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Testis & Epiclidymis

Cryptorchidism (undescended testes) is found in 1% of 1-year-old boys and is mostly unilateral (Right>Left). Testicular descent has two phases; transabdominal and inguino-scrotal. Transabdominal phase is controlled by Mullerian-inhibiting substance whereas inguino-scrotal phase is androgen dependent (mediated by androgen induced release of CGP from genitofemoral nerve). Grossly, testis is small, brown and atrophic. Microscopically, tubules are atrophic with thickened basement membranes. Leydig cells are spared and appear to be prominent. Occasionally, proliferation of Sertoli cells may also be seen. Smaller but definite risk of malignancy is present for contra-lateral, correctly placed testis. Persistently undescended testes require orchiopexy (Placement in scrtol sac) preferably before 2 years before histological deterioration sets in. Orchiopexy dose not guarantee fertility.
Testicular Tumours Q
  1. Tumours of the testis are relatively uncommon, although their incidence has increased in recent years.
  2. They account for less than 1% of all cancer death.
  3. Testicular tumours are important, however, as many occur in young men and are the commonest form of malignancy in males under 35 years.
  4. Many are highly malignant.
  5. Aetiology Q
    1. Maldescent of the testis is the only known risk factor for tumour development.
    2. An undescended testis is 10 times more likely to develop a tumour than an intrascrotal testis. About 10% of all testicular tumours develop in testes that are, or have been, cryptorchid.
  6. Clinical features
    Testicular tumours may present with:
    1. painless unilateral enlargement of testis
    2. secondary hydrocele
    3. symptoms from metastases
    4. retroperitoneal mass
    5. gynaecomastia.
    6. The majority of testicular tumours present as slow, painless enlargement of one testis.
    7. On examination, there is a smooth or irregular firm enlargement of the testis.
    8. There may be a loss of testicular sensation on palpation.
    9. Less often, the patient notices a more rapidly enlarging scrotal swelling due to a secondary hydrocele around the tumour. Q
Some of the more malignant tumours may produce symptoms from metastases initially, for example haemoptysis from lung deposits, or pain from hepatomegaly.
  1. Classification Q
    1. Testicular tumours may be derived from germ cells or non-germ cells; 85-90% are of germ cell origin. 
    2. Germ cell tumours include seminomas, teratomas and their subtypes.
    3. Non-germ cell tumours include those arising from the Sertoli cells of the seminiferous tubules and the interstitial cells. 
The most widely used classification of testicular neoplasms is as follows:
  • seminoma
  • teratoma
  • combined (mixed) germ cell tumour-seminoma and teratoma
  • malignant lymphoma
  • yolk sac tumour
  • interstitial (Leydig) cell tumour
  • Sertoli cell tumour
  • metastatic tumours
  • adenomatoid tumour
  • paratesticular sarcoma. 
Germ Cell Tumours
  1. Seminoma Q
    1. Commonest type of testicular tumour
    2. Germ cell origin
    3. Peak incidence 30-50 years
    4. Histological subtypes: classical-lymphocytic stromal infiltrate; spermatocytic; anaplastic; with syncytiotrophoblast giant cells-contain human chorionic gonadotrophin (hCG); combined with other types of tumour
  2. Seminoma has a germ cell origin, arising in the seminiferous epithelium. 
Five histological subtypes of seminoma are recognised:
  1. classical
  2. spermatocytic
  3. anaplastic
  4. with syncytiotrophoblast giant cells
  5. combined with other types of germ cell tumour.
Classical Seminoma. Q
  1. This is the commonest subtype.
  2. It is composed of uniform cells with well-defined cell borders.
  3. The cytoplasm is vacuolated and contains glycogen.
  4. In most of these tumours the stroma contains a variable lymphocytic infiltrate, a favourable prognostic feature .
  5. Some tumours may have a histiocytic granulomatous response in the stroma with fibrosis, which correlates with a better prognosis.
Spermatocytic Seminoma.
The tumour cells resemble spermatocytes and show a marked degree of nuclear pleomorphism with a high mitotic rateQ. The tumour cells do not contain cytoplasmic glycogen.
  1. Anaplastic seminoma. Q
    This is a histological subtype with marked cellular pleomorphism and a high mitotic rate. The prognosis is slightly worse than for the classical seminoma.
  2. Teratoma Q
    1. Germ cell origin
    2. Peak incidence 20-30 years
    3. More aggressive than seminomas
    4. Histological subtypes: differentiated; intermediate; undifferentiated; trophoblastic
    5. βhCG and alpha-fetoprotein are useful tumour markers
      Teratomas are composed of several types of tissue representing endoderm, ectoderm and mesoderm
There are four histological subgroups of teratoma:
  • differentiated teratoma
  • malignant teratoma intermediate
  • malignant teratoma undifferentiated
  • malignant teratoma trophoblastic.
The above classification has prognostic value, with differentiated teratomas having an excellent prognosis and trophoblastic teratomas a poor prognosis.

