Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this work was to ascertain if diabetes and obesity can affect gastric colonization by Helicobacter pylori. 59 hospitalized subjects with dyspepsia and endoscopic antral gastritis were selected. They were divided into three groups: I) 13 patients with normal body weight and without disease other than gastritis (control group); II) 15 patients with essential obesity of whom 10 had impaired glucose tolerance (IGT); III) 31 patients with type II diabetes mellitus, of whom 14 were obese. Three gastric biopsies were obtained from each patient for histologic examination and H. pylori detection by means of rapid urea test, culture and histological evidence of Helicobacter-Like Organisms (HLO). Age, sex, blood glucose, cholesterol, triglycerides, HDL-cholesterol, basal gastrine, duration of illness, body weight were statistically analysed. Differences between the three groups were not statistically significant. There was a higher prevalence of H. pylori infection both in obese and in diabetic patients with respect to control subjects. Prevalence became still higher in obese patients with impaired glucose tolerance. Among the three tests used for the detection of H. pylori, culture and rapid urea were reliable and specific, while the histologic test was highly sensitive but barely specific. Our data suggest that both obesity and type II diabetes may be associated with an increased incidence of H. pylori-colonization. This could be related to the reduced gastric motility observed in both pathologies and chemical changes in gastric mucosa following non-enzymatic glycosylation processes.
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PMID:Gastric infection by Helicobacter pylori and antral gastritis in hyperglycemic obese and in diabetic subjects. 872 11

Diabetic patients often suffer from symptoms arising from the gastrointestinal tract. Several factors are considered responsible for these alterations, including abnormalities of gastric motility. Recently Helicobacter pylori (HP) has been identified in a relevant aliquot of subjects with or without gastrointestinal abnormalities, but only scarce and controversial data are available on the prevalence of HP and the association between HP and chronic gastritis or peptic ulcer in diabetic patients. In addition, the possible association between alterations of gastric motility induced by autonomic neuropathy (AN) and the presence of HP has never been evaluated in diabetic subjects. In this study we document the presence of HP in the gastric biopsies of 73% out of a series of 29 patients affected by type 2 diabetes and non-ulcer dyspepsia (3 with oesophagitis, 10 with gastritis, 7 with bulbar duodenitis, and 9 with a normal endoscopy), with a significantly higher prevalence (P < 0.01) in subjects with AN (74%) than in subjects without AN (26%). Two other tests have been compared with the histological evidence of HP (used as golden standard), i.e. the urease test (CP-test) and the assay of anti-HP G-immunoglobulins, both of which were positive in a significantly (P < 0.01) higher percentage of neuropathic patients in comparison with non-neuropathic patients. The sensitivity and the specificity of the CP-test were 96% and 100%, respectively. Similarly, both the sensitivity and the specificity of the assay of IgG HP-Ab were 100%. Since patients affected by non-ulcer dyspepsia and NIDDM complicated by autonomic neuropathy are under a higher risk to be carriers of HP than non-neuropathic or non-diabetic patients. The assay of serum IgG HP-Ab could be used as a screening method, thus avoiding the more expensive and time-consuming endoscopy.
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PMID:Non-ulcer dyspepsia and Helicobacter pylori in type 2 diabetic patients: association with autonomic neuropathy. 879 6

