testicular tumor
Introduction
Introduction to testicular tumors Testicular tumors account for 1% to 2% of male malignancies and are classified into primary and secondary. The vast majority are primary, divided into two major categories of germ cell tumors and non-germ cell tumors. Germ cell tumors occur in the reproductive epithelium of seminiferous tubules, accounting for 90% to 95% of testicular tumors, of which seminoma The most common, slow growth rate, the general prognosis is better; non-spermato cell tumors such as embryonic cancer, teratocarcinoma, chorionic epithelial cancer, etc., are relatively rare, but the degree of malignancy is high, early lymphatic and hematogenous metastasis, prognosis difference. Non-germ cell tumors occur in Leydig cells, accounting for 5% to 10%, and are derived from testicular interstitial cells such as fibrous tissue, smooth muscle, blood vessels and lymphoid tissues. Secondary testicular tumors are rare. basic knowledge The proportion of illness: 0.003%--0.004% Susceptible people: good for adult males Mode of infection: non-infectious Complications: testicular cancer
Cause
Testicular tumor cause
(1) Causes of the disease
The etiology of the tumor is still not completely clear, and may be related to viral infection, environmental pollution, endocrine abnormalities, injury and heredity. At present, there are five factors that can promote the occurrence of testicular tumors: cryptorchidism, previously suffered from testicular germ cells. Tumors, family history, true hermaphroditism and infertility, the incidence of cryptorchidism malignant is 30 to 50 times higher than the normal testis to the scrotum, according to the literature, every 20 peritoneal cryptorchidism or every 80 One case of testicular tumor occurred in the inguinal cryptorchidism.
(two) pathogenesis
Testicular tumors are classified into four categories according to their tissue origin: 1 germ cell tumor; 2 interstitial tumor; 3 germ cell and interstitial mixed tumor; 4 testicular network tumor, in which the organization of testicular germ cell tumor has been controversial. In recent years, there have been some new understandings that all types of testicular germ cell tumors, except spermatogenic seminoma, originate from a common precursor, testicular carcinoma in situ, which is called pathologically. Intratubular germ cell neoplasia of the unclassified type (IGCNU), these IGCNU cells and seminoma are identical in morphology and DNA composition, and are caused by other germ cell tumors. The precursor, pure seminoma, can differentiate into nonseminoma germ cell tumors (NSGCT).
Classification of testicular tumors (WHO, 1994):
Germ cell tumor
Precancerous lesions.
Germ cell tumors in the seminiferous tubules (in situ carcinoma).
(1) A tissue type of tumor:
1 spermatocyte type seminoma.
2 variant: accompanied by sarcomatoid components.
3 seminoma (may be associated with syncytiotrophoblast cells).
4 embryo cancer.
5 yolk sac tumor (endodermal sinus tumor).
6 chorionic epithelial cancer.
7 teratoma:
A. Mature teratoma.
B. Dermoid cyst.
C. Immature teratoma.
D. Teratoma with obvious malignant components.
E. Carcinoid (pure carcinoid or associated with teratoma).
F. primitive neuroectodermal tumors.
(2) More than one type of tissue type of tumor:
1 mixed germ cell tumor.
2 multiple embryos.
2. Sexual cord stromal tumor
(1) Sexual stromal cell tumor (Leydig cells).
(2) Supporting cell tumors (Sertoli cells):
1 typical type.
2 hardened type.
3 large cell calcification type.
(3) granulosa cell tumor (adult type C, juvenile type).
(4) Mixed cord stromal cell tumors.
(5) Undifferentiated sex cord stromal tumors.
3. Germ cell and sex cord interstitial mixed tumor
(1) Testicular blastoma.
(2) Others.
4. Testicular tumor
(1) adenoma.
(2) Adenocarcinoma.
(3) adenomatous hyperplasia.
5. Other testicular tissue-derived tumors
(1) Epidermoid cysts.
(2) Tumors derived from mesenchymal tissue.
