No abstract

No abstract

A retrospective study of 177 patients attending Tata Memorial Hospital over a period of 40 years from 1942 through 1981 is presented. These patients who had "primary lesions" in the head and neck region, breast, esophagus, lung, and elsewhere as carcinoma or sarcoma developed "second primary" at different sites, after the treatment for the primary lesion after a variable period over years--as "metachronous lesions" (139 patients). Another group of patients presented with "double primary" at initial clinical examination and investigations, and these were "synchronous" lesions (38 patients). The analysis brings out the relationship of these lesions in both groups to each other with reference to habits in Indian population, viz, pan chewing, tobacco smoking, and alcohol consumption and time interval and histological variations among these lesions. An interesting relationship has been observed in certain aerodigestive tract primary lesions developing second cancer due to continued effect of "carcinogens," as habits are hard to die even after developing cancer. Analysis also brings out an interesting observation of involvement of "physiologically and anatomically" related organs developing second cancer at an interval or concurrently. A solitary pulmonary nodule or an opacity in a patient with extrathoracic cancer should not be considered as "metastatic" unless proved otherwise; metachronous lesions need to be treated energetically, adequately, efficiently, and aggressively in certain clinical situations for better results and salvage.

No abstract

In carcinoma of the esophagus, response to in vivo sensitization with recall antigens and DNCB was markedly depressed with 13% and 16% positivity respectively. Similarly, the number of T-cells was found to be significantly low (24 +/- 14) as compared to normal control (61 +/- 23). Blastogenesis index with PHA was only 1.75 +/- 1.04 in contrast to normal of 6.79 +/- 2.57. This depression was independent of serum albumin level and body weight. Cell-mediated immunity was further depressed following radiotherapy and did not improve following enteral alimentation for 3 weeks. In untreated patients, there was a significant rise in levels of IgA (298 +/- 184 mg/100 ml) as compared to normal (154 +/- 54 mg/100 ml). Levels of IgA did show a downward trend following enteral hyperalimentation. Circulating immune complexes and serum CEA level were elevated in almost 50% of patients. These data confirm the influence of tumor-related impairment of cell-mediated immunity while nutrition appears to affect IgA levels.