Heterogeneity of gastric histology and function in food cobalamin malabsorption: absence of atrophic gastritis and achlorhydria in some patients with severe malabsorption

BACKGROUND: The common but incompletely understood entity of malabsorption of food bound cobalamin is generally presumed to arise from gastritis and/or achlorhydria. AIM: To conduct a systematic comparative examination of gastric histology and function. SUBJECTS: Nineteen volunteers, either healthy or with low cobalamin levels, were prospectively studied without prior knowledge of their absorption or gastric status. METHODS: All subjects underwent prospective assessment of food cobalamin absorption by the egg yolk cobalamin absorption test, endoscopy, histological grading of biopsies from six gastric sites, measurement of gastric secretory function, assay for serum gastrin and antiparietal cell antibodies, and direct tests for Helicobacter pylori infection. RESULTS: The six subjects with severe malabsorption (group I) had worse histological scores overall and lower acid and pepsin secretion than the eight subjects with normal absorption (group III) or the five subjects with mild malabsorption (group II). However, histological findings, and acid and pepsin secretion overlapped considerably between individual subjects in group I and group III. Two distinct subgroups of three subjects each emerged within group I. One subgroup (IA) had severe gastric atrophy and achlorhydria. The other subgroup (IB) had little atrophy and only mild hypochlorhydria; the gastric findings were indistinguishable from those in many subjects with normal absorption. Absorption improved in the two subjects in subgroup IB and in one subject in group II who received antibiotics, along with evidence of clearing of H pylori. None of the subjects in group IA responded to antibiotics. CONCLUSIONS: Food cobalamin malabsorption arises in at least two different gastric settings, one of which involves neither gastric atrophy nor achlorhydria. Malabsorption can respond to antibiotics, but only in some patients. Food cobalamin malabsorption is not always synonymous with atrophic gastritis and achlorhydria, and hypochlorhydria does not always guarantee food cobalamin malabsorption.     

Gastroesophageal reflux disease in chronic renal failure patients with upper GI symptoms: multivariate analysis of pathogenetic factors

OBJECTIVE: The association between gastroesophageal reflux disease and end-stage renal disease remains unclear. We aimed to assess the prevalence of gastroesophageal reflux disease and also to identify possible pathogenetic factors in the development of reflux in symptomatic end-stage renal disease patients. METHODS: The study involved 42 end-stage renal disease patients with upper GI symptoms (group I) and 46 age- and sex-matched controls who did not have renal disease but had the same symptoms (group II). Endoscopy, endoscopic biopsies, and 24-h esophageal pH studies were used to diagnose gastroesophageal reflux disease. Subjects were also investigated for Helicobacter pylori gastritis and GI amyloidosis. RESULTS: The prevalences of gastroesophageal reflux disease in the two groups were similar (81% vs 84.8%, p = 0.423). The prevalence of H. pylori infection was significantly lower in group I than in group II (38.1% vs 67.4%, p = 0.01). There were II cases of GI amyloidosis in group I. Multivariate logistic regression analysis in group I showed that GI amyloidosis (OR = 7.28, 95% CI = 1.13-46.93), chronic ambulatory peritoneal dialysis treatment (OR = 5.54, 95% CI = 1.01-30.43), and absence of H. pylori infection (OR = 3.75, 95% CI = 1.01-13.9) were significantly associated with reflux esophagitis. CONCLUSIONS: Upper GI symptoms are important in predicting gastroesophageal reflux disease in end-stage renal disease patients. Chronic ambulatory peritoneal dialysis, GI amyloidosis, and absence of H. pylori infection seem to be risk factors for the development of gastroesophageal reflux disease in end-stage renal disease patients.     

Clustering of impaired glucose tolerance, hyperinsulinemia and dyslipidemia in young north Indian patients with coronary heart disease: a preliminary case-control study

