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)

Macrophage migration inhibitory factor (MIF) is a unique protein, participating in inflammation, immune response, and cell growth. MIF was first discovered as a lymphokine involved in delayed hypersensitivity and various macrophage functions, including phagocytosis, spreading, and tumoricidal activity. It has been reported that MIF is associated with the pathogenesis of a variety of diseases. MIF expression was increased at inflammatory sites in diseases such as rheumatoid arthritis and glomerulonephritis. In experimental inflammatory disease, blockade of MIF bioactivity inhibited the severity of disease activity. On the other hand, MIF expression is also increased in tumor lesions, and MIF plays a role as a cell growth factor. MIF has been reported to be constitutively expressed in gut, liver, and pancreas. In patients with gastritis, inflammatory bowel disease, hepatitis, and pancreatitis, MIF expression was remarkably increased in both the serum and the local lesions. Blockade of MIF bioactivity inhibited and prevented inflammation in experimental gastritis, colitis, hepatitis, and pancreatitis. On the other hand, MIF expression was higher than that in normal tissues in colonic carcinomas and hepatocellular carcinoma both in vivo and in vitro. Blockade of MIF bioactivity successfully inhibited tumor cell growth in vivo and in vitro. MIF plays important roles in the pathogenesis of gastrointestinal, hepatic, and pancreatic disorders.
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PMID:Pathophysiological roles of macrophage migration inhibitory factor in gastrointestinal, hepatic, and pancreatic disorders. 1577 Mar 93

Rheumatoid arthritis is the commonest form of inflammatory arthritis and affects about 1-3% of the population in the West and even more in the developing world due to the compounded factors of late detection and inadequate treatment in the overall background of poverty, deprivation, and improper macro and micronutrients in the diet in a sizeable segment of the population. Nearly 90% of patients with aggressive disease will become clinically disabled within 20 years. Furthermore, in patients with severe disease or extra-articular symptoms, mortality is equal to that for patients with triple artery coronary artery disease or Stage IV Hodgkin's lymphoma. Anemia is a very common comorbidity of rheumatoid arthritis. Anemia in rheumatoid arthritis is caused by various factors, for instance, cytokine impact of the advanced arthritic process on the host, or lack of proper nutrition and essential micronutrients in the diet, or coexistent helminthiasis, and/or impact of antiarthritic drugs on the host system, i.e., high steroid induced gastritis or ulcerations in gastric mucosa or subclinical or clinical hepatitis due to methotrexate or salazopyrin effects on bone marrow, only to name a few. Other pre-existing or compounding gastrointestinal problems, which alter the available iron stores or cause bone marrow dysfunction, may also help in adding to an anemic condition. If the anemia is 8 g/dl or less, blood transfusion or erythropoietin injection with adequate hematinic reserve is effective in normal situations, but is not that effective in anemia with a chronic disease background like rheumatoid arthritis. Cord blood, because of its rich mix of fetal and adult hemoglobin, high platelet and white blood cell (WBC) counts, and a plasma filled with cytokine and growth factors, as well as its hypo antigenic nature and altered metabolic profile, has all the potential of a real and safe alternative to adult blood transfusion. Seventy-eight units (42 ml -136 ml mean 80.6 ml +/- 3.6 ml SD, median 82.4 ml, mean packed cell volume 48.2 +/- 2.1 SD, mean percent hemoglobin concentration 16.4 g/dl +/- 1.5 g/dl SD) of placental umbilical cord whole blood was transfused (from 1 April 1999 to April 2005) after lower uterine cesarean section (LUCS) from consenting mothers to 28 informed consenting patients with advanced rheumatoid arthritis who had plasma hemoglobin of 8 g/dl or less. After collection, the blood was immediately transfused following the standard adult blood transfusion protocol. Each case was passed through the institutional ethical committee. The patients received two to six units of freshly collected placental umbilical cord blood without encountering any clinical, immunological or non-immunological reactions. Three days after completion of the transfusion of placental umbilical cord blood, the peripheral blood hematopoietic stem cell (CD34) estimation revealed a rise from the pretransfusion base level (.09%), varying from 2.03 to 23%, which returned to base level in most of the cases at the three-month CD34 re-estimation, without provoking any clinical graft vs host reaction in any of the patients.
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PMID:Placental umbilical cord whole blood transfusion to combat anemia in the background of advanced rheumatoid arthritis and emaciation and its potential role as immunoadjuvant therapy. 1676 35

Glucocorticoids are usually given for management of Graves' ophthalmopathy (GO) for their anti-inflammatory and immunosuppressive effects. The overall rate of favorable response for moderately severe and active GO is 77% in patients treated with methylprednisolone iv pulse therapy. When radioiodine therapy is indicated for hyperthyroidism in Graves' patients with high risk factors, the use of glucocorticoid with small doses and short periods is recommended to prevent the development or progression of GO. Cushingoid features, glucose intolerance, gastritis, hypertension, hepatitis, and depression are major adverse effects of glucocorticoids. Fatal liver failure after high dose of pulse therapy (9-12g) was observed in 0.8%. Limiting the cumulative dose to 4.5-6g, assessment of liver virus markers and monitoring liver function before, during and after i.v. treatment are warranted.
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PMID:[Steroid therapy for Graves' ophthalmopathy]. 1715 92

