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PubMed2002

Immunomodulation by the autonomic nervous system: therapeutic approach for cancer, collagen diseases, and inflammatory bowel diseases.

The distribution of leukocytes is regulated by the autonomic nervous system in humans and animals. The number and function of granulocytes are stimulated by sympathetic nerves whereas those of lymphocytes are stimulated by parasympathetic nerves. This is because granulocytes bear adrenergic receptors, but lymphocytes bear cholinergic receptors on the surface. These regulations may be beneficial to protect the body of living beings. However, when the autonomic nervous system deviates too much to one direction, we fall victim to certain diseases. For example, severe physical or mental stress --> sympathetic nerve activation --> granulocytosis --> tissue damage, including collagen diseases, inflammatory bowel diseases, and cancer. If we introduce the concept of immunomodulation by the autonomic nervous system, a new approach for collagen diseases, inflammatory bowel diseases, and even cancer is raised. With this approach, we believe that these diseases are no longer incurable.

Animals↗
PubMed1988

Collagen content and types in the intestinal strictures of Crohn's disease.

The collagen content and the relative amount of collagen types were quantitated in control intestine as well as in both inflamed and strictured intestine resected from patients with Crohn's disease. The major collagen type in control intestine was type I (68%), followed by types III (20%) and V (12%). In strictured intestine both collagen content and the relative amount of type V collagen were significantly increased compared with control intestine. Histologic studies demonstrated that in strictured specimens there was a striking proliferation of smooth muscle cells of the muscularis mucosae associated with an accumulation of collagen in the submucosa. The thickness of the muscularis propria was also increased. Immunohistochemical studies demonstrated small amounts of type V collagen in the submucosa of control bowel. In contrast, large amounts of type V collagen were seen in the fibrotic, expanded submucosa of strictured bowel, particularly in the areas where smooth muscle cells of the muscularis mucosae had proliferated. Intestinal strictures in Crohn's disease are therefore characterized by an accumulation of collagen, a proliferation of smooth muscle cells, and an increase in type V collagen, a collagen type produced in relatively large amounts by smooth muscle cells. These changes appear to result in both a loss of the normal compliance of the intestine and a thickening of the intestine wall, resulting ultimately in the intestinal obstruction so frequently seen in patients with Crohn's disease.

Amino Acids↗
PubMed2003

Diagnosis and management of microscopic colitis.

OBJECTIVE: To describe microscopic colitis (MC) and a stepwise approach to its diagnosis and management. QUALITY OF EVIDENCE: MEDLINE was searched from January 1996 to August 2002. Controlled trials were sought, but due to their relative rarity, most articles cited are well designed retrospective studies and reviews. MAIN MESSAGE: Microscopic colitis in both its collagenous and lymphocytic forms is a relatively common and important cause of diarrhea in middle-aged and elderly patients. It usually presents as chronic watery diarrhea. Results of endoscopic and radiologic examinations are normal; specific histologic findings are seen on colonic biopsy. Once the diagnosis is confirmed, we suggest a stepwise approach to therapy. First-line therapies include antidiarrheal agents; second-line include bismuth subsalicylates and budesonide; third-line include cholestyramine and 5-aminosalicylic acid agents. When patients fail to respond to these therapies, oral corticosteroids or immune modulatory therapy should be considered. For severe unresponsive cases, colectomy is the last resort. CONCLUSION: Microscopic colitis is an important cause of chronic diarrhea. Once the diagnosis is confirmed, a stepwise approach to treatment is suggested.

Adrenal Cortex Hormones↗
PubMed2000

Genetic factors determine extent of bone loss in inflammatory bowel disease.