Metabolic insulin resistance syndrome is a critical factor in the pathogenesis of atherosclerosis and coronary heart disease in Indians. In a preliminary case-control study, 44 young patients (age < 40 years) with coronary heart disease (angina, myocardial infarction), not previously diagnosed to have diabetes mellitus, were recruited seven days to six weeks after the cardiac event (group I), and compared to 20 healthy subjects (group II). After recording history and anthropometric data, they were subjected to oral glucose tolerance test. Each group was divided into A and B subgroups according to the magnitude of impaired glucose tolerance. Hypertension was recorded in 11 (25%) patients in group I, while all the subjects in group II were normotensive (p < 0.05). Groups IB and IIB, consisting of subjects with impaired glucose tolerance displayed significantly high post-load blood glucose values. After excluding patients with the family history of diabetes mellitus, there were 13 (39%) and 3 (17%) patients with impaired glucose tolerance in groups I and II, respectively. Total cholesterol and low-density lipoprotein cholesterol levels were higher in group I as compared to group II (p < 0.01). Group IB showed highest mean values of total cholesterol, triglycerides, low-density lipoprotein cholesterol and lowest level of high-density lipoprotein cholesterol as compared to other subgroups. Serum insulin levels at 30 and 90 minutes were significantly higher in group I (p < 0.05). Group IB and IIB showed higher insulin values at 90 minutes when compared to group IA (p < 0.05) and IIA (p < 0.05). Elevated serum insulin values at 90 minutes during oral glucose tolerance test could differentiate among both groups and subgroups, except IB versus IIB. The study demonstrates significantly high prevalence of hypertension, obesity, impaired glucose tolerance, hyperinsulinemia and dyslipidemia, suggesting fully developed metabolic insulin resistance syndrome in young north Indian patients with manifest coronary heart disease.     

Plasma and gastric tissue selenium levels in patients with Helicobacter pylori infection

GOALS: We investigated plasma and gastric mucosal selenium levels in patients with Helicobacter pylori (HP)-associated histopathologic findings in their gastric antral mucosa. STUDY: Before and after a successful HP eradication therapy, we quantitated the plasma and antral selenium levels in patients with HP-associated chronic antral gastritis using atomic absorption flame emission spectrometry. The same measurements were done in patients with dyspeptic complaints who had normal antral histology and negative urease test. RESULTS: Thirty-four patients were studied, of whom 24 had HP-associated chronic antral gastritis confirmed by histology and positive urease test; the control group included 10 healthy patients. There was no difference between the groups with regard to age, gender, and number of smokers. All patients with HP infection were diagnosed with diffuse antral gastritis. Histopathology showed that 11 (49%) had some degree of atrophy. Of the 11 patients, 7 were classified as having chronic atrophic gastritis (CAG) without intestinal metaplasia (IM), 4 had IM, and none had dysplasia. The plasma concentrations of selenium were found to be very similar in controls and HP-infected subjects (68.0 +/- 25.97 microg/L and 71 +/- 32.9 microg/L, respectively; p > 0.05). The antral biopsy samples of the patients with HP-associated gastritis contained significantly higher levels of tissue selenium than the controls (20.17 +/- 19.74 microg/g and 2.83 +/- 1.42 microg/g, respectively; p < 0.05). Also, it was shown that antral tissue selenium levels decrease after successful HP eradication therapy (20.17 +/- 19.4 microg/g and 7.4 +/- 4.56 microg/g, respectively; t < 0.05). The patients with HP gastritis were assigned to mild, moderate, and severe gastritis groups, according to the histopathologic degree of inflammation present. The antral gastric selenium levels were significantly higher in patients with moderate and severe HP gastritis (21.13 +/- 22.5 microg/g and 22.81 +/- 17.35 microg/g, respectively) than in patients with mild gastric inflammation (9.53 +/- 10.3 microg/g; p < 0.05). The selenium concentrations in the biopsies of patients with CAG were significantly lower than in those with HP gastritis who did not have CAG (9.45 +/- 6.44 microg/g vs. 19.13 +/- 22.48 microg/g, respectively; p < 0.05). CONCLUSIONS: Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation. This reactive increase in gastric mucosal selenium seems to disappear in the presence of precancerous gastric lesions in the setting of HP-associated gastritis.     