6. The source of metastatic tumor hematopoietic system.
(1) Lymphoma.
(2) plasmacytoma.
(3) Leukemia.
Testicular tumors are mainly lymph node metastasis. Half of the patients have undergone different degrees of metastasis at the time of initial diagnosis. The lymphatic drainage of the testis originates from the genital warts near the second lumbar vertebrae, forming in the retroperitoneal region, and the testicles descending into the scrotum. The lymphatics and blood vessels descend to the scrotum through the inner ring of the inguinal region. Therefore, the first lymphatic metastasis is located at the lumbar vertebrae at the level of the renal pedicle. The bilateral lymphatics can communicate with each other across the midline. The upper boundary can reach 2 cm above the renal pedicle. The lateral boundary is On both sides of the kidney and the medial edge of the upper end of the ureter, from the lower boundary to the abdominal aorta crossing and the upper third of the iliac vessels, the metastasis of the inguinal lymph nodes often occurs when the tumor penetrates the tunica and occurs in the epididymis, spermatic cord and scrotal skin. Metastasis, scrotal testicular tumor resection and testicular biopsy can cause local metastasis, the most common distant metastasis is the lung, liver, followed by intra-abdominal metastasis, most of which are direct adjacent invasion.
Another important issue is the clinical stage of testicular tumors, because local or systemic dissemination has important implications for treatment and prognosis. To date, at least nine staging systems have been used worldwide, with more traditional stages (Boden and Gibb in 1951). It is proposed that: 1 tumor is limited to I (A) in the testis, 2 has regional lymph node (ie, retroperitoneal lymph node) metastasis, and no supraorbital and visceral metastasis is II (B), 3 tumor metastasis Above the retroperitoneal lymph nodes, such as the mediastinum, lung or other visceral stage III (C), later scholars on this basis divided the I and II into several sub-phases (grade), 1992 International Union Against Cancer (UICC) Recommended tumor staging is TNM system: T represents the primary tumor; N refers to the invasion of the following regional lymph nodes; M represents the presence or absence of distant organs or regional lymph node metastasis, the clinical stage is based on clinical examination, Imaging studies and pathological examinations, in order to facilitate memory, can be simplified TNM staging, ie 0 to III (Table 1).
Staging of testicular tumors:
Phase I: No transfer.
IA: The tumor is confined to the testis and epididymis.
IB: Tumor invading spermatic cord or tumor occurs in undecreased testes.
IC: Tumor invades the scrotum or groin and scrotum after surgery.
ID: The extent of invasion of the primary tumor cannot be determined.
Stage II: There is a lymph node metastasis under the armpit.
IIA: Metastatic lymph nodes <2 cm.
IIB: At least one metastatic lymph node is 2 to 5 cm.
IIC: retroperitoneal lymph nodes > 5 cm.
IID: The abdomen can be licked and the lumps or inguinal lymph nodes are fixed.
Stage III: mediastinal and supraclavicular lymph node metastasis and/or distant metastasis.
IIIA: There is mediastinal and/or supraclavicular lymph node metastasis, but no distant metastasis.
IIIB: distant metastasis but only the lungs:
"Small lung metastasis" has a number of lung metastases <5 per side and a lesion diameter > 2 cm.
The number of lung metastases on each side of "late lung metastasis" was >5, and the lesion diameter was >2 cm.
IIIC: Hematogenous metastasis outside of any lung.
IIID: After radical surgery, there were no obvious residual lesions, but the tumor was positive.
Tumor markers (referred to as tumor markers) have long been used in the diagnosis and treatment of testicular tumors. They are important for early diagnosis, classification, treatment plan decision, monitoring treatment effect and long-term follow-up, and specific and sensitive testicular tumors. The tumors are labeled with alpha-fetoprotein (AFP) and human chorionic gonadotropin (HCG), both of which are glycoproteins, 70% to 80%. NSGCT type testicular tumor patients may have AFP and (or) elevated HCG levels, increased AFP indicates the presence of embryonic cancer components in testicular tumors, so the treatment should be based on surgical treatment, HCG increased to consider the presence of components of chorionic epithelial or embryonal cancer, in addition to some non-specific The tumor markers have increased performance in testicular tumors, such as carcinoembryonic antigen (CEA), lactate dehydrogenase (LDH) isoenzyme, placental alkaline phosphatase (PALP) and the like.