BACKGROUND & AIMS: Although bone loss and osteoporosis are well-known long-term sequelae of inflammatory bowel disease (IBD), the risk factors for increased bone loss have not been identified. Balances of pro- and anti-inflammatory cytokines influence mechanisms of both chronic inflammation and bone resorption. The aim of this study was to identify genetic risk factors for rapid bone loss in IBD patients as a model of disease- and inflammation-associated bone loss. METHODS: Multiple clinical parameters, biochemical markers of bone metabolism (vitamin D, parathyroid hormone, N-terminal telopeptide of type-I collagen, desoxypyridinoline, bone alkaline phosphatase), and bone mineral density were prospectively assessed in 83 IBD patients over 1.6+/-0.3 years. Eighty-six healthy bone marrow donors served as controls for allelotyping. The allele status of the interleukin 1 receptor antagonist (IL-1ra), IL-6, heat shock protein 70-2 (hsp 70-2), and heat shock protein 70-hom (hsp hom) genes was typed and correlated with clinical course of IBD and extent of bone loss. RESULTS: The extent of bone loss was not correlated to clinical severity of disease or application of corticosteroids. Noncarriage of the 240-base pair allele of the IL-1ra gene and carriage of the 130-base pair allele of IL-6 were independently associated with increased bone loss. Genetic variations of the hsp genes were not associated with degree of bone loss. The combined presence of the named risk factors was significantly associated with increasing bone loss. CONCLUSIONS: Genetic variations in the IL-6 and IL-1ra gene identify IBD patients at risk for increased bone loss.

Absorptiometry, Photon↗
PubMed2004

[Collagen diseases with gastrointestinal manifestations].

Collagen vascular diseases are known to present with a diverse array of gastrointestinal manifestations. These can be classified as: 1) gastrointestinal damage due to the collagen vascular disease itself; 2) adverse events caused by pharmacotherapies; or 3) gastrointestinal infections following immunosuppression due to corticosteroid (CS) administration. The first group includes lupus enteritis and protein-losing gastroenteropathy in systemic lupus erythematosus (SLE), reflux esophagitis, chronic intestinal pseudo-obstruction, and pneumatosis cystoids intestinalis in systemic sclerosis, amyloidosis in rheumatoid arthritis, bowel ulcer and bleeding in rheumatoid vasculitis and microscopic polyangiitis, and ileocecal ulcer in Behcet disease. In particular, colonic ulcers associated with SLE represent refractory lesions resistant to CS. Analysis of reported cases showing colonic lesions with SLE (22 cases in Japan) revealed that mean duration of SLE was 9.9 years and 77% of colonic lesions were observed in the rectum and sigmoid colon. Half of the patients developed intestinal perforation or penetration, and 6 of the 11 patients with perforation died. The second group includes lesions in the small and large intestine due to nonsteroidal anti-inflammatory drugs (NSAIDs) and CSs, in addition to peptic ulcers. As perforation in CS-treated patients displays relatively high incidence with poor prognosis, careful attention to such complications is needed. The third group includes candidal esophagitis and cytomegalovirus (CMV) enteritis. Prompt diagnosis is required to prevent colonic bleeding and perforation due to CMV.

Adrenal Cortex Hormones↗
PubMed2003

Serum laminin and collagen IV in inflammatory bowel disease.

BACKGROUND: / AIMS: Laminin and collagen IV have been proposed as extracellular matrix serum markers. Because fibrosis is a major complication of inflammatory bowel disease, serum concentrations of laminin and collagen IV were measured in patients with ulcerative colitis (UC) and Crohn's disease (CD) and compared with inflammatory and healthy controls. METHODS: Laminin and collagen IV serum concentrations were measured in 170 patients with inflammatory bowel disease (86 UC and 84 CD), in 23 patients with other causes of intestinal inflammation, and in 80 matched healthy controls using commercially available enzyme linked immunosorbent assays. Laminin and collagen IV concentrations were correlated with disease activity, type, localisation, and treatment. RESULTS: Mean (SD) serum laminin concentrations were 281.0 (110.1) ng/ml in patients with UC, 275.6 (106.7) ng/ml in patients with CD, 192.0 (17.8) ng/ml in healthy controls, and 198.5 (32.5) ng/ml in inflammatory controls. Mean (SD) serum collagen IV concentrations were 72.8 (22.9) ng/ml in patients with UC, 71.0 (18.2) in patients with CD, 79.8 (12.2) ng/ml in healthy controls, and 88.9 (24.6) ng/ml in inflammatory controls. There was a significant difference among the four groups (p < 0.0001) for both markers. There was a strong correlation between serum laminin, but not collagen IV, and disease activity in both diseases. No significant association was found between these markers and disease localisation or disease type. CONCLUSIONS: Serum concentrations of laminin are increased, whereas serum concentrations of collagen IV are decreased, in patients with inflammatory bowel disease. They may be useful surrogate markers for sustained inflammation and tissue remodelling.

