This cytokine pattern may favour a chemotactic response and implicates P. acnes and coproporphyrin III in the recruitment of inflammatory cells to the site of infection and in the development of acne lesions.

In December 1970, 8,292 rural Bengali children the ages of 1 and 9 had their height and arm circumference measured. Eighteen months later the fate of 98.8% of these children was ascertained. Overall, 2.3% of the children had died. Those the 9th and between the 10th and 50th percentiles of arm circumference for height were at 3.4 1.5 times greater risk of dying, respectively, than those above the 5oth percentiles. A gradient was present at every age, although it was greatest for the bulnerable 1- to 4-year age group, for whom the relative risks were 4.5, 1.6, and 1.0, respectively. The discriminant efficiency of these categories was greatest immediately following measurement and decreased with time. During the first postmeasurement month the risk of dying the poorest nutritional category was 19.8 times that of the best, and for the first 3 months, 12.2 times. By the last 3 months of followup it was only twice that of the best. Females in all three categories fared slightly worse than males, being at 1.1 times the risk of dying. This same vulnerable group of 1. to 4-year olds could be identified without knowing their age. Limiting the analysis to children whose heights were between 65 and 89 cm resulted in relative risks, for the three categories, of 4.1, 1.6, and 1.0, respectively. These arm circumference to height categories and the QUAC stick survey technique for which they were devised appear to be valid tools for identifying nutritionally disadvantaged individuals and populations at high risk of death.

Elevated circulating CEA levels occur in patients with benign gastrointestinal and hepatic disorders. These are usually less than 10 ng/ml. Of clinical importance is the influence of liver disease on the interpretation of CEA. At least 50% of patients with severe benign hepatic disease have elevated CEA levels, most often active alcoholic cirrhosis, and also chronic active and viral hepatitis, and cryptogenic and biliary cirrhosis. Patients with benign extrahepatic biliary obstruction may have increased plasma CEA, the highest in patients with co-existent cholangitis and especially liver abscess. The liver appears to be essential for the metabolism and/or excretion of CEA. Hence, liver work-up is needed to assess any patient with an elevated CEA. A damaged liver may further augment elevated CEA levels due to cancer. The increased circulating CEA observed in some patients with active ulcerative colitis tends to correlate with severity and extent of disease and usually returns to normal with remission. CEA levels also may be mildly elevated in patients with pancreatitis and in adults with colonic polyps. Smoking may contribute to the increased CEA levels seen in patients with alcoholic liver disease and pancreatitis. Therefore, in interpreting mildy elevated circulating CEA levels in patients with GI tract diseases, one must consider benign as well as malignant etiologies.

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