that both are diseases of male aging, both occur in the same gland, the prostate, and both are related to male hormones.
Clinical staging of prostate cancer.
According to the TNM classification system developed by the International Union Against Cancer (UICC), plus the use of transrectal ultrasound, PSA or rectal finger examination results to classify, which is clinically more practical.
IV. Clinical diagnosis of prostate cancer.
Among all organ malignancies, the natural history of prostate cancer is the most unique; it is variable, varies from person to person, and is unpredictable, unlike malignancies of other organs that end in sinister outcomes. Most patients have tumors that can remain latent for a long time or even go undetected for life. According to US statistics, the incidence of autopsy prostate cancer in men over 50 years of age accounts for 30% of the population, while the clinical incidence of prostate cancer is only 1.05% and the annual mortality rate is only 0.31%. Prostate cancer can be detected in approximately 5% of men using rectal examinations, blood PSA measurements and transrectal ultrasound as screening diagnoses. The diagnosis of prostate cancer must be confirmed by prostate biopsy.
1. Clinical symptoms.
Early stage prostate cancer is asymptomatic. When the tumor enlarges to the extent of blocking the urinary tract, bladder neck obstruction similar to prostate enlargement will appear, with gradually increasing slow urine flow, urinary frequency, urinary urgency, incomplete urination, difficult urination and even urinary incontinence. Hematuria is uncommon. In advanced stages, low back pain, leg pain (nerve compression), anemia (extensive bone metastases), swelling of the lower extremities (obstruction of lymphatic and venous return), bone pain, pathological fractures, paraplegia (bone metastases), difficulty in defecation (rectal compression), oliguria, anuria, and uremic symptoms (bilateral ureteral compression) are seen.
Some patients are seen with metastatic symptoms without primary prostate symptoms.
2. Rectal palpation.
This is the first diagnostic step. The examination should check the size and shape of the prostate gland, the presence of irregular nodules, the size, hardness and extension of the mass and the seminal vesicles. Early stage prostate cancer is often asymptomatic and most of them are detected only when the prostate nodules are palpated during routine physical examination, while primary tumors in the migratory zone are palpated only when they have reached a certain level of enlargement. The tumors are often hard as wood and stone, but vary widely, with extensive infiltration and interstitial lesions that may be softer. The prostate cancer associated with prostate enlargement is sometimes not easily distinguished by rectal examination.
3. Laboratory tests.
Serum prostate-specific antigen (PSA) is the most important prostate cancer marker. The sensitivity of prostate acid phosphatase is poor, and the increase of alkaline phosphatase should be noted whether there is extensive bone metastasis. Advanced prostate cancer compression of bilateral ureters may result in increased blood creatinine, urea nitrogen and decreased carbon dioxide binding capacity.
Tumor markers.
①Prostate acid phosphatase (PAP) is good by radioimmunoassay, but its sensitivity specificity is not ideal. PAP is not ideal as a tumor marker, and PSA has been used instead of PAP test.
②Prostate specific antigen (PSA) it is an enzyme produced by the prostate epithelium and is a glycoprotein. psA is a more sensitive marker than PAP. However, its specificity is still not high for screening and diagnosis of prostate cancer. PSA is specific for prostate tissue but not for prostate cancer.
Serum PSA levels are fairly stable, and concentrations do not correlate significantly with diurnal time variations. PSA can be reduced by transurethral electrodesiccation of the prostate, radical prostatectomy, radiotherapy or hormone therapy. psA can be used as an indicator of treatment failure or recurrence. It is important to note that serum PSA values can double after rectal examination, increase 4-fold after cystoscopy, and increase 53-57-fold after puncture biopsy or transurethral resection of the prostate. PSA values do not decrease to basal values until one week after rectal examination and at least 6 weeks after biopsy, and can increase from prostatic hyperplasia to acute urinary retention. Acute and chronic prostatitis increases PSA.
A PSA value of <4ng/ml is generally normal and between 4-10ng/ml is considered high. If the PSA value is >10ng/ml, it is generally more important to pay attention to the possibility of prostate cancer, about 50% of these patients are prostate cancer patients.
The PSA value can be easily confused with the PSA value, so it should be taken seriously to avoid misdiagnosis in elderly men with elevated blood PSA.