Outcome of coronary artery bypass operations in patients with renal insufficiency with and without renal transplantation

HYPOTHESIS: Renal insufficiency (RI) is associated with an increased risk of morbidity and mortality following coronary artery bypass graft (CABG) operations, particularly among patients who are dependent on dialysis. DESIGN AND SETTING: A retrospective analysis of data collected at a tertiary care center. PATIENTS: One hundred eighty-four consecutive patients with RI who underwent CABG surgery between 1992 and 2004. This group consisted of 152 patients with serum creatinine levels of > or = 1.7 mg/dL (group I) and 32 kidney transplant recipients (group II). Of the patients in group I, 90 were dialysis-free (subgroup IA) and 62 were dialysis-dependent (subgroup IB). MAIN OUTCOME MEASURES: Demographics, perioperative data, and outcomes for each of the three groups were evaluated and compared. RESULTS: Fifty-four percent of the patients were in New York Heart Association classes III and IV, 36% had unstable angina, and 21% had left main coronary disease. The mean ejection fraction was 38%. The median postoperative length of stay in the hospital was 10 days. Of the patients in group IB, 8% required reexploration for bleeding compared to 3% in groups IA and II (p < 0.05). Dialysis was needed postoperatively in five patients in group IA and two patients in group II (5.7%). The raw operative mortality rate was 7.6% and was higher in group IB (9.7%) compared to groups IA and II (6.7% and 6.2%, respectively; p < 0.05). The actuarial 5-year survival rate was higher in group II compared to group I (79% vs 59%, respectively; p < 0.05). The difference in survival rates was more apparent between groups II and IB (79% vs 57%, respectively; p < 0.005). CONCLUSIONS: CABG is associated with an increased rate of perioperative complications and mortality in patients with RI. Dialysis dependence is a major risk factor for patients undergoing CABG surgery. However, with acceptable surgical results, dialysis patients should not be denied CABG surgery. A survival advantage is demonstrated among patients with previous kidney transplants compared to those patients who are dependent on dialysis.     

The gastric mucosa in stomachs with polyps: morphologic and dynamic evaluation

Biopsy specimens from the antral and body mucosa of 183 patients with gastric polyps (adenoma, 4; hyperplastic polyp (HP), 52; foveolar hyperplasia (FH), 49; and inflammatory polyp (IP), 78 cases) have been examined. The prevalence of gastritis in the series was compared with that in 183 age- and sex-matched controls. The dynamics (progression) of gastritis was evaluated by means of an age-adjusted gastritic score. In the HP and FH groups the prevalence and progression of body gastritis were significantly higher and more rapid (p less than 0.001) while the prevalence of antral gastritis was lower (p less than 0.05) and its progression less rapid (p less than 0.001) than in controls. It is concluded that the pernicious anaemia type of gastritis (A-type gastritis) is closely related to gastric polyps of hyperplastic origin. The progression of this gastritis type seemed to increase in the order IP, FH, and HP. In addition, we observed an increase in the prevalence of intestinal metaplasia (p less than 0.001) and marked epithelial dysplasia (0.1 greater than p greater than 0.05; chi-square = 3.75) in stomachs with polyps as compared with in controls.     

Effect of thrombolytic therapy on the prevalence of ventricular late potentials in patients after myocardial infraction

Sudden cardiac death is one of the most important problems of modern cardiology. More than 50% of these deaths are caused by ventricular arrhythmias. It has been known for twenty years that ventricular late potentials (LP) might be the substrate for serious ventricular arrhythmias and prevalence of LP correlates closely, among the others, with myocardium necrosis. The purpose of the study was to assess the influence of applied therapy in acute phase of myocardial infarction on LP presence, evaluation of relationship between the degree of left ventricular LV (V) myocardium damage and LP occurrence and assessment if LP can be non-invasive reperfusion markers. 120 consecutive patients (20 women, 100 men, mean age 53.3) with first acute myocardial infarction (AMI) treated either with thrombolytic or non-thrombolytic therapy were enrolled into the study. The patients were divided into three groups. Group IA--patients treated with thrombolysis with non-invasive features of reperfusion (n = 30), group IB--patients treated with thrombolysis, without reperfusion features (n = 31) and group II--patients treated with non-thrombolytic therapy. Within 24 hours of admission signal-averaged ECG was recorded (before and after treatment) and 24-hour ECG monitoring and echocardiography were performed. The examinations were repeated before discharge (approximately 21 days after AMI). All patients were followed up for one year. The prevalence of LP was 16.7% in the group IA, 48.4% in the group IB and 57.6% in the group II (p < 0.001). LVEF was 48.9% in the group IA, 42% in the group IB and 43.9% in the group II (I vs IB vs II p < 0.001). Significant changes of LP parameters before and after thrombolysis were observed only in the group 1A (in 40% of patients) (tQRS--122.4 +/- 6.1 msec vs 104.1 +/- 7.1 msec p < 0.001, LAS--49.8 +/- 4.8 msec vs 30.7 +/- 4.7 msec p < 0.001, RMS--13.6 +/- 4.4 uV vs 29.1 +/- 8.3 uV p < 0.001). There was no statistical significance in ventricular arrhythmia assessment but there was marked correlation with LP occurrence in all groups. 1-year mortality rate was 6.7% in group IA, 12.9% in group IB and 8.5% in group II (NS). CONCLUSIONS: Successful thrombolysis significantly reduces LP incidence in the late phase of myocardial infarction. LVEF correlates negatively with LP presence. LP presence in the first day of AMI may predict sudden cardiac death. LP occurrence can be significant non-invasive reperfusion markers.     

