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Crohn disease (CD) is a chronic, panenteric intestinal inflammatory disease. Its etiology is unknown.

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Recent epidemiological evidence suggests that there are two forms of Crohn disease (CD): perforating and nonperforating. We hypothesized that, just as with tuberculoid and lepromatous leprosy, differences in the two forms of CD would be both identified and determined by differences in the host immune response. Resected intestinal tissue from control patients as well as perforating and nonperforating CD patients was evaluated for mRNA levels. We employed 32p PCR amplification with published or custom-designed primers of a housekeeping gene (13-actin); a human T-cell marker (CD3-6); and the cytokines tumor necrosis factor a, transforming growth factor (3, granulocyte/macrophage colony-stimulating factor, interleukin (IL) 1(3, IL-lra, and IL-6. Differences were identified with IL-1,B (control = 162 ± 57 vs. perforating = 464 ± 154 vs. nonperforating = 12,582 ± 4733; P c 0.02) and IL-lra (control = 1337 ± 622 vs. perforating = 2194 ± 775 vs. nonperforating = 9715 ± 2988; P < 0.02). These data corroborate the epidemiological observation that there are two forms of CD. Nonperforating CD, the more benign form, is associated with increased IL-1,B and IL-lra mRNA expression. We conclude that it is the host immune response that determines which form of CD becomes manifest in any given individual and discuss the investigative, diagnostic, and therapeutic implications of these observations.

(EG and MA). During the whole study the same two sphygmomanometers were used. With the subject seated, the right arm was used to measure blood pressure and pulse rate. Blood pressure was determined twice within a five minute period. Whenever obesity was apparent a large arm cuff was used. The blood pressure was read to the nearest 2 mmHg. The mean systolic and diastolic blood pressure was calculated from the two readings.