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Abdominosacral resection allows curative resection of midrectal cancer with excellent preservation of sphincter function. In the last ten years 427 patients underwent resection for rectal carcinoma at University Hospital by one surgeon. (SAL) The operation, selected by preoperative sigmoidoscopic measurement, was anterior resection (AR) in 239, abdominosacral resection (ASR) in 100, and abdominoperineal resection (APR) in 88. Operative mortality was 1.7% for AR, 2% for ASR and 2.3% for APR. All patients were completely continent of stool and flatus after AR and ASR. Follow-up is complete in 194 of 195 patients treated five to ten years ago. Five year survival for curative resection (no distant metastases) was 67.3% after AR (66/98), 58.3% after ASR (21/36), and 50% after APR (15/30). For patients without tumor in lymph nodes, survival rates were 78.3% for AR, 64.3% for ASR and 63.2% for APR. With involvement of regional nodes, survival fell to 41.4% for AR, 37.5% for ASR and 27.3% for APR. For lesions at 5-8.5 cm, five year survival was 61.1% for ASR and 58.3% for APR. No statistical difference in survival time was noted when patients were matched for age, sex, level of lesion and extent of spread. Pelvic recurrences were detected in 16.7% after ASR, 15.3% after AR and 33.3% after APR. All of the pelvic recurrences after ASR and the majority of those after AR and APR occurred in patients with tumor invasion of perirectal fat. These data strongly support the applicability of ASR as an important advance in the treatment of midrectal cancer. Although technically demanding, ASR has permitted preservation of anal continence without sacrifice of long-term cure in approximately 50% of patients who would otherwise have required APR.

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In addition to the bile pigments, there are present in the urine and stool another series of pyrrole pigments, the porphyrins. Hemoglobin, myoglobin, and other respiratory pigments contain as their prosthetic group a porphyrin of Type III configuration. The porphyrin excreted in urine and feces by normal individuals, and in most pathological states, is coproporphyrin Type I. This substance cannot be derived by degradation of the Type III porphyrins present in the respiratory pigments (1). Dobriner and his associates have shown that coproporphyrin I is formed as a by-product in the course of hematopoiesis (2a, b, c). Furthermore, they showed that the rate of production and excretion of coproporphyrin I depends upon the activity of orderly hematopoiesis (3a, b, c). Dobriner (4a, b) and Watson (5a, b, c, d,e) have established that the excreted coproporphyrin is chiefly, if not entirely, endogenous in origin. The greater proportion of the coproporphyrin is excreted by the liver into the intestinal tract and is found in the stool. There is a similarity between the pathways of excretion of coproporphyrin and the bile pigments.Salkowski (7) and Garrod (9), in their early work on porphyrins, observed an increased urinary output of porphyrins in liver disease. Elevated urinary porphyrin excretion has been recorded in cases of passive congestion of the liver, cholangitis, catarrhal jaundice, luetic hepatitis, hemachromatosis, secondary carcinoma of the liver, acute and subacute liver atrophy, and cirrhosis (4a, 6, 10a, b, lla, b, 12, 13, 15, 16, 17, 18).No suitable fecal coproporphyrin studies have been reported in cases of diseases of the liver. Brugsch (1 la, b) and Vigliani (6) did not separate the fecal porphyrins into their components, hence their quantitative data for fecal porphyrin excretion comprise the total fecal porphyrins, and include deuteroporphyrin and protoporphyrin, which are partially exogenous in origin (4b, Se).Brugsch (lla, b) suggested that there might be value in the determination of the relative excretion of urinary and fecal porphyrins in cases of liver disease. It was reasoned that, since the coproporphyrin is excreted by the liver as well as by the kidney, the injured liver might be unable to excrete the total amount of coproporphyrin presented to it, and therefore this substance would accumulate in the blood stream and be excreted in the urine. Thus the urinary excretion would be increased at the expense of the fecal output. In cases of liver insufficiency, the ratio of urinary to fecal coproporphyrin should be elevated. In order to determine the amount of porphyrin cleared by the liver, only the coproporphyrin need be determined, since it alone is excreted in both urine and feces. METHODSThe quantitative separation methods for coproporphyrin used in our studies are those of Dobriner (4a, b, 20). Quantitative measurements were done by means of a spectroscopic colorimeter (21).All of the patients studied were on a regular diet. The entire urine and stool were collected for a period of seven...