Blood pressure and heart rate responses during 24-hour ambulatory monitoring and exercise in men with diabetes mellitus

The heart rate (HR) variation of 25 normotensive and asymptomatic men, mean age 58 +/- 7 years, with diabetes mellitus (group I) was studied during deep respiration. Thirteen subjects (52%) had a variation of 10 beats/min or less, consistent with an autonomic neuropathy (AN) (group IA); 12 had variation in HR of more than 10 beats/min and were considered to have no neuropathy (group IB). The 24-hour ambulatory HR and systolic blood pressure (BP) values of group I were compared with those of 13 healthy men, mean age 48 +/- 8 years (group II). The mean of 5 maximal HR measurements during the 24-hour period was higher for group IA (106 +/- 11 beats/min) than for group IB (100 +/- 13 beats/min) or for group II (92 +/- 9 beats/min) (p less than 0.01). The mean of 5 maximal BP measurements was greater for group I (149 +/- 28 mm Hg) than for group II (128 +/- 13 mm Hg) (p less than 0.01), but no difference was observed between groups IA and IB. Maximal treadmill exercise was performed with 22 of the patients (11 with and 11 without AN), and no difference in HR was observed between the 2 groups during all stages of exercise or at maximal exertion. The increase in systolic BP and duration of exercise in these 2 groups were also similar. Seventeen of 25 diabetic men had peripheral neuropathy (PN). Of 13 patients with AN, 10 had PN; of 12 without AN, 7 had PN and 5 did not.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postextrasystolic aortic pressure pulse response in coronary artery disease.

The response of the aortic systolic pressure after an extrasystole was evaluated in 100 consecutive patients with coronary artery disease. The patients were divided into four groups depending on the response of the first postextrasystolic beat. Group IA (45 patients), had lower systolic pressure, whereas group IB (40 patients), had a similar systolic pressure in the postextrasystolic beat, as compared to beats preceding the extrasystole. Group IIA (12 patients) and group IIB (3 patients), demonstrated an increased systolic pressure in the first postextrasystolic beat with subsequent beats in group IIB, also demonstrating pulsus alternans. Congestive heart failure and cardiomegaly were significantly more frequent in group II, as compared to group I patients. In group IIA and IIB, triple vessel disease was present in 83 and 100 per cent, respectively, as compared to 44 per cent in group I patients. Left ventricular end-diastolic pressure (mm. Hg) was 14 ± 6 and 12 ± 7 in group IA and IB respectively, as compared to 19 ± 9 (p < 0.025) in group IIA and 31 in group IIB. Comparing groups IA and IB with each other for cardiac output, stroke volume, end-diastolic volume and ejection fraction, revealed no significant difference. The cardiac output (L./min./M.²) was 2.2 ± 0.6 for group IIA, as compared (p < 0.01) to 2.8 ± 0.5 and 2.9 ± 0.5 in groups IA and IB. Stroke volume (ml./M.²) and ejection fraction were 30 ± 10 and 0.30 ± 0.08, respectively, for group IIA, which is signficantly less, as compared to group I patients. The end-diastolic volume (ml./M.²) in group IIA was 102 ± 28, which is significantly (p < 0.001) higher, as compared to group IA and IB. All patients in group IIB had an abnormal cardiac output, end-diastolic volume and ejection fraction. Thus, the differences in response between group I and group II patients to an extrasystole clearly define two distinct hemodynamic groups. The responses observed to an extrasystole are best explained by variable response of each group to postextrasystolic potentiation and aortic impedance.     