A high prevalence of upper gastrointestinal symptoms is described in diabetic patients and, at least in part, this has been attributed to abnormal emptying of the stomach. In an unselected small series of dyspeptic patients with Type 2 diabetes mellitus (DM2), we previously described a higher prevalence of Helicobacter pylori (Hp) infection associated with autonomic neuropathy (AN) than in non-diabetic subjects. To evaluate the prevalence of Hp and its relationship with AN, we studied 164 DM2 patients, matched for sex, age ( +/- 5 years) and body weight ( +/- kg) to 164 non-diabetic subjects, all affected with dyspepsia of unknown origin. Results document that the prevalence of peptic ulcer is similar in both groups of patients (20.1 vs 29.3% P = n.s.); chronic gastritis was 50% in the control group and 35.4% in the DN2 group (P < 0.01) and dyspepsia without ulcer and gastritis (simple dyspepsia) was significantly more frequent in DM2 patients than in non-diabetics (44.5 vs 20.7%, P < 0.01). Hp infection was documented by histology of gastrointestinal mucosa in 74.4% of the DM2 patients and in 50% of the controls (P < 0.01) (ulcer: 97 vs 71%, P < 0.05; gastritis: 72 vs 43.5%, P < 0.05; simple dyspepsia: 66 vs 35%, P < 0.01, respectively). Autonomic neuropathy was found in 65.2% of the DM2 patients (90.9% of patients with ulcer, 65.5% with gastritis and 53.4% with simple dyspepsia). A significant concordance (84.7%, P < 0.001) was found between the presence of AN and Hp infection. Data provide, for the first time, direct evidence for a higher frequency of Hp infection in dyspeptic patients affected with DM2 than in non-diabetic subjects. In addition, in diabetic patients the frequency of non-ulcer, non-gastritis dyspepsia is two times higher than in non-diabetics and is strictly associated with autonomic neuropathy, acting as a favoring factor for occurrence and recurrence of gastrointestinal disease.
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PMID:The role of autonomic neuropathy as a risk factor of Helicobacter pylori infection in dyspeptic patients with type 2 diabetes mellitus. 988 32

The relationship between diabetes and Helicobacter pylori (HP) infection is controversial. In this study, we examined the possible relationship between HP infection and type 2 diabetes in Chinese subjects. Sixty-three Chinese type 2 diabetic patients (mean age +/- SD: 49.9 +/- 12.0 years; range: 17-76 years) were recruited irrespective of the duration of diabetes or type of therapy. Twenty-nine (46%) of them had upper gastrointestinal symptoms and the other 34 (54%) did not. Another 55 age- and sex-matched non-diabetic subjects (mean age +/- SD: 45.6 +/- 15.6 years, p=0.098; range 18-79 years) with dyspepsia indicated for upper endoscopy were recruited as a comparison group. Upper endoscopy was performed with antral mucosal biopsy specimens taken for rapid urease test (CLO test). HP infection was considered to be present if the rapid urease test was positive. The rates of HP infection of the diabetic and non-diabetic individuals were 50.8% and 56.4% respectively (p: NS). The rate of HP infection was similar between the 2 groups of diabetic patients with or without gastrointestinal symptoms (42.9% vs. 56.3%, p: NS). Using logistic regression analysis (forward stepwise) with age, sex, glycaemic control, duration of diabetes and upper gastrointestinal symptoms as independent variables to predict the risk of HP infection in diabetic patients, none of the parameters enter into the model. In conclusion, the rate of HP infection in Hong Kong Chinese subjects with type 2 diabetes is around 50%, which is similar to control subjects. No association was found between HP infection, glycaemic status, and duration of diabetes and upper gastrointestinal symptoms in these diabetic subjects.
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PMID:Helicobacter pylori infection in Chinese subjects with type 2 diabetes. 1142 8

Metformin is an effective and commonly administered drug for controlling plasma glucose concentrations in patients with type 2 diabetes mellitus. Gastrointestinal adverse effects such as abdominal pain, nausea, dyspepsia, anorexia, and diarrhea are common and widely accepted when occurring at the start of metformin therapy. Diarrhea occurring long after the dosage titration period is much less well recognized. Our patient began to experience nausea, abdominal cramping, and explosive watery diarrhea that occasionally caused incontinence after several years of stable metformin therapy A trial of metformin discontinuation resolved all gastrointestinal symptoms. A review of the literature revealed two reports that suggest diarrhea occurring long after the start of metformin therapy is relatively common, based on surveys of patients with diabetes. Metformin-induced diarrhea is differentiated from diabetic diarrhea, which is clinically similar, except diabetic diarrhea is rare in patients with type 2 diabetes. Patients with type 2 diabetes who are taking metformin and experience diarrhea deserve a drug-free interval before undergoing expensive and uncomfortable diagnostic tests, even when the dosage has been stable over a long period.
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PMID:Metformin as a cause of late-onset chronic diarrhea. 1171 16

