Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although most studies reporting on the examination of Helicobacter pylori infection have focused on the clearance of the bacteria and the rapid disappearance of the neutrophil infiltrates, the evolution of inflammatory and architectural changes in the antral and corporal mucosa following the eradication of H. pylori has not been addressed systematically. This study examines in detail the histopathologic appearance of the antral and corporal mucosa in a group of patients infected with H. pylori and follows the spectrum of morphologic changes in each of them after the eradication of the infection. At least 11 biopsies ("gastric mapping") were obtained from the antrum and body of each of 15 patients with H. pylori. Complete mapping was then repeated 1, 4, and 10 to 12 mo after the eradication of H. pylori by a course of "triple therapy." Each biopsy was assessed in a semi-quantitative fashion for presence of H. pylori, neutrophils, eosinophils, lymphocytes, lymphoid follicles, and intestinal metaplasia. Other features (integrity of surface epithelium, architecture, fibrosis) were evaluated descriptively. Results were compared with those obtained from a control group of 16 uninfected, healthy adult volunteers. H. pylori infection was eradicated in 11 subjects. The disappearance of neutrophils and the normalization of the surface epithelium closely paralleled that of H. pylori. Persistence of even small numbers of neutrophils was a predictor of relapse. Eosinophils and lymphocytes decreased slowly and did not return to normal levels within 1 yr. Lymphoid follicles decreased very slowly in all patients but were still present in all gastric locations at one year after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in the gastric mucosa following eradication of Helicobacter pylori. 834 76

We report the case of a 63 year-old female who presented with a seven-year history of epigastric pain and a sudden overall deterioration. Gastroscopy demonstrated inflammatory aspect and ulceration in the antrum and fundus. Histology showed a lymphocytic infiltrate consistent with low grade mucosa-associated lymphoid tissue lymphoma and cytomegalovirus gastritis. There was no evidence of Helicobacter pylori infection. Other investigations demonstrated two pulmonary foci consistent with lymphomatous infiltration and a reduced CD4 + T-lymphocyte count (85/mm3). Other screening tests including HIV serology were negative. This case of idiopathic CD4 lymphopenia, in conjunction with the other rare cases in the literature, allows us to reevaluate this condition and its unusual clinical presentation with two opportunistic pathologies.
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PMID:[Multifocal MALT lymphoma and acute cytomegalovirus gastritis revealing CD4 lymphopenia without HIV infection]. 1021 14

The two-stage neuroinflammatory process, containment and progression, proposed to underlie neurodegeneration may predicate on systemic inflammation arising from the gastrointestinal tract. Helicobacter infection has been described as one switch in the pathogenic-circuitry of idiopathic parkinsonism (IP): eradication modifies disease progression and marked deterioration accompanies eradication-failure. Moreover, serum Helicobacter-antibody-profile predicts presence, severity and progression of IP. Slow gastrointestinal-transit precedes IP-diagnosis and becomes increasingly-apparent after, predisposing to small-intestinal bacterial-overgrowth (SIBO). Although IP is well-described as a systemic illness with a long prodrome, there has been no comprehensive overview of the blood profile. Here, it is examined in relation to Helicobacter status and lactulose-hydrogen-breath-testing for SIBO. A robust finding of reduced lymphocyte count in 126 IP-probands and 79 spouses (without clinically-definite IP), compared with that in 381 controls (p < 0.001 in each case), was not explained by Helicobacter-status or breath-hydrogen. This complements a previous report that spouses were 'down-the-pathway' to 'clinically-definite' disease. In 205 other controls without clinically-definite IP, there were strong associations between sporadic cardinal features and immunoglobulin class concentration, not explained by Helicobacter-status. Premonitory states for idiopathic parkinsonism associated with relative lymphopenia, higher serum immunoglobulin concentrations and evidence of enteric-nervous-system damage may prove viral in origin.Although only 8% of the above 79 spouses were urea-breath-test-positive for Helicobacter, all 8 spouses with clinically-definite IP were (p < 0.0001). Transmission of a 'primer' to a Helicobacter-colonised recipient might result in progression to the diagnostic threshold. Twenty-five percent of the 126 probands were seropositive for anti-nuclear autoantibody. In 20 probands, monitored before and serially after anti-Helicobacter therapy, seropositivity marked a severe hypokinetic response (p = 0.03). It may alert to continuing infection, even at low-density. Hyperhomocysteinemia is a risk factor for dementia and depression. Serum homocysteine exceeded the target in 43% of the 126 IP-probands. It was partially explained by serum B12 (12% variance, p < 0.001), but not by Helicobacter-status (gastric-atrophy uncommon in IP) or levodopa treatment. Immune-inflammatory activation increases homocysteine production. Since an estimated 60% of probands are hydrogen-breath-test positive, SIBO, with its increased bacterial utilisation of B12, is a likely cause. Thus, two prognostic indicators in established IP fit with involvement of Helicobacter and SIBO.
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PMID:Blood profile holds clues to role of infection in a premonitory state for idiopathic parkinsonism and of gastrointestinal infection in established disease. 1994 60