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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral lichen ruber (OLR) is a chronic, recurrent disease with a worldwide prevalence of 0.9%-2.2%. In Croatia, the disease has been on a constant increase over the last 10 years, and its prevalence has reached the upper limit. The aim of the study was to identify OLR specificities in a Croatian population. The study included 100 subjects, 84 women and 16 men, mean age 53 +/- 13.88 years, with recurrent OLR. Results showed a four-fold prevalence of OLR in women as compared to men. In women, the disease was found to develop later than in men. Oral changes indicated the reticular form of the disease in 62% and erosive in 33%, whereas all other types were present in 5% of study subjects. Systemic disorders underlying OLR were found in 93% of study patients, predominantly isolated or in combination. Pathologic values of laboratory tests were recorded in 23% of study subjects. Significant differences were obtained in OLR associated with gastritis and diabetes mellitus (p < 0.05), and with gastritis and cholecystopathy (p < 0.001). Increased values of bilirubin (p < 0.01), triglycerides (p < 0.01) and blood glucose (p < 0.001) were recorded in men. The level of total lipids was significantly higher in OLR associated with cholecystopathy (p < 0.05). Accordingly, the occurrence of OLR in the Croatian population was found to be most commonly associated with the hepatobiliary system diseases, followed by gastric disorders and diabetes mellitus.
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PMID:Characteristics of oral lichen in the Croatian population. 995 Nov 44

Although much is known about the pathology of human chronic atrophic (type A, autoimmune) gastritis, its cause is poorly understood. Mouse experimental autoimmune gastritis (EAG) is a CD4+ T cell-mediated organ-specific autoimmune disease of the stomach that is induced by neonatal thymectomy of BALB/c mice. It has many features similar to human autoimmune gastritis. To obtain a greater understanding of the genetic components predisposing to autoimmune gastritis, a linkage analysis study was performed on (BALB/cCrSlc x C57BL/6)F2 intercross mice using 126 microsatellite markers covering 95% of the autosomal genome. Two regions with linkage to EAG were identified on distal chromosome 4 and were designated Gasa1 and Gasa2. The Gasa1 gene maps within the same chromosomal segment as the type 1 diabetes and systemic lupus erythematosus susceptibility genes Idd11 and Nba1, respectively. Gasa2 is the more telomeric of the two genes and was mapped within the same chromosomal segment as the type 1 diabetes susceptibility gene Idd9. In addition, there was evidence of quantitative trait locus controlling autoantibody titer within the telomeric segment of chromosome 4. The clustering of genes conferring susceptibility to EAG with those conferring susceptibility to type 1 diabetes is consistent with the coinheritance of gastritis and diabetes within human families. This is the first linkage analysis study of autoimmune gastritis in any organism and as such makes an important and novel contribution to our understanding of the etiology of this disease.
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PMID:A major linkage region on distal chromosome 4 confers susceptibility to mouse autoimmune gastritis. 1022 80

In order to study the health status of 3,333 old people (over 60) in Chengdu city, a survey was carried out from May 1996 to Nov. 1996. Results revealed that 79.4% of old people had a history of chronic diseases. The first ten common chronic diseases were stated as follows: rheumatic arthritis, hypertension, benign prostatic hypertrophy, chronic bronchitis, cataract, chronic gastritis, osteoarthrosis, asthma and diabetes mellitus. There were significant differences of body weight index, vision and auditus disorder among old people according to their age (P < 0.01). As ageing grows, old people's physical condition and daily-life-capacity decline. In order to improve the quality of life among the aged, following aspects as popularizing health education on self care, strengthening programs on prevention and care of chronic diseases, expanding the medical and nursing services in community and easier access to hospitalization etc should be promoted.
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PMID:[Study on health status of 3,333 old people in Chengdu City, Sichuan Province]. 1032 99