Diabetic autonomic neuropathy (DAN) is a serious and common complication of diabetes. Despite its relationship to an increased risk of cardiovascular mortality and its association with multiple symptoms and impairments, the significance of DAN has not been fully appreciated. The reported prevalence of DAN varies widely depending on the cohort studied and the methods of assessment. In randomly selected cohorts of asymptomatic individuals with diabetes, approximately 20% had abnormal cardiovascular autonomic function. DAN frequently coexists with other peripheral neuropathies and other diabetic complications, but DAN may be isolated, frequently preceding the detection of other complications. Major clinical manifestations of DAN include resting tachycardia, exercise intolerance, orthostatic hypotension, constipation, gastroparesis, erectile dysfunction, sudomotor dysfunction, impaired neurovascular function, "brittle diabetes," and hypoglycemic autonomic failure. DAN may affect many organ systems throughout the body (e.g., gastrointestinal [GI], genitourinary, and cardiovascular). GI disturbances (e.g., esophageal enteropathy, gastroparesis, constipation, diarrhea, and fecal incontinence) are common, and any section of the GI tract may be affected. Gastroparesis should be suspected in individuals with erratic glucose control. Upper-GI symptoms should lead to consideration of all possible causes, including autonomic dysfunction. Whereas a radiographic gastric emptying study can definitively establish the diagnosis of gastroparesis, a reasonable approach is to exclude autonomic dysfunction and other known causes of these upper-GI symptoms. Constipation is the most common lower-GI symptom but can alternate with episodes of diarrhea. Diagnostic approaches should rule out autonomic dysfunction and the well-known causes such as neoplasia. Occasionally, anorectal manometry and other specialized tests typically performed by the gastroenterologist may be helpful. DAN is also associated with genitourinary tract disturbances including bladder and/or sexual dysfunction. Evaluation of bladder dysfunction should be performed for individuals with diabetes who have recurrent urinary tract infections, pyelonephritis, incontinence, or a palpable bladder. Specialized assessment of bladder dysfunction will typically be performed by a urologist. In men, DAN may cause loss of penile erection and/or retrograde ejaculation. A complete workup for erectile dysfunction in men should include history (medical and sexual); psychological evaluation; hormone levels; measurement of nocturnal penile tumescence; tests to assess penile, pelvic, and spinal nerve function; cardiovascular autonomic function tests; and measurement of penile and brachial blood pressure. Neurovascular dysfunction resulting from DAN contributes to a wide spectrum of clinical disorders including erectile dysfunction, loss of skin integrity, and abnormal vascular reflexes. Disruption of microvascular skin blood flow and sudomotor function may be among the earliest manifestations of DAN and lead to dry skin, loss of sweating, and the development of fissures and cracks that allow microorganisms to enter. These changes ultimately contribute to the development of ulcers, gangrene, and limb loss. Various aspects of neurovascular function can be evaluated with specialized tests, but generally these have not been well standardized and have limited clinical utility. Cardiovascular autonomic neuropathy (CAN) is the most studied and clinically important form of DAN. Meta-analyses of published data demonstrate that reduced cardiovascular autonomic function as measured by heart rate variability (HRV) is strongly (i.e., relative risk is doubled) associated with an increased risk of silent myocardial ischemia and mortality. The determination of the presence of CAN is usually based on a battery of autonomic function tests rather than just on one test. Proceedings from a consensus conference in 1992 recommended that three tests (R-R variation, Valsalva maneuver, and postural blood pressure testing)or longitudinal testing of the cardiovascular autonomic system. Other forms of autonomic neuropathy can be evaluated with specialized tests, but these are less standardized and less available than commonly used tests of cardiovascular autonomic function, which quantify loss of HRV. Interpretability of serial HRV testing requires accurate, precise, and reproducible procedures that use established physiological maneuvers. The battery of three recommended tests for assessing CAN is readily performed in the average clinic, hospital, or diagnostic center with the use of available technology. Measurement of HRV at the time of diagnosis of type 2 diabetes and within 5 years after diagnosis of type 1 diabetes (unless an individual has symptoms suggestive of autonomic dysfunction earlier) serves to establish a baseline, with which 1-year interval tests can be compared. Regular HRV testing provides early detection and thereby promotes timely diagnostic and therapeutic interventions. HRV testing may also facilitate differential diagnosis and the attribution of symptoms (e.g., erectile dysfunction, dyspepsia, and dizziness) to autonomic dysfunction. Finally, knowledge of early autonomic dysfunction can encourage patient and physician to improve metabolic control and to use therapies such as ACE inhibitors and beta-blockers, proven to be effective for patients with CAN.
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PMID:Diabetic autonomic neuropathy. 1271 21

