Direct health-care cost utilization in Hong Kong inflammatory bowel disease patients in the initial 2 years following diagnosis.

BACKGROUND AND AIM: There are scanty data on the health-care utilization from Asia where the incidence of inflammatory bowel disease (IBD) is rising rapidly. We aim to determine the direct health-care costs in the first 2 years of diagnosis in an IBD cohort from Hong Kong and the factors associated with high cost outliers. METHODS: This is a retrospective cohort study that included patients newly diagnosed with IBD in a territory-wide IBD registry. Patients' clinical information, hospitalization records, investigations, and IBD treatments were retrieved for up to 2 years following diagnosis of IBD. RESULTS: Four hundred and thirty-five newly diagnosed IBD patients were included: 198 with Crohn's disease and 237 with ulcerative colitis. Total direct medical expenditure for this cohort 2 years after the IBD diagnosis was $7 072 710: hospitalizations (33%), 5-aminosalicylic acid (23%), imaging and endoscopy (17%), outpatient visits (10%), surgery (8%), and biologics (6%). Mean direct medical costs per patient-year were significantly higher for Crohn's disease ($9918) than ulcerative colitis ($6634; P, 0.001). The total direct health-care cost decreased significantly after transition to the second year (P < 0.01). High cost (> 90th percentile) outliers were associated with surgery (OR 7.1, 95% CI 2.9-17.2) and low hemoglobin on presentation (OR 0.83, 95% CI 0.70-0.96). CONCLUSIONS: Hospitalization and 5-aminosalicylic acid usage accounted for 56% of total direct medical costs in the first 2 years of our newly diagnosed IBD patients. Direct health-care costs were higher in the first year compared with the second year of diagnosis. Surgery and low hemoglobin on presentation were associated with high cost outliers.

Action of alpha-momorcharin, a ribosome inactivating protein, on cultured tumor cell lines.

1. alpha-Momorcharin, a glycoprotein isolated from seeds of the bitter gourd, Momordica charantia inhibited incorporation of [3H]thymidine, [3H]leucine and [3H]uridine into P388 (mouse monocyte-macrophage), J774 (Balb/c macrophage), JAR (human placental choriocarcinoma) and sarcoma S180 cell lines. 2. The most potent inhibitory effect was exerted on P388 cells and the smallest effect on sarcoma cells. 3. alpha-Momorcharin also enhanced the tumoricidal effect of mouse macrophages on mouse mastocytomal (P815) cells.

Activation of peritoneal macrophages by polysaccharopeptide from the mushroom, Coriolus versicolor.

Polysaccharopeptide (PSP) is a substance produced by an edible mushroom, Coriolus versicolor which has been claimed to possess antitumor activity. However, neither tumoricidal activity nor cytotoxicity was observed when five tumor cell lines and mouse peritoneal macrophages were cultured in vitro in the presence of 2.5-10 micrograms/ml PSP. An increase in the production of reactive nitrogen intermediates, reactive oxygen intermediates (superoxide anions) and tumor necrosis factor was measured in peritoneal macrophages collected from inbred C57 mice which had received PSP in the drinking water for 2 weeks. Northern blot analysis also demonstrated that PSP activated the transcription of tumor necrosis factor gene in these cells, indicating that PSP exerted an immunomodulatory effect on the defensive cells.

Stimulation of murine splenocytes by melatonin and methoxytryptamine.

Male C57 mice kept under a 14:10 (L:D) photoperiod received vehicle (VEH), melatonin (MEL) and methoxytryptamine (MTA) in the drinking water for 2 weeks. Splenocytes from MEL-treated mice showed an augmented mitogenic response to concanavalin A and lipopolysaccharide (LPS) while splenocytes from MTA-treated mice demonstrated an enhanced mitogenic response to LPS when compared to the VEH-treated control. Splenocytes from MEL-treated and MTA-treated mice also produced higher levels of gamma interferon and interleukin-2. Lymphokines prepared from splenocytes of MEL-treated mice stimulated peritoneal macrophages to produce more nitrite than those from splenocytes of MTA-treated and control mice, suggesting that MEL had a stronger stimulating effect on the lymphocytes than MTA. Understimulation of lymphokines from MEL-treated mice, peritoneal macrophages from MTA-treated mice produced a greater inhibition of the growth of murine mastocytoma P815 cells than that produced by macrophages from control and MEL-treated mice, suggesting that MTA was more potent than MEL in rendering the macrophages responsive to lymphokines. The results point to immunostimulatory actions of the pineal indoles MEL and MTA.

Antiproliferative effect of pineal indoles on cultured tumor cell lines.

The in vitro antiproliferative action of pineal indoles on several tumor cell lines including melanoma (B16), sarcoma (S180), macrophage-like cell line (PU5), fibroblasts (3T3), and choriocarcinoma (JAr) was examined by measuring the incorporation of 3H-thymidine by the tumor cells, and, in the case of melanoma cells, by also measuring the incorporation of 3H-leucine and 3H-uridine. Uptake of crystal violet was used to assess the viability of the tumor cells. The order of inhibitory potency of the indoles was found to be methoxytryptamine > melatonin, methoxytryptophol, hydroxytryptophol, and methoxyindoleacetic acid > serotonin and hydroxyindoleacetic acid. The possibility of an adverse effect of the indoles on the viability of normal cells was also investigated by employing a primary culture of rat hepatocytes. The release of glutamate-oxaloacetate transaminase by hepatocytes was not affected by the indoles, although the release of glutamate-pyruvate transaminase was increased to a small extent and the uptake of crystal violet was slightly inhibited.