Helicobacter pylori (HP) is the most common cause of nonerosive nonspecific gastritis. Gastric and duadenal ulcer both are found to be associated with HP infection. Another consequence of HP infection is that it may progress to chronic atrophic gastritis which is a well recognized risk factor for adenocarcinoma of the stomach. So by extension, HP infection can be accepted as a risk factor for gastric cancer. From this aspect, identification of risk groups is increasingly important. It is well-known that patients with diabetes mellitus are more prone to infection. Besides this, presence of gastroparesis diabeticorum may lead to bacterial overgrowth in the upper gastrointestinal (GI) tract. The present crossectional study was planned to study the presence of HP infection in diabetic patients with alterations in upper GI motility and to compare the results with healthy control group. Group I consisted of 51 patients with type II diabetes mellitus (as defined by National Data Group criteria) without any dyspeptic symptoms. Twenty-five age-matched healthy people served as a control in group II. Radionuclide-labelled solid meals were used to calculate gastric emptying time (GET). According to the results, patients in group I were divided into two groups. Patients with prolonged GET were grouped as group IA, while group IB consisted of patients with normal or shortened GET. Presence of HP gastritis is determined by histopathologic examination of endoscopic biopsy specimen. The results showed that the prevalence of HP gastritis in group I and II were 80.4% and 56% respectively and the difference was significant statistically (p: 0.03). In group IA, the prevalence of HP infection was estimated to be 88.2%, while in group IB it was 76.5% but the difference was not significant (p: 0.31). We have not found any correlation between HbA1c levels and the presence of HP infection in both group IA and IB (p values 0.26 and 0.15 respectively). We conclude that the prevalence of HP gastritis is higher in asymptomatic diabetic patients compared with healthy people. But there is no association between the alterations in GET and the presence of HP gastritis as indicated by our results. So prolonged GET may not be regarded as a specific pathogenic mechanism or a cause of HP infection in NIDDM patients.
Exp Clin Endocrinol Diabetes 1999
PMID:Helicobacter pylori associated gastric pathology in patients with type II diabetes mellitus and its relationship with gastric emptying: the Ankara study. 1037 41

Unusual pneumococcal infections occurred frequently in the preantibiotic age but rapidly declined with the advent of the antibiotic era. Unfortunately, the morbidity and mortality associated with invasive pneumococcal disease remain high despite antibiotic therapy and monumental advances in medical technology. The incidence of invasive pneumococcal disease has increased recently because of the onset of the human immunodeficiency virus (HIV) epidemic and the emergence of antibiotic-resistant pneumococcus. Robert Austrian described the clinical triad of pneumococcal pneumonia, meningitis, and endocarditis, a syndrome that now bears his name. Although seen infrequently today, unusual manifestations of pneumococcal infection such as those Austrian reported still occur. A review of these cases is warranted because, as drug-resistant organisms continue to emerge worldwide, more unusual pneumococcal infections will be seen. Streptococcus pneumoniae is responsible for a remarkable array of disease processes; our literature review uncovered 95 different types of unusual pneumococcal infections representing 2,064 cases. Examples of these infections included pancreatic and liver abscesses, aortitis, gingival lesions, phlegmonous gastritis, inguinal adenitis, testicular and tubo-ovarian abscesses, and necrotizing fasciitis. We also reviewed predisposing underlying illnesses and conditions. Alcoholism, HIV infection, splenectomy, connective tissue disease, steroid use, diabetes mellitus, and intravenous drug use remain common risk factors for invasive pneumococcal infections. Currently, multidrug-resistant S. pneumoniae remains susceptible to vancomycin and several new third-generation fluoroquinolones. As what some fear will be a possible postantibiotic era approaches, clinicians must be able to recognize and manage unusual pneumococcal infections.
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PMID:Unusual manifestations of invasive pneumococcal infection. 1045 Oct 5

The history of a 45-year-old male type 1 diabetic patient is presented. At the age of 29 years, he was diagnosed to have an autoimmune hepatitis with incipient liver cirrhosis. Five years later, a successful liver/pancreas transplantation was performed. Eighteen months later, however, pancreatic insufficiency occurred due to thrombosis of the pancreatic graft. Besides these conditions, iron deficiency, pernicious anemia, and autoimmune gastritis were also diagnosed. Serum parietal cell antibodies (PCA) and intrinsic factor antibodies (AIF) were positive. At 45, this patient was found to have a gastric carcinoid tumor. The clinical importance of PCA is discussed with regard to chronic atrophic gastritis and pernicious anemia, which both predispose toward gastric carcinoid tumors. Autoimmune type 1 diabetic patients who have a high prevalence of PCA should be screened for gastric autoimmune manifestations and tumors, as the history of this patient illustrates.
J Diabetes Complications
PMID:Autoimmune hepatitis, autoimmune gastritis, and gastric carcinoid in a type 1 diabetic patient: a case report. 1095 74