Prevention
Testicular tumor prevention
Tobacco contains carcinogenic substances such as arsenic, and smoking can cause changes in sex hormones. Therefore, scientists have suspected that smoking may be one of the risk factors for testicular cancer. The current research shows that smoking does increase the risk of testicular cancer.
People with higher consumption of dairy products are also at a higher risk of developing testicular cancer, especially those with high cheese consumption, who are 87% more likely to develop testicular cancer than the average person.
Therefore, quitting smoking and adjusting bad eating habits are the key to prevention.
Complication
Testicular tumor complications Complications testicular cancer
Testicular tumors are mainly lymph node metastasis, which is common in the iliac crest, sputum total, abdominal aorta and mediastinal lymph nodes. The metastases can be large, the abdomen can be touched, and patients complain of waist, back pain, testicular villus cancer, breast hypertrophy, The nipple areola pigmentation.
Symptom
Testicular tumor symptoms Common symptoms Joint pain, difficulty breathing, nodule, cough
Testicular tumors often inadvertently find a mass in the scrotum, and also have local pain and heavy feeling. The cryptorchidism may have a groin and a lower abdominal mass. A sudden increase in atrophic testicles should be thought of as a tumor. Acute pain is not common, but 10% may have symptoms similar to orchitis or aphlegm. About 10% of patients are mainly characterized by metastatic cancer, such as enlarged lymph nodes on the supraclavicular bone, cough and lung dyspnea.
Testicular examination begins on the healthy side as a comparison of size, stiffness and contour. Tumors are generally insensitive and do not feel like normal tissue. The epididymis is clearly separated, the sheath and scrotum are non-adhesive, and there is often no effusion. The size of the tumor and the presence or absence of metastatic cancer often manifest as irregular masses in normal testicular tissue. The spread to the epididymis and spermatic cord accounts for 10% to 15%, and the prognosis is poor.
Examine
Test for testicular tumors
1. Tumor markers (tumor markers), especially AFP and HCG provide valuable reference for the diagnosis, staging, monitoring and prognosis of testicular germ cells. Germ cell tumors are classified into two categories: 1 and embryo Related carcinoembryonic substances (alpha-fetoprotein AFP and human chorionic gonadotropin HCG) occur; 2 certain cellular enzymes (lactate dehydrogenase LDH and placental alkaline phosphatase PLAP).
(1) AFP single-chain glycoprotein, molecular weight of about 70,000, half-life of 5 to 7 days, pure embryonic cancer, teratocarcinoma, yolk sac tumor, AFP increased by 70% to 90%, pure chorionic epithelial carcinoma and pure spermatogonia The tumor AFP is normal.
(2) HCG polypeptide glycoprotein consisting of and chains with a half-life of 24 to 36 h [but subunits are relatively rapidly cleared -subunit (-uCG) 20 min, -subunit (-uCG) 45 min], fluff Membrane epithelial cancer and 40% to 60% of embryonic carcinoma have increased HCG, and pure seminoma is increased by 5% to 10%.
(3) LDH lactate dehydrogenase cell enzyme, molecular weight 134,000, LDH is ubiquitous in different tissue cells, so the specificity is low, prone to false positive, germ cell tumor can cause LDH increase, and is related to tumor size, staging, For example, LDH increased by 8% in stage I, 32% in stage II, and 81% in stage III. The recurrence rate was 77% in LDH before I and II, and 40% in LDH.
(4) PLAAP placenta alkaline phosphatase alkaline phosphatase isoenzyme, the structure is different from adult alkaline phosphatase, 95% seminoma, increased PLAP, specificity 57% to 90%.