Seroprevalence ofHelicobacter pylori and association with atrophic gastritis in patients with Sjögren’s syndrome

To investigate the association betweenHelicobacter pylori (HP) infection and atrophic gastritis in Sjögren’s syndrome (SS), we conducted an age-matched case-control study examining serum HP-IgG antibodies and pepsinogen (PG) I and II levels using ELISA. The sera of 82 primary SS (1-SS), and 57 secondary SS (2-SS) were studied, as well as 198 controls having a diagnosis of connective tissue disease (CTD), except for SS which were obtained according to age. The titers of HP-IgG in 1-SS were significantly much higher than those in either 2-SS or control. The HP-IgG level revealed an exclusively positive correlation with the serum PG II level and a negative correlation with the PG I/II ratio. Serum PG II levels and PG I/II ratios were associated with the positivity of HP-IgG antibodies. The age-specific seroprevalence rates of HP infection in SS patients compared with controls showed a high positivity in patients less than 49 years old, but no difference among the higher age groups because of increasing positive rates with advancing age in the control. The matched odds ratio with HP infection in all SS (1-SS and 2-SS) and in 1-SS were 2.33 (95% CI: 1.43–3.81) and 2.75 (95% CI: 1.50–5.05), respectively. However, the positive PG I/II ratio did not show a statistically significant odds ratio for SS. We conclude that SS patients have a highly positive association with HP infection and that atrophic gastritis with SS may occur as a result of HP infection.     

Severity of atrophic gastritis related to antiparietal cell antibody and gastric carcinogenesis, including p53 mutations

BACKGROUND AND AIMS: Infection with Helicobacter pylori (Hp) has been linked to atrophic gastritis, an inflammatory precursor of non-cardia gastric carcinoma. Mutations in the p53 gene are one of the most frequent genetic alterations in gastric carcinoma. In a subgroup of atrophic gastritis, antiparietal cell antibody (APCA) has been detected. This study was aimed to clarify the role of APCA in the progression of atrophic gastritis and gastric carcinogenesis, and to determine the relationship of the severity of atrophic gastritis to gastric carcinoma and to p53 mutations. METHODS: In 494 control subjects and 284 gastric carcinoma patients, serum APCA was evaluated and all subjects and patients were classified into four groups using serologic markers (anti-Hp IgG antibody and pepsinogen (PG) test: positive; PG I < 70 microg/L and PG I/II ratio < 3.0) as follows: A, HP- PG-; B, HP+ PG-; C, HP+ PG+ and D, HP- PG+. p53 mutations were analyzed in 174 of 284 patients. RESULTS: Antiparietal cell antibody seropositivity increased from group B to D, however, no difference in its positivity was found between controls and patients. The incidence of gastric carcinoma increased from A to D, especially the intestinal subtype. The frequency of p53 gene mutations was higher in PG+ than in PG- gastric carcinoma. CONCLUSIONS: Antiparietal cell antibody seropositivity is involved in the progression of a subgroup of atrophic gastritis, but not associated with gastric carcinogenesis. Severe atrophic gastritis is associated with susceptibility to gastric carcinoma, especially the intestinal subtype, and p53 mutations.     

Seroprevalence of Helicobacter pylori and association with atrophic gastritis in patients with Sjögren’s syndrome

Abstract

To investigate the association between Helicobacter pylori (HP) infection and atrophic gastritis in Sjögren’s syndrome (SS), we conducted an age-matched case-control study examining serum HP-IgG antibodies and pepsinogen (PG) I and II levels using ELISA. The sera of 82 primary SS (1-SS), and 57 secondary SS (2-SS) were studied, as well as 198 controls having a diagnosis of connective tissue disease (CTD), except for SS which were obtained according to age. The titers of HP-IgG in 1-SS were significantly much higher than those in either 2-SS or control. The HP-IgG level revealed an exclusively positive correlation with the serum PG II level and a negative correlation with the PG I/II ratio. Serum PG II levels and PG I/II ratios were associated with the positivity of HP-IgG antibodies. The age-specific seroprevalence rates of HP infection in SS patients compared with controls showed a high positivity in patients less than 49 years old, but no difference among the higher age groups because of increasing positive rates with advancing age in the control. The matched odds ratio with HP infection in all SS (1-SS and 2-SS) and in 1-SS were 2.33 (95% CI: 1.43–3.81) and 2.75 (95% CI: 1.50–5.05), respectively. However, the positive PG I/II ratio did not show a statistically significant odds ratio for SS. We conclude that SS patients have a highly positive association with HP infection and that atrophic gastritis with SS may occur as a result of HP infection.     

