An 18-year-old female patient with Crohn's disease presented with left lower lobe pneumonia and pleural effusion which were resistant to treatment with antibiotics. Colo-bronchial fistula had not been recognized until she coughed up yellow sputa with feculent odor and developed acute respiratory distress syndrome. This type offistula is a rare complication ofCrohn's disease, but the present case certainly alerts physicians to search for a fistula between the bronchus and gastrointestinal tract when encountering patients with Crohn's disease accompanied by antibioticresistant chronic pneumonia. (Internal Medicine 35: 957-960, 1996)
When rabbit peritoneal exudate cells were incubated for 24 and 48 h with phytohemagglutinin-activated lymphocytes or their culture supernatants, two times as many cells remained adherent to culture slides as in the controls. More spreading cells were found among the adherent cells in the stimulatea cultures. Eighty percent of spreading cells that were induced by supernatants were negative or faintly positive for f-galactosidase. On the other hand, half of the spreading cells induced by activated lymphocytes were positive (1+ to 4+) for 38galactosidase. Enhanced reduction of nitroblue tetrazolium was found in the spreading cells that were stimulated by either phytohemagglutinin-activated lymphocytes and their supernatants. Under similar conditions, unstimulated peritoneal cells showed less marked activation. These findings show that macrophages can appear morphologically activated and yet not be enzymatically activated by lymphokines. Possible mechanisms of direct interaction of activated lymphocytes and macrophages are discussed.
Pulmonary washings from rabbits were freed of cells and added to the monolayers of homologous alveolar macrophages (AM). At 1 h after incubation with the pulmonary washings, many more cells adhered to glass, spread out, and showed enhanced Nitro Blue Tetrazolium reduction. The maximal effect of the pulmonary washings on AM activation was obtained 12 h after incubation. The AM activated by the pulmonary washings showed a higher capacity to inhibit the growth of intracellular BCG, and that capacity was correlated with the intensity of Nitro Blue Tetrazolium reduction by the AM. Gel filtration of the pulmonary washings through Sepharose 4B yielded five fractions. The factor that activated the AM functions was in fraction 4. When the immunoglobulin G in the fraction was removed by an immunoadsorbent column, AM activity was abolished. The effect of the immunoglobulin G was dose dependent, and minimal responses to 106 cells per ml were obtained at a protein concentration of 20 ,ug/ml. Lymphokines had no effect on AM activation with respect to the morphological alterations and Nitro Blue Tetrazolium reduction during the 24-h observation time. In summary, AM from normal rabbits were soon activated markedly by lavage-procured immunoglobulin G, but not by lymphokines.
The presence of defects on resting thallium (201Tl) myocardial scintigraphy has been previously demonstrated in myocardial sarcoidosis. To examine cardiac sympathetic nerve activity in patients with cardiac sarcoidosis, we performed 201Tl and I-123 MIBG (meta-iodobenzylguanidine) myocardial scintigraphy in patients with sarcoidosis. Sixteen patients with sarcoidosis were classified into 2 groups according to the presence or absence of defects on 201Tl scintigraphy. Myocardial images by both 201Tl and I-123 MIBG were then divided into 20 segments and scored using a 6-point scoring system. Defect Score was defined as a the sum of significant scores in each image. The mean Defect Score in I-123 MIBG images was higher in the 201Tl defect group (44.3 +/- 13.3) than in both the normal 201Tl group (25.1 +/- 10.5) and the control group (22.7 +/- 11.4). Moreover, the locations of defects on I-123 MIBG scans were consistent with those on 201Tl scans. This study suggests that cardiac adrenergic function may be impaired in cardiac sarcoidosis, and I-123 MIBG scintigraphy may be more sensitive in detecting cardiac sarcoidosis than 201Tl scintigraphy, although the clinical significance of these findings requires further study.
The soft, gelatin capsule of VP-16-213 (etoposide) was given orally and evaluated in a Phase II study of 56 patients with histologically confirmed small cell lung cancer. The drug was given in a dose of 200 mg/body/day orally for 5 consecutive days, and the courses were repeated every 3 to 4 weeks depending upon the individual patient recovery from myelosuppression. An overall objective response was obtained in 17 patients (30%), five previously treated (23%) and 12 untreated (35%). The median days for response after the start of treatment was 14 d (range, 5 to 64), and the median duration of response was 62 days (range, 28 to 278). The dose-limiting factor was leukopenia, while thrombocytopenia was also experienced. Gastrointestinal reactions to toxicity and alopecia were also observed, but they were not overwhelming. The study demonstrated that the VP-16-213 soft gelatin capsule given orally is effective against small cell lung cancer without clinical cross-resistance to other cytotoxic agents. Its usefulness in combination chemotherapy is thus suggested.
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