2. Ultrasonography is of great value in the diagnosis of scrotal contents diseases. The diagnostic accuracy rate is 97%. It can directly and accurately determine the size and shape of testicular tumors. In addition, it has diagnostic value for lymph node metastasis of testicular tumors and abdominal organ metastasis.
3. Chest and lateral radiographs to understand the lungs and mediastinum.
4. CT is more sensitive to the detection of pulmonary metastasis and retroperitoneal lymph node metastasis, has replaced intravenous urography and lymphangiography, and can find lymph node metastases less than 2cm in diameter.
Diagnosis
Diagnosis and differentiation of testicular tumors
diagnosis
(A) tumor markers (tumor markers) The most widely used are the fetal armor (AFP) and human gonadotropin (HCG).
AFP: normal value <40ng/ml, half-life 4 days to 5 days. All yolk sac tumors in testicular tumors, 50% to 70% of embryonal carcinomas, and teratogenic cancers were elevated; pure choriocarcinoma and pure seminoma were not elevated.
HCG: normal value <1ng/ml, all choriocarcinoma and 40% to 60% embryonic cancer HCG positive, "pure" seminoma is 5% to 10% positive.
Using the above two tumor markers, 90% of non-seminomas are positive for one or both. Pure spermatogonoma HCG positive accounted for 5% to 10%, that is, more than 90% of pure seminoma does not produce tumor markers, non-seminoma does not produce tumor markers 10%, so once clinical diagnosis of testicular tumors should be Immediate testicular resection is performed without waiting for the outcome of the tumor.
The tumor marker can be used as an indicator for observing the curative effect. The rapid prognosis after surgery or chemotherapy or radiotherapy has a good prognosis. Those with slow or no decline may have residual tumors. Therefore, once the clinical diagnosis of the testicular tumor, the sputum resection should be performed immediately, without waiting for the tumor result.
The tumor marker can be used as an indicator for observing the curative effect. The rapid prognosis after surgery or chemotherapy or radiotherapy has a good prognosis. Those with slow or no decline may have residual tumors.
(B) B-ultrasound can be used to determine the presence of metastatic lymph nodes and other diseases in the testicular tumor and groin.
(C) CT and MRI can be found in the retroperitoneal lymph node metastasis <2cm lesions.
There are also lymphadenography and urography.
Differential diagnosis
1. Testicular sphincter fluid examination The mass of the testis is sac sexy, tough, elastic, and positive in light transmission test, but the sheath wall thickness or partial calcification is difficult to identify, testicular tumor sometimes can produce a small amount of hydrocele, but there are Heavy feeling, negative light transmission test, B-ultrasound, CT examination is helpful for identification.
2. Acute epididymis, orchitis epididymis, testicular swelling can be confused with testicular tumors, but patients have chills, high fever, local pain is heavier, testicular tenderness is obvious, and often involve the vas deferens, white blood cells increase.
3. Testicular hematoma has a history of trauma, physical examination of the scrotum with blood spots, B-ultrasound showed a hypoechoic area within the testicular echo.
4. Epididymal tuberculosis can involve the testicles, producing nodules, confused with testicular tumors, but epididymal tuberculosis often involves the vas deferens, forming a bead-like nodule, the epithelial tail lesions can adhere to the scrotal skin to form a sinus.
5. Clinical manifestations of testicular torsion are characterized by sudden testicular pain, swelling, tenderness, physical examination of the testicular position often in the upper part of the scrotum, color Doppler ultrasound and dynamic radionuclide scanning showed significant reduction or disappearance of blood flow.
6. Semen cysts Semen cysts are cysts located in the testicular epididymis formed by sperm accumulation, mostly in young adults, long history, slow progress, clear tumor boundaries, positive light transmission test, B-ultrasound, CT examination showed that the mass is a liquid Sex.
7. Testicular syphilis: The age of onset is relatively late, and the local appearance is similar to that of the tumor, mainly based on the history and serum septic response.