In April 2007, an international Colloquium bridging scientific and clinical disciplines was held to discuss the role of cellular and tissue damage in the initiation, development and persistence of autoimmune disease. Five potential etiologic and pathophysiologic processes fundamental to autoimmune disease (i.e. inflammation, infection, apoptosis, environmental exposure and genetics) were the focus of the presentations and integrative discussions at the Colloquium. The information presented on these topics is condensed in this review. Inflammation has close clinico-pathologic associations with autoimmunity, but future analyses will require better definition and metrics of inflammation, particularly for the earliest cellular and molecular components dependent on recruitment of elements of innate immunity. Although infection may be associated with increased levels of autoantibodies, most infections and virtually all vaccinations in humans lack well-established links to autoimmune diseases. Further application of well-designed, long-term epidemiologic and population-based studies is urgently needed to relate antecedent exposures with later occurring stigmata of autoimmunity with a goal of discerning potentially susceptible individuals or subpopulations. Suspect infections requiring closer interrogation include EB virus (SLE and other diseases), HCV (autoimmune hepatitis), beta hemolytic streptococci (rheumatic carditis) and Helicobacter pylori (autoimmune gastritis) among others. And even if a micro-organism was to be incriminated, mechanisms of initiation/perpetuation of autoimmunity continue to challenge investigators. Plausible mechanisms include potentiation and diversion of innate immunity; exposure or spillage of intracellular autoantigens; or provision of autoantigenic mimics. Integrity of apoptosis as a critical safeguard against autoimmunity was discussed in the contexts of over-reactivity causing autoantigens to gain enhanced exposure to the immune system, or under-reactivity producing insufficient elimination of autoreactive clones of lymphocytes. Although environmental agents are widely believed to serve as necessary "triggers" of autoimmune disease in genetically predisposed individuals, only a few such agents (mainly drugs and some nutrients) have been clearly identified and their mechanism of action defined. Finally an essential genetic foundation underlies all these hazards for autoimmunity in the form of risk-associated polymorphisms in immunoregulatory genes. They may be predictive of future or impending disease.
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PMID:Cell damage and autoimmunity: a critical appraisal. 1819 28

A 24-year-old Vietnamese woman presented with a 3-month history of non-itchy erythematous plaques on the face, trunk and limbs. Borderline lepromatous leprosy was confirmed by clinical findings, acid-fast bacilli on skin biopsy specimen and skin smear and a history of exposure. Around the twentieth day of World Health Organization (WHO) multibacillary standard treatment (rifampin 600 mg per month, dapsone 100 mg per day, clofazimine 300 mg per month and 50 mg per day for 1 year), she developed fever, general malaise, blurred vision, cough, nausea, epigastric pain, and arthralgia. The skin lesions also became swollen. During hospitalization, her illness was complicated by retrobulbar optic neuritis, secondary bacterial pneumonia, pleuritis, ascites, hepatitis, antral gastritis, progressive normocytic anemia, and peripheral sensory loss. The patient recovered after receiving systemic steroid pulse therapy (prednisolone equivalent dose 1250 mg) with systemic antibiotics (cefuroxime), adjustment of her anti-lepromatous therapy, and supportive care. She resumed the WHO multibacillary regimen uneventfully. This patient presented with a diverse type 1 reaction, which is a complex immune response in leprosy. We found that the judicious use of high dose steroids followed by a slow tapering course is beneficial in managing patients with a severe type 1 reaction. At the 1-year follow up, the patient had generalized skin hyperpigmentation resulted from long-term clofazamine use and numbness on feet without other systemic sequelae.
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PMID:Corticosteroid pulse therapy for leprosy complicated by a severe type 1 reaction. 1856 21

CMV infection is one of the major causes of morbidity and mortality after HSCT. The aim of this single center retrospective study was to analyze risk factors for CMV infection in pediatric patients who underwent HSCT. We retrospectively reviewed the medical records of 117 pediatric patients who underwent allogeneic HSCT at Asan Medical Center between December 2000 and January 2007. After HSCT, CMV antigenemia was detected by identifying CMV pp65 early antigen in white blood cells. The incidence of CMV antigenemia was 24% (28/117) at a median of 38 days (range: 19-123 days) after HSCT. In multivariate analysis, CMV antigenemia occurred significantly more often in CMV seropositive recipients, patients who received grafts from alternative donors, T-cell depleted grafts, patients on ATG-containing conditioning regimens, or patients who received steroid for acute GVHD (p < 0.05). CMV antigenemia tend to develop earlier in patients who received ATG-containing conditioning regimens (p = 0.09). A second episode of CMV antigenemia was observed in three out of 28 patients (11%). The incidence of CMV disease was 5.9% (7/117) at a median of 97 days (range: 34-120 days). Manifestation of CMV disease included retinitis in two, pneumonitis in two, hepatitis in one, hepatitis with colitis in one, and gastritis in one. Six of the 12 patients (50%) with HG antigenemia (CMV pp65 antigen positivity > or =40 cells) developed clinical CMV disease, a rate that was significantly higher than seen in patients with LG antigenemia (6.25%; p < 0.01). We recommend that patients with these risk factors should carefully undergo regular evaluations for CMV infection. We also suggest that earlier and more aggressive preemptive treatment and serial follow-up of CMV disease is necessary in patients with HG-antigenemia.
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PMID:Cytomegalovirus infection in children who underwent hematopoietic stem cell transplantation at a single center: a retrospective study of the risk factors. 1903 14

