From November 1985 to August 1988, the National Study Group for Oesophageal Cancer collected and centralized data on 1926 new cases of oesophageal cancer in South Africa. A standard data sheet was used to record the age, sex, and condition of the patients, the site, length, and circumferential extent of the tumor, the presence of extraoesophageal and distant spread, associated pulmonary disease, and the therapeutic technique selected for each case. A computerized audit of cases was reviewed to examine the performance status, stage of disease, and methods of treatment. There were 1438 men and 488 women (male to female ratio, 3 to 1) and their ages ranged from 20 to 100 years (mean age, 56 years). Twenty-four percent were admitted to the hospital with total dysphagia. The performance status was excellent or good in 49% of the patients and fair in 29%. Those in poor or desperate condition included 13% of the patients with oesophago-airway fistulae. The most common site of cancer was the mid-thoracic oesophagus (53% of the cases), but 8.3% had tumors longer than 10 cm involving two or more oesophageal segments. Using the American Joint Committee (AJC) system of staging, 2.8% of the patients were assessed as Stage I, 19.8% as Stage II, and 77.4% as Stage III. Thirty-seven percent of the patients were treated by oesophageal intubation, 35% by radiation therapy, and 22% by chemotherapy. Surgery was selected for 17% of the patients. Although the number of young patients appears to have increased, the typical South African patient with oesophageal cancer is a man 56 years of age, in excellent or good condition, with a mid-thoracic tumor 6 cm in length and Stage III disease. This patient is frequently treated by palliative intubation of the oesophagus but may be a candidate for more intensive anti-cancer therapy.

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The clinical details and post-mortem findings are given of a patient who had primary `acquired' hypogammaglobulinaemia and was found at necropsy to have amyloidosis. The relationship of gamma globulin deficiency to amyloidosis is discussed, and the possible relevance of the hypogammaglobulinaemia to the formation and nature of amyloid is noted. It is suggested that a disordered immune response may be an essential prerequisite for the development of amyloidosis.

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