Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine H2-receptor antagonists metiamide and cimetidine were used in the treatment of severe peptic ulceration in Zollinger-Ellison syndrome. The ulcerations were completely healed in all four patients after treatment lasting from six weeks to four-and-a-half-months. Two patients developed recurrent ulcer after the treatment had stopped, but responded to a second course. One patient developed hepatitis B during cimetidine treatment and it is possible that the course of the hepatitis was unfavourable affected by cimetidine. But no other side effects were noted nor was there a significant change in basal serum-gastrin concentration or an increase in H+ secretion. Total gastrectomy remains the treatment of choice in Zollinger-Ellison syndrome, but cimetidine should be considered if the patient refuses operation or operation is not feasible because of a poor general state.
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PMID:[Treatment of peptic ulcer in the Zollinger-Ellison syndrome with histamine H2-receptor antagonists (author's transl)]. 2 85

Inhibition of gastric acid secretion by drugs remains the most important rational approach to the treatment of acid related diseases. Histamine H2-antagonists and more recently the proton pump blockers have become the first line treatment for acid peptic diseases. Proton pump blockers bind specifically to the proton pump of the parietal cells and thus inhibit the final acid secretion independently from the activating stimuli. Because of this specific mechanism fewer adverse effects on other systems in the body are expected with proton pump blockers than with histamine antagonists. An analysis of the spontaneous reports which the Swiss Drug Monitoring Center (SANZ) received from 1981 to 1995 showed striking differences in the adverse drug reaction profile: hypersensitivity reactions with fever and anaphylactic reactions, liver disorders such as cholestatic hepatitis, most with severe progression and requiring hospitalization, as well as endocrine disorders were reported more frequently with histamine antagonists, skin reactions and joint disorders, however, were reported more often with proton pump blockers. Our data also support the conclusion that adverse drug reactions to proton pump blockers and histamine antagonists are rare in the spontaneous reporting scheme (reporting rate < 1%). There was a somewhat higher rate of serious reports with histamine antagonists. These data do not allow conclusions concerning long-term effects or effects with larger than recommended dosages.
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PMID:[Ulcer drugs: profile of side effects of proton-pump blockers in comparison to H2 blockers in the spontaneous reporting system]. 899 98

Histamine is a classical, but still interesting inflammatory mediator. Many people have long believed that histamine is derived from mast cells or basophils alone. However, the histamine-forming enzyme, histidine decarboxylase (HDC), is induced in a variety of tissues in response (i) to gram-positive and gram-negative bacterial components (lipopolysaccharides, peptidoglycan, and enterotoxin A) and (ii) to various cytokines (IL-1, IL-3, IL-12, IL-18, TNF, G-CSF, and GM-CSF). HDC is induced even in mast-cell-deficient mice. The histamine newly formed via the induction of HDC is released immediately and may be involved in a variety of immune responses. Reviewing our work and that of Schayer and Kahlson, the pioneers in this field, lead us to the conclusion that nowadays we need to understand that histamine can be produced via the induction of HDC by a mechanism coupled with the cytokine network. We call this histamine "neohistamine", to distinguish it from the classical histamine derived from mast cells or basophils. Neohistamine is involved in physiological reactions, inflammation, immune responses and a variety of diseases such as periodontitis, muscle fatigue (or temporomandibular disorders), stress- or drug-induced gastric ulcers, rheumatoid arthritis, complications in diabetes, hepatitis, allograft rejection, allergic reactions, tumor growth, and inflammatory side effects of aminobisphosphonates.
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PMID:[Induction of histidine decarboxylase in inflammation and immune responses]. 1149 27

Inflammation of the liver may be caused by a variety of factors that include infectious agents and toxins. Reactive oxygen species (ROS) generated by the NADPH oxidase in Kupffer cells and infiltrating leukocytes play an important role in the pathogenesis of early alcohol-induced hepatitis. Histamine dihydrochloride (histamine) suppresses the generation of ROS through the histamine type-2 receptor (H2 receptor). Histamine was studied as a potential protective treatment against early alcohol-induced liver injury in an experimental hepatitis model. Female Wistar rats were given ethanol (5 g/kg) intragastrically by gavage once daily for 4 weeks, while a control group not receiving ethanol was fed an isocaloric high-fat diet. Animals receiving ethanol had elevated serum levels of alanine and aspartate transaminase (ALT/AST) and developed steatosis, inflammation, and necrosis of the liver. Histamine treatment (0.5 or 5.0 mg/kg, twice daily) protected against this liver injury as evident by normal serum transaminase levels and significantly reduced liver pathology scores. Ranitidine (10 mg/kg), an H2 receptor antagonist, blocked the protective effect of histamine, indicating that the histamine effect is predominantly mediated through the H2 receptor. In conclusion, these results suggest that histamine protects against early alcohol-induced liver injury in rats.
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PMID:Histamine dihydrochloride protects against early alcohol-induced liver injury in a rat model. 1463 89

Histamine is well known for its roles in allergic diseases and anaphylaxis through H(1)-receptor stimulation. The H(1)-receptor stimulation by histamine results in an increase in vascular permeability, vasodilatation, and stimulation of nerve terminals in primary sensory neurons, thereby accelerating the inflammatory responses. On the other hand, histamine has been demonstrated to be involved in the regulation of innate and acquired immune responses through H(2)-receptors. In a previous study with human peripheral blood mononuclear cells, we observed that histamine exerts various regulatory effects on monocyte/macrophage function. In this review, we discuss how inducible histamine protects mice from lethal hepatitis, induced by heat-killed P.acnes (1 mg, i.v.) followed by challenge with a low dose of lipopolysaccharide (1 microg), by reducing the excessive cytokine response in the liver. In addition, from in vivo studies with histidine decarboxylase knockout and H(1)-, H(2)-receptor knockout mice, the protective effect of histamine against fulminant hepatitis is shown to be elicited through H(2)-receptor stimulation.
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PMID:[Inducible histamine protects mice from hepatitis through H2-receptor stimulation]. 1823 72