Circulating adhesion molecules in patients with chronic obstructive pulmonary disease

The place of adhesion molecules that have a role in the immigration of intravascular leukocytes to the tissue with inflammation in the pathogenesis of chronic obstructive pulmonary disease (COPD) is controversial. Our purpose in this study was to examine the levels of soluble intracellular adhesion molecule-1 (sICAM-1) and Mac-1 (CD11b/CD18), lymphocyte function associated antigen-1 (LFA-1) in both neutrophils and lymphocytes in stable patients with COPD and in the healthy control groups consisting of non-smokers, and in smokers without COPD and also to evaluate the relationship between the parameters related to the severity of the disease. Peripheral venous blood samples of all the individuals were collected, and levels of sICAM-1 was measured quantitatively with ELISA method. Flow cytometry was used for Mac-1 and LFA-1 levels. Twenty-four stable patients with COPD (group I), 13 smokers (group II) and 14 healthy non-smokers (group III) were included in this study. In the COPD group, 12 smokers patients were considered as group IA, and 12 patients with non-smokers and biomass exposure were considered as group IB. No statistically significant differences were seen in LFA-1 examined in peripheric blood (PB) neutrophils and lymphocytes and sICAM in groups I, II, and III. Mac-1 examined in PB neutrophils was found to be significantly lower in group I when compared to groups II and III, however no difference could be seen in smokers' group of II and the control group III. Mac-1 examined in PB lymphocytes were found to be higher in group I according to group II, however no statistically significant difference was seen between group I and control group. No statistically significant differences were seen in all adhesion molecules levels in group IA and group IB. As a result; it was found that Mac-1 levels in PB neutrophils were decreased with the developing of COPD and Mac-1 levels in PB lymphocytes were decreased in smokers, however increased following the development of COPD. No differences existed in sICAM and LFA-1 levels dependent on smoking and/or COPD.     

Relationship between pepsinogen I/II ratio and age or upper gastrointestinal diseases in Helicobacter pylori-positive and -negative subjects]

BACKGROUND/AIMS: Although previous reports suggested that pepsinogen (PG) I/II ratio was the index of gastric atrophy, PG I/II ratio was also related to other factors such as Helicobacter pylori (H. pylori) infection, various gastrointestinal diseases, and aging. The aim of this study was to evaluate the relationship between serum PG I/II ratio and age or upper gastro-intestinal diseases according to H. pylori infection status. METHODS: A total of 529 individuals (307 male; mean age, 57.2 years) were divided into 4 groups (94 gastric ulcers, 35 duodenal ulcers, 105 reflux esophagitis, and 295 atrophic gastritis) according to endoscopic diagnosis. H. pylori infection was determined by H. pylori IgG antibody (ELISA) and PG was measured by latex immunoassay. RESULTS: H. pylori infected patients showed markedly increased serum PG II levels (24.0+/-14.7 ng/mL vs. 13.8+/-16.6 ng/mL, p0.001) and low PG I/II ratio (3.9+/-2.0 vs. 6.0+/-2.5, p0.001) than non-infected subjects. In H. pylori infected patients, mean PG I/II ratios in the gastric ulcer and atrophic gastritis group were significantly lower than those of the duodenal ulcer and reflux esophagitis group (p0.001, ANOVA, Turkey's multiples comparison test). The mean ratio of open type atrophic gastritis was lower than that of close type atrophic gastritis (3.0+/-1.4 vs. 3.8+/-1.7, p0.005). PG I/II ratio gradually decreased with age in H. pylori-infected patients with atrophic gastritis (R(2)=0.9, p=0.005, linear regression analysis). CONCLUSION: Serum PG I/II ratio reflects H. pylori infection and gastric atrophy. In the presence of H. pylori infection, gastric atrophy progresses with age.     