Intra-Tubular Germ Cell Neoplasia
  1. The testicular tissue at the edge of most germ cell tumours shows a proliferation of atypical cells within the seminiferous tubules. Q
  2. This is considered as an in situ stage of malignancy and the precursor lesion of germ cell tumours.
  3. Immunohistochemical demonstration of placental-like alkaline phosphatase (PLAP) is helpful in the identification of these atypical cells.
  4. Combined germ cell tumours Q
    1. A mixed pattern occurs in 14% of all testicular tumours.
    2. Areas of seminoma and teratoma may be intermingled within the same tumour or occur as separate nodules.
    3. In these combined tumours, immunocytochemistry is of value in identifying small foci of more aggressive tissue components such as trophoblast.
    4. The prognosis in mixed tumours is determined by the subtype of teratoma.
Non-Germ Cell Tumours
  1. Malignant lymphoma
    1. Malignant lymphoma comprises about 7% of testicular tumours with a peak incidence between 60 and 80 years.
    2. The tumours are often bilateral and, in some cases, may be the first manifestation of a diffuse disease involving lymph nodes, liver and spleen.
    3. The testis is enlarged and replaced by a homogeneous fleshy white tumour.
    4. This is a non-Hodgkin's lymphoma, Q usually a poorly differentiated B-cell lymphoma with a diffuse pattern.
    5. Typically, the neoplastic cells infiltrate between the seminiferous tubules without destroying the tubular architecture.
    6. There is also neoplastic infiltration of the walls of veins within the tumour. 
  2. Yolk sac tumour
    1. Yolk sac tumour usually occurs before the age of 3 years and is the commonest type of testicular tumour in the child; its other name is orchioblastoma. Q
    2. It may also occur in adults, usually as one component of a mixed germ cell tumour and less often in pure form.
    3. Histology shows an adenopapillary pattern with columnar or flattened cells containing intracytoplasmic eosinophilic globules.
    4. Tumours arising from the interstitial or Leydig cells of the testis are uncommon, comprising only 2% of testicular tumours.
    5. The peak age incidence is between 30 and 45 years. Q
    6. This type of tumour may produce androgens and cause precocious sexual development in boys.
    7. Paradoxically, gynaecomastia may be the initial manifestation.
  3. Interstitial cell tumourQ
    An interstitial cell tumour forms a solid yellow-brown nodule within the body of the testis, composed of uniform eosinophilic cells arranged in sheets or columns.
    The majority of interstitial cell tumours are benign.
  4. Metastatic tumours
    1. Various tumours may occasionally metastasise to the testis but such metastases are usually found only incidentally at autopsy and very rarely present clinically as testicular enlargement.
    2. Carcinoma of the bronchus or prostate and malignant melanoma are among the more frequent primary tumours involved.
Dissemination :
  1. Testicular tumours initially invade the body of the testis and spread locally to the rete testis and epididymis.
  2. Invasion of the fibrous tunica albuginea occurs at a late stage. Q
  3. Invasion of lymphatic spaces leads to spread along the spermatic cord to the internal iliac and para-aortic lymph nodes and then to the mediastinal nodes.
  4. Vascular invasion results in visceral metastases, most frequently in the lungs and liver, as well as skeletal deposits. Q
  5. Seminomas tend to spread by lymphatics to para-aortic nodes; teratomas tend to spread haematogenously and, occasionally, to lymph nodes.
  1. Prognosis  
    1. There has been a marked improvement in the prognosis for patients with testicular tumours during the last few decades.
    2. Seminoma is a very radiosensitive tumour which has an excellent prognosis.
    3. The main improvements, however, have occurred in patients with non-seminomatous germ cell tumours and are due to three main factors: the development of more precise imaging techniques to improve staging; the development of assays for tumour markers; and the use of improved chemotherapeutic agents.
    4. As a result, the cure rate is now similar to that of seminoma. 
    5. Until recently, the management usually involved orchidectomy followed by prophylactic irradiation of the para-aortic lymph nodes. This regimen resulted in a 90-95% cure rate for seminoma.
    6. A more recent and now accepted management of both seminoma and teratoma is orchidectomy followed by surveillance with imaging techniques and serum markers; recurrences of tumour are then treated with chemotherapy. If the patient survives for 2 years after completion of chemotherapy with no evidence of recurrence then cure is likely. 

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