Upper and lower gastrointestinal endoscopical investigation in elderly patients with iron deficiency anaemia

Iron deficiency anaemia is frequently observed in male adults and postmenopausal women due to chronic occult bleeding, usually from the gastrointestinal tract. Practically, as endoscopical investigation of the gastrointestinal system is an invasive procedure, iron replacement treatment was generally started without investigation of the underlying aetiology even in first-line health institutions. This study evaluates the role of endoscopy in the investigation of the aetiology of anaemia in 95 patients (51 males, 44 females), aged 64.9+/-12.5 years (range 50-90 years). All patients having iron deficiency anaemia were investigated by upper gastrointestinal endoscopy and colonoscopy. Upper and lower gastrointestinal pathologies were seen in 10 (10.6%) and 55 (57.8%) patients, respectively. However, no gastrointestinal lesion was found in 30 (31.6%) patients with iron deficiency anaemia. Out of the 95 patients, 16 (16.9%) had erosive gastritis, 15 (15.8%) duodenal ulcer, 8 (8.4%) gastric ulcer, 7 (7.3%) gastric tumours, 7 (7.3%) oesophagitis. 5 (5.4%) colon tumours, 3 (3.2%) haemorrhoids, 2 (2.1%) non-tropical sprue, 1 (1%) colonic polyp, and 1 (1%) colitis. In the majority of elderly patients with iron deficiency anaemia, upper gastrointestinal system disease was found. In 12 (12.7%) patients in the study group, malignancies were detected. In elderly patients with iron deficiency anaemia, the aetiology should be highlighted before giving iron supplementation.     

Risk of tuberculous infection among healthcare workers in a tertiary-care hospital in Ankara, Turkey.

OBJECTIVE: To determine risk factors for tuberculin skin test (TST) positivity among healthcare workers (HCWs). DESIGN: Two-step TST was performed in 2002. SETTING: Tertiary-care hospital in Ankara, Turkey. PARTICIPANTS: A sample of 491 hospital HCWs were included. Information related to demographics, profession, work duration, department, and individual and family history of tuberculosis (TB) was obtained by a structured questionnaire. RESULTS: Four hundred eight (83%) had two-step TST positivity. On multivariate analysis, male physicians (relative risk [RR], 1.5; 95% confidence interval [CI95], 1.23-1.69; P = .001), nurses (RR, 1.5; CI95, 1.29-1.66; P = .005), radiology technicians (RR, 1.7; CI95, 1.35-1.73; P = .002), laboratory technicians (RR, 1.6; CI95, 1.3-1.74; P = .007), and male housekeepers (RR, 1.6; (HCWs). CI95, 1.38-1.7; P < .001) had a higher risk than did female physicians. Among laboratory technicians, radiology technicians had the highest TST positivity (85%). HCWs working for less than 1 year (RR, 0.8; CI95, 0.72-0.98; P = .027) had a lower risk of infection. The HCWs having bacille Calmette-Guerin vaccination (RR, 1.12; CI95, 1.08-1.45) had higher TST positivity. CONCLUSION: Male physicians, nurses, and laboratory technicians had increased risk of Mycobacterium tuberculosis infection in this setting, but community exposure likely accounted for most infections.     

Double probing of human spermatozoa for persistent histones, surplus cytoplasm, apoptosis and DNA fragmentation

Individual spermatozoa were assessed with pairs of probes for persistent histones and cytoplasmic retention, persistent histones and DNA fragmentation, and persistent histones and apoptotic markers. The individual spermatozoa were treated sequentially with combinations of probes for these cytoplasmic and nuclear biochemical markers. Sperm fields were recorded with computer-assisted imaging, and staining patterns with the two probes in the same spermatozoa were examined and scored as light, intermediate or dark (mature to arrested-maturity spermatozoa). The effects of arrested sperm maturation were similar with respect to the cytoplasmic and nuclear characteristics of spermatozoa in 84% of cells, indicating that cytoplasmic and nuclear attributes of arrested sperm maturation are related. However, there were moderate (intermediate-dark or intermediate-light patterns, 14.5% of cells) or major (light-dark patterns, 1.6% of cells) discrepancies in the intensity of the double staining patterns. Thus, testing with single maturity markers may not be fully reliable. These findings are important with respect to: (i) arrested sperm maturation; (ii) potential efficacy of antioxidant and similar therapeutic strategies in subfertile men, as spermatozoa with infrastructure defects due to mismaturation or maturation arrest are unlikely to respond to interventions; and (iii) detection of adverse male environmental exposures.     

Long‐Term Exposure to Biomass Fuel and Its Relation to Systolic and Diastolic Biventricular Performance in Addition to Obstructive and Restrictive Lung Diseases

Background: Previous studies have demonstrated an increased risk for cardiovascular events and pulmonary disease in patients with biomass fuel exposure (BFE). However, biventricular heart function has yet to be investigated in these patients. Left ventricular (LV) myocardial performance index (LVMPI), which is an index of global ventricular function, incorporates ejection, isovolumic relaxation, and contraction times. In this study, pulmonary function and biventricular heart function were investigated in nonsmoking female patients with BFE. Methods: Our study population consisted of 46 female patients with BFE (group 1) and 31 control subjects (group 2). Pulmonary function tests and transthoracic echocardiographic examination were performed. Right ventricular myocardial performance index (RVMPI) and LVMPI were obtained by tissue Doppler imaging echocardiography (TDI). Results: BFE caused obstructive and restrictive spirometric impairments. RVMPI was higher in group 1 (0.55 ± 0.07) than group 2 (0.46 ± 0.06) (P = 0.042) and LVMPI was higher in group 1 (0.54 ± 0.08) than group 2 (0.47 ± 0.05) (P = 0.032). Also, pulmonary artery systolic pressure was higher in group 1 than group 2 (P = 0.02). Conclusions: BFE causes both obstructive and/or restrictive lung disease and systolic and diastolic biventricular dysfunction. Nonetheless, long‐term studies are needed to understand on BFE‐related ventricular dysfunctions and to document subsequent cardiovascular events. (Echocardiography 2011;28:52‐61)     

