Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many studies show a strong association between diabetes mellitus and risk for periodontal disease destruction. Patients with non-insulin-dependent diabetes mellitus have an increased risk of developing destructive periodontal disease. Under similar plaque conditions, adult patients with long-term, poorly controlled diabetes mellitus have more attachment and bone loss than controlled diabetic patients. Most patients with diabetes mellitus respond to conventional periodontal treatment, but in some cases the response may be related to the degree of metabolic control. Periodontal treatment may have a beneficial effect on the metabolic status of poorly controlled diabetes. Tetracycline therapy may be an effective adjunctive treatment in the management of periodontal disease in diabetic patients by blocking collagenase-dependent periodontal tissue destruction. Pyostomatitis vegetans is frequently associated with chronic inflammatory bowel disease and is a marker for the disease. Plaque control with chlorhexidine gluconate should be preceded by mechanical removal of plaque and calculus in patients with leukemia undergoing chemotherapy. A distinct gingival lesion is associated with Wegener's granulomatosis, a potentially fatal disease that, if detected early, has a favorable prognosis.
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PMID:Periodontal manifestations of systemic disease and management of patients with systemic disease. 840 43

Crohn's disease (CD) and ulcerative colitis (UC), the chronic inflammatory bowel diseases (CIBD), are common causes of gastro-intestinal disease in the Western world, with a combined prevalence of 100-200/100,000 (ref. 1). Epidemiological studies, particularly concordance rates in twin pairs and siblings, strongly implicate genetic susceptibility in the pathogenesis of CIBD. In fact, the relative contribution of genetic factors to the pathogenesis of CD may be greater than in schizophrenia, asthma or hypertension, and at least equivalent to that in insulin-dependent diabetes. Systematic screening of the entire human genome now provides a strategy for the identification of susceptibility genes in complex polygenic disorders. We undertook a two-stage genome search for susceptibility genes in inflammatory bowel disease involving 186 affected sibling pairs from 160 nuclear families. We provide strong evidence for the presence of susceptibility loci for both CD and UC on chromosome 3, 7 and 12. We obtained the highest lod score (5.47; P = 2.66 x 10(-7) with the marker D12S83 and lod scores of 3.08 and 2.69 for D7S669 and D3S1573, respectively. Our data suggest that CD and UC are closely related, but distinct, polygenic disorders that share some, but not all, susceptibility genes.
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PMID:Two stage genome-wide search in inflammatory bowel disease provides evidence for susceptibility loci on chromosomes 3, 7 and 12. 884 Nov 95

The chemistry, pharmacology, pharmacokinetics, and clinical efficacy of acarbose, a new antidiabetic agent, are reviewed. Acarbose reversibly inhibits intestinal alpha-glucosidases, enzymes responsible for the metabolism of complex carbohydrates into absorbable monosaccharide units. This action results in a diminished and delayed rise in blood glucose following a meal, resulting in a reduction in post-prandial hyperglycemia, area under the glucose concentration-time curve, and glycosylated hemoglobin. Other effects include a reduction in postprandial insulin and variable changes in plasma lipid concentrations. In placebo-controlled trials, acarbose caused significant improvements in glycemic control indicators, including glycosylated hemoglobin. Acarbose has demonstrated additional glycemic control when added to other antidiabetic therapies, including sulfonylureas and insulin. Efficacy of acarbose appears to be comparable to or slightly less than that of sulfonylureas or metformin, although it has not been compared with maximal dose of these agents. The most commonly reported adverse drug reactions with acarbose are abdominal pain, diarrhea, and flatulence, which tend to lessen with time. Acarbose may affect the bioavailability of metformin and may be less effective when used in conjunction with intestinal adsorbents and digestive enzyme preparations. Concurrent use with hypoglycemic agents (sulfonylureas and insulin) may cause an increased frequency of hypoglycemia. Acarbose should not be used in individuals with certain intestinal disorders, including inflammatory bowel disease. The dosage should start at 25 mg one to three times daily given with the first bite of each main meal and should be adjusted to a maximum of 50 mg three times daily for patients weighing up to 60 kg or 100 mg three times daily for heavier patients. Acarbose may be considered for first-line antidiabetic therapy in certain patients and may be useful as combination therapy in selected instances. Acarbose is efficacious in improving metabolic control in non-insulin-dependent diabetes mellitus. Further evaluation of its effects on the long-term complications of diabetes is needed.
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PMID:Acarbose: an alpha-glucosidase inhibitor. 889 66