Adult↗
PubMed1985

Incidence of cancer in rheumatoid arthritis and other disorders after immunosuppressive treatment.

A prospective study in the United Kingdom of 1,634 patients without transplants treated with immunosuppressive drugs (68 percent with azathioprine, 28 percent with cyclophosphamide) found an excess of non-Hodgkin's lymphoma and squamous cell skin cancer, suggesting that the excesses (although larger) of the same malignancies found among transplant recipients are not due solely to the foreign antigens of the graft. A separate analysis of the 643 patients with rheumatoid arthritis found a 13-fold increase of non-Hodgkin's lymphoma (whether treated with azathioprine or cyclophosphamide). This increase is not significantly different from the excess in similarly treated patients with other disorders in the study. In patients with rheumatoid arthritis not receiving immunosuppressive drugs, this excess is greater than that in a Finnish population and lower than that in another United Kingdom population. The findings are consistent with other evidence that immunosuppression favors the development of non-Hodgkin's lymphoma, which includes the excess of malignancies found among transplant recipients, long-term renal dialysis patients, and patients with certain primary immunodeficiency disorders. The higher risk among transplant recipients may reflect the effects of the foreign antigens, the more intensive immunosuppressive therapy, or both of these factors. In addition, the predilection for the brain, which is a well-known feature of the lymphomas after transplantation, may also apply (to a lesser extent) to other patients after immunosuppressive treatment, judging from the increasing numbers of case reports in such patients of this exceedingly rare type of malignancy. In view of the evidence of an increase of non-Hodgkin's lymphoma in rheumatoid arthritis in the absence of immunosuppressive treatment, any additional increase is likely to be small in absolute terms. Nevertheless, it needs to be weighed against the clinical benefits.

Adolescent↗
PubMed2005

Sex-related differences in tuberculin reaction, free and total testosterone concentrations in patients with autoimmune disorders and controls.

Earlier studies reported the associations among testosterone hormone, autoimmunity, and left-handedness. In the present study, sex differences in tuberculin reaction, a measure of cell-mediated hypersensitivity, serum free and total testosterone levels in controls and patients with autoimmune diseases were studied. There was a sex difference in right and left tuberculin reactions in controls, but not in patients. Both right and left tuberculin reactions were smaller in male and female patients than male and female controls. Free and total testosterone levels were higher in male controls than in male patients. Total testosterone levels were higher in female controls than in female patients. These results suggest that autoimmune diseases may be associated with a decrease in the blood testosterone concentrations.

Adolescent↗
PubMed1999

A colorectal cell line with alterations in E-cadherin and epithelial biology may be an in vitro model of colitis.

BACKGROUND: It has been shown previously in ulcerative colitis tissue that E-cadherin can occasionally be mutated in the extracellular domain early in neoplastic progression. E-cadherin is known to maintain differentiation and inhibits invasion in vivo. AIMS: To assess the mechanisms by which such dysfunction occurs. METHODS: Four human colorectal cancer cell lines, HCA-7 colonies 1, 3, 6, and 30, derived from a single heterogeneous colorectal cancer were studied. The HCA-7 cell line has p53 mutations and a random errors of replication "positive" phenotype, as is seen in early colitis associated cancers or hereditary nonpolyposis coli cancer (HNPCC). RESULTS: Cell lines 6 and 30 expressed E-cadherin abundantly and this correlated positively with their degree of differentiation and organisation; however, both cell lines had loss of heterozygosity of E-cadherin. Interestingly, E-cadherin production was downregulated in the poorly differentiated cell line 1, and this was associated with major chromosomal rearrangements of 16q. This cell line also had a mutation in the homophilic binding domain of exon 4, which was associated with disaggregation by low titres of a function blocking antibody, and an invasive phenotype. CONCLUSIONS: These multiple biological alterations further characterise the complex association that E-cadherin has with tumour heterogeneity and suggest that this series of cell lines may be a useful model of colitis associated or HNPCC associated tumorigenesis.

Agar↗