A 75-year-old patient presented with a superior vena cava syndrome (SVCS) lasting 3 years. A prostatic carcinoma was found and a supraclavicular lymph node biopsy specimen disclosed metastasis of the prostatic carcinoma. Antiandrogen and luteinizing hormone-releasing hormone analogue therapy produced a marked improvement. Prostatic carcinoma, although a very rare cause, must be considered in the diagnosis of cases of SVSC with a protracted course, since it is a treatable disease.
Carcinoma of the prostate is a very common neoplasm in men. On the other hand, superior vena cava syndrome (SVSC) is also common and in most cases due to lung neoplasms. We present the unusual case of a patient presenting with a SVCS due to metastic carcinoma of the prostate.
A 75-year-old patient was referred with a history of dyspnea. He had a long history of chronic pulmonary airways disease and a prostatic adenoma had been diagnosed 7 years previously. Three years before, he had been studied in another hospital where supraclavicular lymphadenopathy and collateral venous circulation were found. Computed tomographic (CT) scan disclosed upper mediastinal lymph node enlargement and superior vena cava and left subclavian and jugular venous obstruction that was confirmed in a venogram. Superior vena cava syndrome was diagnosed, but lymph node specimen was not obtained and no further studies were performed. The patient came to the hospital due to increased dyspnea in the previous 3 months. Physical examination disclosed raised bilateral venous jugular pulse, facial swelling and cyanosis, venous engorgement of the head, neck, and upper chest, and very large supraclavicular masses, averaging in the largest diameter 7 cm on the left side and 4 cm on the right side (Fig 1). Nodular structures suggesting lymph nodes along with dilated varicose veins were felt within the masses. Thoracic auscultation disclosed tracheal stridor. No lymph node enlargement was found in othere areas. The thyroid gland was not palpable and oropharyngeal exploration, heart, and abdomen were normal. Digital rectal examination disclosed a nodular and firm prostatic gland. In the analytical examinations, results of blood and routine biochemical determinations were normal. Immunoglobulins and coagulation test were normal. Hypercoagulability could not be demonstrated. Prostatic and phosphatase level was 554 ng/ml and prostate-specific antigen was 4.154 ng/ml. Chest radiograph showed and enlarged upper mediastinum and a CT scan lymph node enlargement in the supraclavicular, infraclavicular, upper mediastinal (Fig 2. top), obturator, pelvic and retroperitoneal areas. The prostate gland was enlarged with heterogeneous density. Thyroid scan, serum thyroid hormones, and thyroid-stimulating hormone levels were normal. Bone scan showed multiple areas of abnormal contrast uptake in the cervical and dorsal spine and left rib cage. Prostatic ultrasonography demonstrated a hypoechoic lesion within the gland and an aspiration needle cytologic study demonstrated prostatic adenocarcinoma. Supraclavicular lymph node biopsy specimen showed metastatic adenocarcinoma (Fig 3, top) with a high positivity for prostatic acid phosphatase and prostatic antigen stains (Fig 3, bottom). The patient was started on a regimen of oral anticoagulants and antiandrogen (Flutamide) and luteinizing hormone-releasing hormone (LHRH) analogue (Triptorelin) treatment. He improved progressively and four months later the supraclavicular lymph node enlargement had disappeared on the right side and was markedly reduced on the left, although dilated veins persisted. A CT scan showed a decrease in the size of the mediastinal nodes (Fig 2, bottom) and a venogram disclosed partial stenosis of the right subclavia vein and total occlusion of innominate, left subclavia and axillary veins with patent collateral circulation. Serum levels of prostatic acid phosphatase and prostatic-specific antigen lowered to 2.4 ng/ml and 238 ng/ml, respectively.
The diagnosis of a prostatic carcinoma in this patient with the findings of a hard prostate, elevated acid phosphatase and prostate-specific antigen serum levels, hypoechoic lesions on ultrasonography, and a postive prostatic cytologic study was straightforward. However, the finding of the huge and long-lasting supraclavicular lymphadenopathy with a protracted SVCS raised the question of another disease. Although benign causes of SVCS are possible, such as superior vena cava thrombosis (primary or associated with hematologic disease, Behcet's syndrome, and central intravenous catheters or devices), syphlitic aortic aneurysm, thyroid goiter, or tuberculous, fungous, or pyogenic mediastinitis they amount only to 15 to 20 percent of all cases. The majority of cases are due to neoplasms, lung carcinoma representing 70 percent of cases, lymphoma 6 percent, and other primary or metastic disease such as breast carcinoma and testicular seminoma 9 percent.[1-3] In this patient, the diagnosis of either a nonmalignant cause of the SVCS or a second slowly growing malignancy such as low-grade lymphoma, thyroid carcinoma, or salivary gland tumor was considered, but the biopsy specimen of the supraclavicular node demonstrated the prostatic origin of the lymph node metastasis. Dissemination of prostatic carcinoma occurs by direct, lymphatic, or hematogenous extension. Lymph node extension spreads in approximate decreasing order to the obturator, hypogastric, internal, and common iliac and paraaortic lymph nodes.[4-5] Dissemination to lymph nodes in the neck, hilus of the lungs, and mediastinum can be demonstrated at autopsy in 18.2 percent, 14.6 percent, and 2.8 percent, repectively, but they are not clinically relevant. Hematogenous dissemination through the venous vessels is common and the most common metastatic deposits occur in the skeleton, the liver, lungs, and adrenals and only rarely jin other organs, such as the brain, skin, or digestive tract.[4-6] Although metastasis to the lung increases in incidence with the extension of the metastatic spread and can be found at autopsy in 49 percent of cases, they are apparent in most cases only on microscopic analysis and very rarely produce clinical pulmonary disease. The presentation of a prostatic carcinoma with a SCVS, as in this patient, is an absolutely exceptional finding. We have not been able to find any previous reference in classic textbooks or in reviewing articles[1-3,5,6] and we have not found reference in the MED-LINE database. The treatment of the SVCS in this patient is also worthy of discussion: chemotherapy was not believed to be a good initial treatment due to its expected limited and belatedf responses; antifibrinolytic agents were not included due to the long-lasting course of the venous osbstruction. Radiation therapy and surgical decompression were considered, but the presence of chronic pulmonary disease and the advanced age of the patient led us to initiate androgen deprivation as first-choice therapy, and this proved to be very effective.
Although carcinoma of the prostate is a very uncommon cause of SVCS, it should be considered in patients with mediastinal lymphadenopathy and a protracted course. This is not academic, since metastatic prostatic carcinoma is a treatable disease where an appropriate treatment can, at least temporarily, decrease the size of the lymph node metastasis, control the symptoms of the disease, improve the performance and, ultimately, prolong the life of the patient.
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