There is strong evidence that non-insulin-dependent-diabetes mellitus (NIDDM) has a polygenic mode of inheritance. Nevertheless, major gene effects may be involved in its pathogenesis, especially in forms with an early age of onset. We performed linkage analyses between 4 candidate genes for insulin resistance and NIDDM in a set of 55 multigenerational French Caucasian families, using the affected sib-pair approach. No significant results were obtained with glycogen synthase (GSY), insulin receptor substrate-1 (IRS-1) and apolipoprotein C-II (APOC-II) genes. However, a significant trend towards linkage was found between NIDDM and the phosphoenolpyruvate carboxykinase gene (PCK1) located on chromosome 20q (p = 0.005 for the mean estimated proportion of alleles shared identically by descent, mean IBD = 0.55), particularly among sib-pairs with diabetes diagnosed before the age of 46 years (p = 0.0003, mean IBD = 0.66). These results suggest that the PCK1 gene or a nearby locus contributes to the development of NIDDM in the French population.
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PMID:Indication for genetic linkage of the phosphoenolpyruvate carboxykinase (PCK1) gene region on chromosome 20q to non-insulin-dependent diabetes mellitus. 898 54

Cytokines and insulin-like growth factors (IGFs) are involved in the induction and/or perpetuation of inflammatory bowel disease. The effect of fasting on inflammatory bowel disease was studied in a mouse experimental model of acute colitis caused by adding dextran sulfate sodium (DSS) to drinking water. Animals were either fed ad libitum or fasted (water only) for 2 days before death. Inflammation and tissue damage, measured as a colitis activity score, were markedly reduced in fasted (2.4 +/- 0.1) compared to fed (5.3 +/- 0.1) DSS animals (P < 0.0001). Colon interleukin-1 beta (IL-1 beta), IGF-I, and tumor necrosis factor-alpha messenger RNAs (mRNAs) were quantified by Northern blot hybridization and expressed as a percentage of mRNA abundance in fed controls. In DSS mice, IL-1 beta mRNA was elevated in the fed group (954 +/- 155%; P < 0.001), but was suppressed in fasted animals (71.1 +/- 11%). IGF-I mRNA also was elevated in fed DSS mice (421 +/- 71%; P < 0.01). This increase was attenuated in fasted DSS mice (202 +/- 17%; P < 0.01 compared to fed DSS mice). Tumor necrosis factor-alpha mRNA was increased in fed DSS mice (162 +/- 15%; P < 0.01), but was not significantly lower in fasted animals. By in situ hybridization, IL-1 beta mRNA was localized to the lamina propria of colonic mucosa in fed DSS animals, but was not detectable in other groups. We conclude that fasting has a protective effect on the progression of acute DSS, induced colitis. This is associated with decreased expression of IL-1 beta and IGF-I mRNAs in the colon.
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PMID:Fasting prevents experimental murine colitis produced by dextran sulfate sodium and decreases interleukin-1 beta and insulin-like growth factor I messenger ribonucleic acid. 900 9

During the past decade nitric oxide has emerged as an important mediator of physiological and pathophysiological processes. Elevated nitric oxide bio-synthesis has been associated with nonspecific immune-mediated cellular cytotoxicity and the pathogenesis of chronic, inflammatory autoimmune diseases including rheumatoid arthritis, insulin-dependent diabetes, inflammatory bowel disease, and multiple sclerosis. Recent evidence suggests, however, that nitric oxide is also immunoregulatory and suppresses the function of activated proinflammatory macrophages and T lymphocytes involved in these diseases. This article reviews the role of nitric oxide in the biology of central nervous system glial cells (astrocytes and microglia) as it pertains to the pathogenesis of multiple sclerosis in humans and experimental allergic encephalitis, the animal model of this disease. Although nitric oxide has been clearly implicated as a potential mediator of microglia-dependent primary demyelination, a hallmark of multiple sclerosis, studies with nitric oxide synthase inhibitors in the encephalitis model have been equivocal. These data are critically reviewed in the context of what is know from clinical research on the nitric oxide pathway in multiple sclerosis. Specific recommendations for future preclinical animal model research and clinical research on the nitric oxide pathway in patients are suggested. These studies are necessary to further define the role of nitric oxide in the pathology of multiple sclerosis and to fully explore the potential for nitric oxide synthase inhibitors as novel therapeutics for this disease.
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PMID:The role of nitric oxide in multiple sclerosis. 910 72