Helicobacter pylori (Hp) infection plays a role in gastric emptying (GE) in type 1 diabetic patients and may have implications for glycaemic control. The aim of our study was to investigate this relationship. Gastric emptying was studied in 13 patients with type 1 diabetes and Hp infection. The Hp infection status was assessed by serology and urease breath test (UBT). In addition upper gastrointestinal endoscopy with gastric mucosal biopsy was performed to look for gastritis. A radionuclide-labeled solid meal was used to study GE before and after eradication therapy (amoxicillin, clarithromycin and omeprazole) for Hp infection. All patients were evaluated for autonomic and peripheral neuropathy and were asked for symptoms of gastrointestinal motor dysfunction. Blood glucose levels were determined before the meal and at 30,60,90 and 120 min after the start of the meal. Home blood glucose self-monitoring and HbA(1c) were performed to document glycaemic control during the study. Three months after treatment, five patients were free of Hp infection and were without gastritis (group I: no Hp infection, no gastritis); eight of the patients continued to have gastritis after treatment (group II) and of these eight patients, six had gastritis without Hp infection and two had gastritis plus persistent Hp infection. These last two patients were re-treated with eradication therapy. Patients with gastritis were re-evaluated 6 months after initial treatment; at which time four were now free of gastritis and were added to group I (n=9) while four continual to have gastritis although without Hp infection (group II, n=4). In group I, GE half-time showed an increase (30.6+/-10.3 min vs. 60.2+/-15.4 min; P<0.05) while no change (28.8+/-9.5 vs. 26.9+/-8.7 min; n.s.) was observed in group II. GE half-time was not altered by autonomic and peripheral neuropathy or blood glucose during solid meal test. HbA(1c) did not change significantly after treatment in either groups but the blood glucose levels were more stable in group I compared to group II. A delay in GE was observed with disappearance of gastritis associated to H. pylori infection after eradication treatment in patients with type 1 diabetes. This change in GE could help to stabilise the blood glucose levels in these patients treated with insulin before each meal.
Diabetes Res Clin Pract 2001 Apr
PMID:Effect of the treatment of Helicobacter pylori infection on gastric emptying and its influence on the glycaemic control in type 1 diabetes mellitus. 1118 11

As available data on Helicobacter pylori infection in patients with diabetes are scattered and discordant, we evaluated the prevalence of H. pylori and its relationship to dyspeptic symptoms in adult patients with diabetes and subjects with dyspepsia. H. pylori infection (evaluated using the 13C urea breath test) and dyspeptic symptoms (nausea, bloating, and epigastric distress) were investigated in 71 consecutive diabetic outpatients; the presence of gross lesions, histologic gastritis, and Helicobacter was verified in the patients with a positive urea test who agreed to undergo upper gastrointestinal tract endoscopy. Seventy-one age- and gender-matched subjects with dyspepsia were used as controls. Helicobacter pylori infection was detected in 49 (69%) patients with diabetes and in 33 (46%) subject with dyspepsia (p = 0.007). Helicobacter pylori was present in 27 (77%) of 35 patients with diabetes with dyspeptic symptoms and in 22 (61%) of 36 patients without dyspeptic symptoms. Endoscopy revealed peptic ulcers in 13 of 23 patients; H. pylori infection was histologically confirmed in the gastric antrum of all patients with diabetes, and in the body of the stomach in 74%. The significantly higher prevalence of H. pylori infection in the patients with diabetes may partially explain their dyspeptic symptoms. The high prevalence of H. pylori infection, esophagitis, and peptic ulcers found in our patients with diabetes (with or without dyspepsia) suggests that this population should be considered "at risk" for H. pylori infection and suitable candidates for treatment.
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PMID:Helicobacter pylori prevalence in patients with diabetes and its relationship to dyspeptic symptoms. 1124 46

Recently, H. pylori has been associated with several extradigestive diseases such as cardio-vascular, cutaneous, autoimmune, allergic, liver, hematologic disorders, diabetes mellitus, pediatric diseases (sudden infant death syndrome, growth retardation), extragastric MALT-type lymphomas and even colorectal cancer. The potential role of H. pylori infection in the pathogenesis of these extradigestive disorders has been based on the following facts: 1) local gastric infection with H. pylori may exert systemic effects; 2) during chronic H. pylori induced gastritis several different inflammatory mediators are released that are able to cause disorders remote to the primary site of infection and 3) the successful eradication of H. pylori infection improves partly or completely the extradigestive disorders. The available data is conflicting because of the presence of several confounding factors in epidemiological studies. On the basis of the published data any of these associations has been proved. Further prospective studies to explain the association between H. pylori and extradigestive disorders are needed.
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PMID:[Extragastric manifestations of H. pylori infection]. 1136 80

Helicobacter pylori infection has been described in association with increases in glycated hemoglobin (HbA(1c)) levels in patients with type 1 diabetes. The purpose of the present study was to use an animal model of Helicobacter infection to test, under controlled conditions, the hypothesis that infection is associated with high HbA(1c) levels. Diabetes was induced in C57BL/6 mice by administration of streptozotocin, and the mice were orally inoculated with H. felis. Six weeks after inoculation, infected mice (n=10) showed gastritis scores significantly greater (P=.01) than those of uninfected mice (n=10). HbA(1c) levels were significantly higher in infected mice with gastritis (11.6%; n=6) than in infected mice without gastritis (8.4%; n=4) or uninfected mice (7.6%; n=10). It was concluded that gastritis induced by H. felis is associated with increased HbA(1c) levels in the mouse model of streptozotocin-induced diabetes.
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PMID:Association between Helicobacter felis-induced gastritis and elevated glycated hemoglobin levels in a mouse model of type 1 diabetes. 1199 82


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