Life expectancy analysis in patients with Chagas' disease: prognosis after one decade (1973-1983)

We studied the evolution of chronic Chagas' disease in 107 patients with a positive Guerreiro-Machado reaction and 22 non-chagasic, non-heart disease control subjects for a follow-up period of 3 to 10 years (mean follow-up of 4.9 years). After completion of invasive and non-invasive studies, chagasic patients were classified into four groups: IA (normal ECG, without heart disease; 18 patients); IB (normal ECG, early left ventricular segmental abnormalities; 13 patients); II (abnormal ECG, advanced myocardial damage, no signs of heart failure; 42 patients); and III (abnormal ECG, end-stage, congestive heart failure; 34 patients). One out of five group IA patients re-studied with invasive methods evolved to group IB (20%); 4 group IB patients evolved to group II (33%) and 6 group II patients evolved to group III (15%). The life expectancy of patients in groups IA and IB (normal ECG) was similar to that of our control group, whereas in groups II and III it was significantly decreased (P less than 0.001). Nine group II patients (23%) and 28 group III patients (82%) died during the follow-up period. Main terminal events were refractory congestive heart failure, sudden death and systemic thromboembolism. Our findings suggest that chronic Chagas' disease follows an evolutionary course from asymptomatic, normal ECG group I stage to arrhythmic (II) and congestive (III) stages. Subjects with a positive Guerreiro-Machado reaction showed a significantly lower life expectancy than our control group, but only when clinical and/or ECG abnormalities were identified.     

Influence of thyroid status on hemoglobin A2 expression

We studied the electrophoretic pattern of hemoglobin (Hb) and red blood cell indices in 128 women divided into four groups: group I, 36 nonanemic hyperthyroid women, divided in two subgroups: 36 with untreated hyperthyroidism (subgroup IA) and 9 made euthyroid by antithyroid drug therapy (subgroup IB); group II, 12 nonanemic women with untreated hypothyroidism; group III, 30 women known to be heterozygous for beta-thalassemia; and group IV, 50 healthy women. The mean (+/- SEM) HbA2 level was higher (P less than 0.001) in subgroup IA (3.21 +/- 0.06%) than in subgroup IB (2.42 +/- 0.09%) and group IV (2.48 +/- 0.04%), but lower (P less than 0.001) than in group III (5.26 +/- 0.12%). The mean HbA2 level was lower (P less than 0.001) in group II (1.99 +/- 0.08%) than in group IV. Hb fetal was detectable in eight patients of subgroup IA and undetectable in subgroup IB and groups II and IV. The mean cellular volume was lower (P less than 0.001) in subgroup IA than in other nonanemic groups. The mean cellular volume was higher (P less than 0.001) in group II than in group IV. Follow-up of nine patients who became euthyroid with treatment showed the normalization of these erythrocyte parameters. These results suggest that thyroid hormones can modulate the synthesis of delta- and gamma-globin chains.     

Impaired endothelial function in patients with myocardial bridge

OBJECTIVE: The relationship between myocardial bridging (MB) and ischemic heart disease is still controversial. In this study, we aimed to evaluate the existing atherosclerosis and noninvasive endothelial function of brachial artery in patients with MB. METHODS: The present study included 50 patients (group I) who had MB in left anterior descending (LAD) on coronary angiography. All of the coronary artery segments were evaluated by intravascular ultrasound (IVUS). Endothelial function was assessed with measurement of flow-mediated dilatation (FMD) and nitrate-dependent dilatation in the brachial artery. The study also included 30 healthy control subjects (group II). Patients in the group I were further subdivided into two subgroups based on the findings on IVUS: group IA included 20 patients without atherosclerotic lesions and group IB included 30 patients with atherosclerotic coronary artery disease in addition to MB. RESULTS: FMD values were found to be significantly lower in the patients with MB (group I) than in the control (6.4 +/- 3% vs 11 +/- 4%, P <0.001). In regard to FMD values in subgroups, FMD was 7 +/- 2% in the group IA and 5.8 +/- 1% in the group IB (P = 0.023). On IVUS, atherosclerotic plaque was found proximal to the bridge in the same coronary artery segment in addition to MB in 75% of the patients in group I (group IB). No atherosclerotic plaque was found in within or distal segments of MB. CONCLUSION: Endothelial function is impaired in patients with MB and there is an increased tendency for atherosclerosis proximal to the bridge in the patients with MB. Endothelial dysfunction is more severe in the patients with atherosclerosis proximal to the bridge.     

Helicobacter pylori: a risk and severity factor of non-steroidal anti-inflammatory drug induced gastropathy.