Adolescence is a period of rapid growth and physical change; a central question is whether consuming alcohol during this stage can disrupt development in ways that have long-term consequences. In general, the existing evidence suggests that adolescents rarely exhibit the more severe chronic disorders associated with alcohol dependence such as liver cirrhosis, hepatitis, gastritis, and pancreatitis. Adolescents who drink heavily, however, may experience some adverse effects on the liver, bone, growth, and endocrine development. Evidence also is mounting, at least in animal models, that early alcohol use may have detrimental effects on the developing brain, perhaps leading to problems with cognition later in life. This article summarizes the physiological effects of alcohol on adolescents, including a look at the long-term behavioral and physiological consequences of early drinking.
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PMID:The effects of alcohol on physiological processes and biological development. 1909 86

Helicobacter pylori infection is associated with chronic gastritis, peptic ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Some reports also suggest that it causes extragastric disease, including hepatitis. In this study, the pathological changes in the liver and gall bladder in H. pylori-colonized C57BL/6 mice were investigated. Twenty mice were inoculated orally with H. pylori strain SS1, and ten controls were injected with phosphate-buffered saline. Gastric colonization with H. pylori was assessed at 2 months after inoculation. Mice were examined at 8 months by histopathology, culture for H. pylori, and PCR for specific H. pylori genes. All C57BL/6 mice infected with H. pylori for 8 months developed severe gastric mucosal inflammation. Three mice showed mild-to-moderate multifocal hepatitis. The gall bladder mucosa of one H. pylori-infected mouse showed thickening of the mucous membrane with mild submucosal lymphocytic infiltration. H. pylori was observed morphologically in four liver specimens and six gall bladders from infected mice by immunohistochemistry. Specific H. pylori genes were also detected in six liver samples from infected mice, six samples of bile, and two blood samples by nested PCR. Thus, H. pylori inoculated orally may reach the hepatobiliary system and cause inflammation as an independent aetiological factor. The pathway to the liver may be via the blood or the biliary system.
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PMID:The pathological effect of Helicobacter pylori infection on liver tissues in mice. 1939 1

Chronic mucocutaneous candidiasis is a primary immunodeficiency characterized by persistent or recurrent candidal infections of the skin, nails and/or mucosal tissues. CMC can be associated with endocrinopathies such as hypoparathyroidism, Addison's disease, hypothyroidism, type 1 diabetes mellitus or hypogonadism. Other associated conditions include autoimmune diseases such as autoimmune gastritis and autoimmune hepatitis. We report a patient with CMC and decreased T cell, natural killer cells without other associated condition.
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PMID:[Chronic mucocutaneous candidiasis: Case report]. 2046 98

The proton pump inhibitors (PPIs) as a class are remarkably safe and effective for persons with peptic ulcer disorders. Serious adverse events are extremely rare for PPIs, with case reports of interstitial nephritis with omeprazole, hepatitis with omeprazole and lansoprazole, and disputed visual disturbances with pantoprazole and omeprazole. PPI use is associated with the development of fundic gland polyps (FGP); stopping PPIs is associated with regression of FGP. In the absence of Helicobacter pylori infection, the long-term use of PPIs has not been convincingly proven to cause or be associated with the progression of pre-existing chronic gastritis or gastric atrophy or intestinal metaplasia. Mild/modest hypergastrinemia is a physiological response to the reduction in gastric acid secretion due to any cause. The long-term use of PPIs has not been convincingly proven to cause enterochromaffin-like cell hyperplasia or carcinoid tumors. PPIs increase the risk of community acquired pneumonia, but not of hospital acquired (nosocomial) pneumonia. There is no data to support particular care in prescribing PPI therapy due to concerns about risk of hip fracture with the long-term use of PPIs. Long-term use of PPIs does not lead to vitamin B12 deficiencies, except possibly in the elderly, or in persons with Zollinger-Ellison Syndrome who are on high doses of PPI for prolonged periods of time. There is no convincingly proven data that PPIs increase the risk of Clostridium difficile-associated diarrhea in persons in the community. The discontinuation of PPIs may result in rebound symptoms requiring further and even continuous PPI use for suppression of symptoms. As with all medications, the key is to use PPIs only when clearly indicated, and to reassess continued use so that long-term therapy is used judiciously. Thus, in summary, the PPIs are a safe class of medications to use long-term in persons in whom there is a clear need for the maintenance of extensive acid inhibition.
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PMID:Safety of the long-term use of proton pump inhibitors. 2048 May 16


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