Data concerning the prevalence of Helicobacter pylori (H. pylori) in diabetic patients are scanty and controversial. The aim of this study was to evaluate the prevalence of H. pylori infection in patients with diabetes mellitus (DM), and to assess whether the presence of bacterium was associated with severity of dyspeptic symptoms and endoscopic findings in such patients. The study involved 42 patients (19 men, 23 women; mean age 55 years, range 34-75 years) with DM and dyspeptic symptoms. Sixteen patients (38%) were classified as having type 1 diabetes and 26 (62%) patients as having type 2 diabetes. All patients had chronic dyspepsia, and each patient has completed a self-report questionnaire to obtain information concerning the presence and severity of upper gastrointestinal tract symptoms. H. pylori status was confirmed by 13C-urea breath test (13C-UBT), and diabetic patients underwent upper gastrointestinal endoscopy. Twenty-six (61.9%) of patients with DM were positive for 13C-UBT. There were no statistically significant differences in the infection rate between patients with type 1 and type 2 diabetes, and the prevalence of H. pylori infection was not associated with the known duration of diabetes. There was no significant difference in the symptoms score between H. pylori-positive and H. pylori-negative diabetic patients, and endoscopic findings in patients with DM were in the same range with those found in dyspeptic subjects from the same region. In conclusion, H. pylori infection is not associated with DM, duration of diabetes, or severity of dyspeptic symptoms in patients with DM.
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PMID:Helicobacter pylori infection in patients with diabetes mellitus. 1475 71

The recent identification of tissue transglutaminase (tTG) as the autoantigen for celiac disease-associated anti-endomysial antibodies (EMA) has allowed the use of rapid immunoassay to detect the presence of autoantibodies, anti-tTG, in the serum of patients. In this study, we examined the prevalence of IgG or IgA anti-tTG in sera from patients with elevated levels of IgM rheumatoid factors, which are autoantibodies reactive with the Fc portion of IgG. We report here on four cases of anti-tTG positivity for patients with elevated IgM rheumatoid factor (RF) without evidence of celiac sprue. The study population consisted of 65 patients (26 men, 39 women; mean age, 49 years; range 4 - 92 years) with elevated RF (>20 U/ml ), and 23 healthy subjects (12 men, 11 women; mean age, 46 years; range, 21 - 54 years). IgG and IgA anti- tTG levels were detected using a commercially available ELISA kit (Immuno-Biological Laboratories, Germany). Out of 65 patients, one (1.5%) and three (4.6%) patients were positive for IgG and IgA anti-tTG antibodies, respectively, and this was a higher frequency than occurred in healthy subjects (0/23). The clinical features of the four cases positive for IgG or IgA anti-tTG were as follows: The first case (female, 63 yrs) positive for IgA anti-tTG antibody suffered from rheumatoid arthritis, type II diabetes mellitus, iron deficiency anemia and gastric indigestion without symptoms of malabsorption. She denied any gluten sensitivity on her diet. Her esophagogastroduodenoscopic biopsy showed mucosal atrophy with no elongated crypts or infiltration of inflammatory cells in the lamina propria. The remaining three cases positive for anti-tTG antibodies had interstitial pneumonia, a herniated lumbar disc, and mild scoliosis, respectively. They all denied any malabsorption symptoms or gluten sensitivity. Jejunal biopsy could not be performed in all four cases.
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PMID:Tissue transglutaminase autoantibodies in patients with IgM rheumatoid factors. 1551 14