This prospective study aimed to determine the prevalence of Helicobacter pylori infection in relation to the occurrence and severity of NSAIDs induced gastropathy. A total of 111 patients were studied-66 were taking NSAIDs and 45 were control patients. All patients underwent endoscopy during which antral biopsy specimens were taken to determine H pylori status (Gram and Giemsa staining, urease test, and cultures). The NSAID group comprised: group I, patients without mucosal damage (n = 28); group II, patients with gastropathy (n = 26); and group III, patients with bleeding associated with NSAID induced gastropathy (n = 12). Control patients had neither dyspeptic symptoms nor endoscopic lesions. There were no differences in age, sex ratio, or presence of H pylori (26% v 24%) between the NSAID and the control groups. Among patients taking NSAIDs, H pylori infection was more frequently (p < 0.02) diagnosed in those who presented with gastropathy (groups II and III: 37%) than in those without lesions (group I: 11%). The frequency of H pylori infection increased significantly with the severity of gastropathy (group I = 11%; group II = 31%; group III = 50%; p < 0.03). H pylori infection was associated with chronic active gastritis (group I = 21%; group II = 35%; group III = 67%; p < 0.05). These data suggest that H pylori may be a risk factor of NSAID induced gastropathy.     

Atrophic gastritis, but not antibody to Helicobacter pylori, is associated with body mass index in a Japanese population

Background  The relationship between Helicobacter pylori (HP) infection and body mass index (BMI) is controversial. Several reports have indicated that eradication of HP infection induces an increase in BMI. In contrast, epidemiological case-control studies have failed to show an association between HP infection and BMI. Therefore, we investigated whether HP and atrophic gastritis (AG) were associated with BMI. Methods  A total of 617 individuals were recruited for the measurements of BMI, serum leptin, pepsinogens (PGs) I and II, and IgG antibody to HP (HP-IgG). BMI and leptin of the subjects were compared when the subjects were stratified by HP-IgG and PGs. Results  The subjects were divided into AG-positive and AG-negative groups according to PGs (AG-positive: PG I ≤ 70 ng/ml and PG I/II ratio ≤3.0). BMI after adjusting for sex and age was significantly lower in the AG-positive group than in the AG-negative group (23.47 ± 3.05 vs. 24.18 ± 3.25, P = 0.010). When the subjects were divided into two groups according to HP-IgG, BMI tended to be lower in the HP-IgG-positive group, though the difference was not large. When the subjects were divided into four groups for different combinations of AG and HP-IgG, BMI was the lowest in the AG-positive and HP-IgG-negative group. Conclusions  BMI was associated with AG, as diagnosed by PGs, but not with HP infection status. These results mean that HP infection affects BMI via atrophic gastritis.     

Upstaging by vessel invasion improves the pathology staging system of non-small cell lung cancer

BACKGROUND: There is a need for a more complete classification system of lung cancer. To address this issue, we assessed whether the new staging could differentiate patients with early-stage cancers who have poorer prognosis and improve the unbalanced patient numbers with overlapping prognoses arising from the current TNM staging system. METHODS: The study included 995 patients with pathology stages I and II non-small cell lung cancer (NSCLC) who underwent surgical resection at two institutions. We subclassified patients with stage IA and IB NSCLC based on the presence of vessel invasion (Vi). Stage IA Vi and stage IB non-Vi were combined into new stage IB, as were stages IB Vi and IIA into new stage IIA. RESULTS: The numbers of patients of stages IA, IB, IIA, and IIB were 477, 314, 55, and 149, and their 5-year survival rates were 86.0%, 66.2%, 60.7%, and 50.4%, respectively. Vi groups showed significantly poorer prognosis than non-Vi groups at stage IA (p = 0.011) and at stage IB (p = 0.036). The numbers of patients of new stages IA, IB, and IIA were 333, 260, and 253, and their 5-year survival rates were 88.7%, 76.4%, and 61.2%, respectively. Regression analysis indicated that the new staging improved predictability of overall survival according to disease stage, and Akaike information criterion (3023.7) was significantly lower than that for current staging system (3032.5). CONCLUSION: Upstaging of Vi groups allows differentiation of patients with early-stage cancers with poor prognosis and improves the unbalanced numbers of patients and prediction of prognosis in cases of lung cancer.