In addition, it is important to know the ratio of free PSA to total PSA. If the ratio is <15%, it is more likely to be prostate cancer, and vice versa, if it is >15%, it is more likely to be benign prostatic hyperplasia. This has a discriminatory significance for those with a blood PSA value of 4-10ng/ml. In combination with anal examination, if there are nodules, biopsy will confirm the diagnosis of prostate cancer. In addition blood PSA measurement can also be used as a follow-up indicator after prostate cancer treatment.
The elderly patients must also have experience with oral Prolotherapy for BPH. However, it is important to note that taking oral Prostagland for more than 3 months can decrease the blood PSA test value by about half. The blood PSA value must be multiplied by 2 to be its true value when measured in patients taking oral Prostaglandin. Clinical vigilance is necessary!
4.Tranorectal ultrasound examination is a more accurate examination method, which can detect cancer nodules with volume of 4ml or more, and the tumors are often hypoechoic, single or multiple. A few isoechoic cancers are not detected during ultrasound examination. Ultrasonography can accurately understand the three-dimensional image of tumor and can measure the volume of tumor.
5.Prostate biopsy via rectal system biopsy: three puncture points in the direction of the middle parsagittal plane of the second lateral lobe in a fan shape, with a total of six pieces of tissue. Transrectal ultrasound-guided puncture biopsy has a high accuracy rate.
6.Other: CT and MRI have no value for the diagnosis of stage A and B prostate cancer, while stage C and D can show whether the tumor expands to the extraperitoneum and seminal vesicle, and whether it compresses the ureter causing hydronephrosis.
X-ray examination: IVP can reveal advanced prostate cancer extending to the bladder, compression of the ureter causing hydronephrosis, and the function of both kidneys. When bone metastasis occurs, it can cause osteogenic bone destruction on X-ray plain film, and pathological fracture may occur. Bone scan can detect bone metastasis of prostate cancer earlier than X-ray plain film.
V. Screening tests for prostate cancer patients.
Screening examination for prostate cancer from routine physical examination of people over 50 years old mainly relies on several methods of rectal examination (DRE), PSA test, transrectal ultrasound (TRUS) and puncture biopsy, which can be referred to the following scheme: ① if DRE is normal and PSA ≤ 4ng/ml, continue to observe; ② if DRE is normal and PSA 4.1-10ng/ml, do TRUS, such If PSA is >10 ng/ml, regardless of DRE, TRUS and systematic biopsy should be done immediately. If DRE or TRUS is suspicious or positive and PSA is 4.1-10 ng/ml, do systemic biopsy.
VI. Treatment of prostate cancer.
1.Treatment of early limited prostate cancer (T1 or T2 stage treatment) Prostate cancer generally develops slowly and limited tumors rarely cause death within 10 years, so treating any treatment for early prostate cancer has been controversial, observation waiting, radical resection of prostate cancer or radiation therapy can achieve better results. The final treatment plan for a patient should be based on the patient’s age, general condition, clinical stage and pathological grade. The patient’s age is an important factor in deciding the treatment plan whether the tumor needs treatment or not and whether the tumor can be treated.
Radical prostate cancer surgery aims to cure the tumor, which is theoretically the best treatment for early prostate cancer with a 15-year survival rate of 86-93%. If the pericardium is found to be punctured and the seminal vesicles are involved during surgery, the chance of healing is reduced, and those with pelvic lymph nodes should give up radical surgery. Radical surgery is only indicated for young patients in relatively good general condition, and is contraindicated for those with a predicted life expectancy of less than 10 years.
Radiation therapy is generally considered to take a similar outcome to that based on prostatectomy, but does not absolutely eliminate all cancer cells in the treated area.
The recommended treatment for early stage limited prostate cancer is as follows: patients with stage Tia who have a predicted life expectancy of <10 years should be observed and waited without treatment, while those with a predicted life expectancy of >10 years may be treated with radical prostatectomy, radiation therapy, or observation and waiting.
T1b, T1c, T2a, T2b, T2c with life expectancy less than 10 years are treated with radiation therapy or endocrine therapy, and those with predicted life expectancy greater than 10 years are treated with radical surgery, radiation therapy, or endocrine therapy.
2.Endocrine therapy for prostate cancer
LHRH, which is commonly used clinically, mainly acts on the pituitary-testicular axis, and its effect is similar to orchiectomy. It can make the LHRH receptors in the anterior pituitary gland decrease in regulation and the surface receptors decrease. The pituitary gland receives a decrease in LHRH stimulation, resulting in a decrease in LH secretion by the pituitary gland, which can eventually lead to a decrease in testosterone to depot levels. Neither surgical nor pharmacological depot can effectively reduce dihydrotestosterone in the prostate to the lowest level. Therefore, in 1982, the use of anti-androgens in combination with orchiectomy or inhibition of nandrolone was introduced for the treatment of advanced prostate cancer. Inhibiton is 3.75 mg, qM (subcutaneous injection).