Erection is a neurovascular event that involves spinal and supra spinal pathways. The final common pathway involves the release of nitric oxide (NO) from both endothelial cells and neurons, which acts as a vasodilator causing penile engorgement and erection. NO is degraded by the enzyme phosphodiesterase (PDE) type 5 in the penis. Erectile dysfunction (ED), defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance, results when the neurovascular pathway is interrupted by medical conditions or drugs. A 15-item self-administered questionnaire, the International Index of Erectile Function (IIEF), is one of the most useful tools to evaluate erectile function (EF) in clinical trials, although of much less use in routine clinical practice. The MMAS (Massachusetts Male Aging Study) was the first major epidemiological investigation to study the prevalence of ED. The study found that ED was three times more common in patients with diabetes mellitus. The aetiopathogenesis of ED in diabetes is multifactorial, with vascular and neural factors being equally implicated. Hyperglycaemia is believed to give rise to biochemical perturbations that lead to these microvascular changes. In the MMAS, ED in diabetes was strongly correlated with glycaemic control, duration of disease and diabetic complications. The incidence increased with increasing age, duration of diabetes and deteriorating metabolic control, and was higher in individuals with type 2 diabetes than those with type 1.ED in men with diabetes often affects their quality of life and, as patients are often reluctant to come forward with their symptoms, a carefully taken history is one of the most useful approaches in identifying affected individuals. The PDE inhibitors have revolutionised the management of ED and oral drug therapy is currently first-line therapy for the condition. These agents act by potentiating the action of intracavernosal NO, thereby leading to a more sustained erection. Sildenafil was the first PDE5 inhibitor to undergo evaluation and has been studied extensively. More recently two other agents, vardenafil and tadalafil, have been introduced. All the drugs have been shown to be effective across a wide range of aetiologies of ED, including diabetes. The drugs have been shown to improve EF domain scores, penetration and maintenance of erection, resulting in more successful intercourse. Their effects are greater at higher doses. Sildenafil and vardenafil are shorter-acting agents, while tadalafil has a longer half-life allowing the user more flexibility in sexual activity. Common adverse effects include headache, nasal congestion and dyspepsia, all actions related to inhibition of PDE5. The drugs are generally well tolerated and withdrawal from the clinical studies as a result of drug-related adverse effects were rare. The use of PDE5 inhibitors in the presence of oral nitrates is absolutely contraindicated. The clinical studies to date have not evaluated the use of one drug in the case of treatment failure with another agent. Sublingual apomorphine, which stimulates central neurogenic pathways, is a new agent and may be a suitable alternative in those patients in whom PDE5 inhibitors are ineffective or contraindicated. In clinical trials, all IIEF domains except sexual desire were found to have improved after apomorphine. The median times to erection in these studies were 18.9 and 18.8 minutes for the 2 and 3mg doses, respectively. Intraurethral and intracavernosal alprostadil may be a useful alternative when oral drug therapy is ineffective or contraindicated. The management of ED in the diabetic patient may often involve a multidisciplinary approach where psychosexual counselling and specialist urologist advice is required in addition to the skills and expertise of the diabetologist. Finally, the introduction of the new oral agents have completely revolutionised the management of ED and allowed more individuals to come forward for treatment.
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PMID:New treatment options for erectile dysfunction in patients with diabetes mellitus. 1553 69

Gastroparesis is the most severe form of gastric neuromuscular dysfunction along a continuum that encompasses gastric visceral hypersensitivity, gastric dysrhythmias, and pylorospasm. Gastroparesis may present with vague dyspepsia symptoms or with vomiting of undigested food and weight loss. A careful history and physical examination may suggest the diagnosis of gastroparesis, but symptoms associated with gastric neuromuscular disorders are non-specific. Gastroparesis in patients with diabetes, particularly type 2 diabetes, is more common than appreciated. If gastroparesis is confirmed, then reversible causes such as mechanical obstruction of stomach and chronic mesenteric ischemia must be excluded. ''Idiopathic'' gastroparesis may follow viral infections or be due to degenerative processes that affect gastric enteric neurons, smooth muscle, and/or interstitial cells of Cajal. An approach to the diagnosis and treatment of gastroparesis and gastric neuromuscular disorders is reviewed including dietary counselling and new medical devices.
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PMID:Gastroparesis and neuromuscular disorders of the stomach. 1648 77


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