Although monogenic diseases often show extreme clinical phenotypes, the major burden of genetic ill health lies in the more prevalent polygenic disorders, such as diabetes, hypertension and multiple sclerosis. These conditions affect many thousands of individuals and their management consumes vast amounts of health care resources: in the UK some 80,000 people have multiple sclerosis; the estimated financial cost to society of introducing treatments, such as beta interferon, could be as high as 250 million pounds per year. Knowledge on the genetics of these common diseases is poor, but has potentially received a considerable boost with the arrival of whole genome screening. The genome screen in insulin-dependent diabetes mellitus (IDDM) reported in 1994 was the first in a human polygenic disease. Since this publication, whole genome screening has been performed in a variety of human polygenic diseases, including schizophrenia, bipolar affective disorder, non-insulin-dependent diabetes mellitus (NIDDM), inflammatory bowel disease, asthma and multiple sclerosis.
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PMID:The genetic analysis of multiple sclerosis. 919 29

1. Autoimmune diseases are common conditions which appear to develop in genetically susceptible individuals, with expression of disease being modified by permissive and protective environments. Familial clustering and data from twin studies provided the impetus for the search for putative loci. Both the candidate gene approach in population-based case-control studies and entire genome screening in families have helped identify susceptibility genes in a number of autoimmune diseases. 2. After the first genome screen in type 1 (insulin-dependent) diabetes mellitus it seems likely that most autoimmune diseases are polygenic with no single gene being either necessary or sufficient for disease development. Of the organ-specific autoimmune diseases, genome screens have now been completed in insulin-dependent diabetes mellitus and multiple sclerosis. Furthermore, the clustering of autoimmune diseases within the same individuals suggests that the same genes may be involved in the different diseases. This is supported by data showing that both HLA (human leucocyte antigen) and CTLA-4 (cytotoxic T-lymphocyte-associated-4) appear to be involved in the development of insulin-dependent diabetes mellitus and Graves' disease. 3. Genome screens have also been completed in some of the non-organ-specific autoimmune diseases including rheumatoid arthritis, inflammatory bowel disease and psoriasis. Many candidate genes have also been investigated although these are predominantly in population-based case-control studies. 4. Substantial progress has been made in recent years towards the identification of susceptibility loci in autoimmune diseases. The inconsistencies seen between case-control studies may largely be due to genetic mismatching between cases and controls in small datasets. Family-based association studies are being increasingly used to confirm genetic linkages and help with fine mapping strategies. It will, however, require a combination of biology and genetics, as has been necessary with the major histocompatibility complex in insulin-dependent diabetes mellitus, to identify primary aetiological mutations.
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PMID:Genetic susceptibility to the development of autoimmune disease. 949 84

The Central Medical Pharmaceutical Committee of the Health Insurance Council informs the medical profession annually about the effects of drugs through the Pharmacotherapeutical Compass. The 1998 edition now contains a chapter on pharmacokinetics as well. Compared with previous editions the main alterations of the contents concern an introduction and advice on the antidepressants, two protocols with respect to the medical treatment of patients suffering from epilepsy, advice with respect to oral drugs for the treatment of inflammatory bowel disease, an introduction and advice regarding the treatment of allergic rhinitis, the treatment of patients suffering from AIDS with antiretroviral drugs, the treatment of genital herpes, the taking of insulin lispro by patients with diabetes and the taking of bisphosphonates to prevent or to treat osteoporosis. Two corrections to the 1998 edition are given.
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PMID:[Pharmacotherapeutic compass 1998]. 975 45

Breast-feeding protects the newborn against infectious diseases in developing as well as in industrialized countries. Protection is conferred against gastrointestinal and respiratory tract diseases as well as against otitis media. This protection provided by specific (antibody dependent) and broad, nonspecific protective factors in human milk (proteins, glycoproteins, and lipids) is associated with lower global morbidity and mortality of breast-fed infants as compared with formula-fed infants. While protection against diseases that develop later in life, such as insulin-dependent diabetes mellitus, inflammatory bowel disease, and childhood cancer, has been reported, well-planned prospective studies are essential in order to confirm these observations. Similar studies are essential in order to ascertain the small but consistently reported higher cognitive ability of breast-fed infants.
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PMID:Early and late effects of breast-feeding: does breast-feeding really matter? 969 Nov 58


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