(2) Anti-androgen drugs: Flutamide (retardation) and domestic flutamide, which can block the binding of dihydrotestosterone to the receptor, have less side effects, but we should pay attention to the liver damage side of it. Flutamide cannot solve androgen non-dependent cancer and is more expensive. The domestic one is flutamide, 250mg tid (three times daily) orally. The long-term application of retardation tumor prostate symptoms reappear, PSA is elevated, the withdrawal of retardation tumor after the rapid improvement of symptoms, PSA decreased called retardation tumor withdrawal syndrome. The incidence of this syndrome is 44-75% in patients with remission tumors when their condition worsens. At this time, the first consideration should be to discontinue this drug, or switch to Casodex (another anti-androgen), which is still effective. Intermittent androgen blockade therapy can delay the progression of prostate cancer to the non-dependent type for 6 months, and then stop until PSA rises by 20ng/ml.
The combination therapy can be enhanced by the addition of aminoglutethimide, which blocks the cytochrome P450 system and inhibits the synthesis of adrenal glucocorticoids and sex hormones.
Ketoconazole inhibits the synthesis of androgens in the body and has a rapid effect, but has more side effects. Some are used for bleeding in prostate cancer. Ketoconazole 400mg Q8h (200mg per tablet) reduced blood testosterone levels to depot levels in all patients within 24 hours. The main side effect is the problem of impairment of liver function.
Radiotherapy is feasible for patients with severe pain with bone and soft tissue metastases and is generally effective, with 80% of patients experiencing pain relief. Patients with multiple bone metastases have rapid symptomatic relief with hemibody radiotherapy.
Estracyt (estradiol phosphate nitrogen mustard). It is suitable for the treatment of patients who have failed endocrine therapy. 30-50% of patients respond and PSA decreases by more than 50%, which is the most effective treatment option today. (140mg/tablet) There is also the possibility of applying chemotherapy, and immunotherapy is also the future direction of treatment.
VII. What is androgen non-dependent cells?
After orchiectomy, only 60% of the androgens in the prostate are reduced, while 40% of the hormones from the adrenal glands are not removed.
2. Clonal cells insensitive to androgens exist in prostate cancer.
3. The glandular basal cells contain a large number of anti-apoptotic genes.
4. Mutations occur in the androgen receptor. The mutation occurs in the DNA binding region of the receptor and is mostly a point mutation, after which the receptor is insensitive to androgens and therefore loses the effect of anti-androgen therapy.
5. Loss of receptor expression. Therefore, there is a lack of in-depth understanding about the biological characteristics of prostate cancer. Androgen non-dependent cancer is undoubtedly the key to the treatment of prostate cancer.
VIII. Criteria for deterioration of prostate cancer after treatment.
1. new lesions in the prostate or soft tissue. lesions in PR cases increased more than 50% than before treatment, lesions in NC cases increased more than 125% before treatment.
2. Bone metastasis. New lesions were found on bone scan or X-ray.
3. PSA. PSA more than doubles in CR cases, more than 50% increase in PR cases than before treatment, and more than 125% increase in NC cases than before treatment.
4. New clinical symptoms such as wasting, physical decline, pain, etc. appear.
IX. Treatment principles for those who deteriorate after prostate cancer treatment.
1.Discontinuation of anti-androgen drugs, Flutamide 50%, Casodex 29% may decrease PSA after discontinuation.
2. No special drugs are available at this stage.
3, cytotoxic drugs, multi-drug combinations are better than single drugs, can be combined with hormonal drugs, such as estradiol phosphate nitrogen mustard.
4.Radiation therapy. Bone metastasis pain relief, intrapelvic metastasis symptoms, bone marrow compression: steroids, surgical decompression and postoperative radiation therapy can be performed first.
X. Prevention of prostate cancer.
1.Fat within total food calories is less than 20%.
2. 20-40g of soy products daily.
3.Selenium 200ug daily (seafood, skin of cereals, fruits (watermelon, tomatoes), internal organs (kidney and liver))
4.VitE 400-800IU.
5.Drink more green tea.