Patent Foramen Ovale among Patients with Mild Chronic Obstructive Pulmonary Disease and Unexplained Hypoxia

Purpose: To evaluate whether patent foramen ovale (PFO) is a contributing factor to hypoxia in patients with chronic obstructive pulmonary disease (COPD). Methods: Twenty‐one patients over 40 years of age with mild COPD (Forced expiratory volume (FEV1)/Forced Vital Capacity (FVC): > 50%) who had hypoxia (PO₂ < 80 mmHg, SaO₂ < 95%) that could not be explained by COPD alone were included in this study. Arterial oxygen pressures (PO₂) and arterial oxygen saturations (SaO₂) were recorded from laboratory evaluations of arterial blood gases. Respiratory function tests were performed to analyze the degree of COPD. Standard and contrast echocardiography was used to calculate pulmonary artery pressure (PAP) levels and to determine patients with a PFO. Results: The mean age of the patients was 64 ± 12 years. Four patients (19%) had a PFO. The mean PO₂, mean SaO₂, and mean PAP levels were 57.4 ± 6.8 mmHg, 90 ± 3.2%, and 33.8 ± 5.4 mmHg, respectively, in patients without PFO. The mean PO₂, mean SaO₂, and mean PAP levels were 46.5 ± 13.7 mmHg, 79.3 ± 12.8%, and 42.5 ± 6.5 mmHg, respectively, in patients with PFO. There were no statistically significant differences noted between the two groups in the PO₂ levels (P = 0.172) and SaO₂ levels (P = 0.065). A comparison of the PAP levels revealed a statistically significant difference between the two groups, with values that were more elevated in the PFO group than in the non‐PFO group (P = 0.031). Conclusion: This study demonstrated that PFO is not a contributing factor to deep hypoxia in COPD patients with lower PO₂ and SaO₂ levels; however, higher PAP levels were detected in patients with a PFO. Further studies involving a larger number of patients are needed to be conclusive. (Echocardiography 2010;27:687‐690)     

In vivo effect of losartan on platelet aggregation in patients with hypertension

The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 ± 12.8 and 149.2 ± 17.3mmHg, respectively. Mean DBP decreased from 93.7 ± 8.2 to 87.7 ± 10.3mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% ± 24.3% before and 58.3% ± 18.1% after the treatment. The same variables with ristocetin were 66.8% ± 21.6% and 60.8% ± 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.     

Is the Change of Late Potential Over Time Related to Enzyme Levels?Ichemic Burden in Acute Myocardial Infarction

Background: The ventricular late potential (VLP) detected using the technique of signal average electrocardiography (SAECG) interacts with several factors, primarily time. Method: In this study, we examined the interaction, over time, of VLP with the initial ischemic burden and enzyme levels in acute myocardial infarction. Patients diagnosed as having acute myocardial infarction were included in the study. On the first day, the patients underwent enzyme analysis and electrocardiography (ECG) follow‐up every 6 hours. A 24‐hour ambulatory ECG was performed on the seventh day in order to determine the ischemic burden. SAECG findings (TQRS, RMS, LAS were obtained on the seventh day, in the first and third months. The study was continued with the patients who did not require angioplasty as decided with angiographic evaluation in the first month. Results: The study included 30 patients with acute myocardial infarction (mean age 51 ± 12, 28 males and 2 females). The initial mean CK‐MB levels and the mean ischemic burden were 98 ± 31 U/L and 44 ± 96 minutes. The TQRS (ms), LAS (ms), and RMS (μV) values (mean ± SD) obtained at day 7, month 1, and month 3 are 97 ± 12, 96 ± 9, 103 ± 11, P = 0.01; 31 ± 10, 31 ± 11, 32 ± 10, P = 0.46; 43 ± 28, 41 ± 26, 33 ± 25, P = 0.01, respectively. We observed that the TQRS and RMS values changed significantly with time, but these levels of significance disappeared when adjusted for the initial ischemic burden and CK‐MB levels (P = 0.06; P = 0.53). The VLP frequency was 33% at day 7 and 23% at month 3. Unlike the CK‐MB level, the initial ischemic burden was significantly different between the patients with and without VLP at month 3 (150.85 ± 149.28, 12.34 ± 26.48, P = 0.001). When tested together with age and gender, it was found that the high initial ischemic burden increased the possibility of VLP (OR: 24, Cl: 2.09–279.52, P = 0.01) at month 3. Conclusion: SAECG findings in patients with myocardial infarction changed with time; however, this change occurred depending on the initial ischemic burden and CK‐MB levels. Of these, only the initial ischemic burden, especially in high levels, was a determinant for the presence of VLP in the late period of myocardial infarction. A.N.E. 2002;7(3):242–246     

HLA-DR B1 and DQ B1 polymorphisms in patients with coronary artery ectasia

OBJECTIVES: The purpose of our study was to evaluate the significance of polymorphisms in HLA class II genes in coronary artery ectasia (CAE) patients. METHODS AND RESULTS: Twenty-six patients with CAE without associated cardiac defects were enrolled in the study. CAE was defined as luminal dilation of 1.5- to 2.0-fold of normal limits. Ninety-five healthy subjects who were donors for different organ transplantations, were chosen as control group. Physical examination, electrocardiography and chest X-ray were completely normal in these cases. Both the patients and the control group were screened and compared for their HLA class II genotypes. HLA-DR B1*13, DR16, DQ2 and DQ5 genotypes were significantly more frequent in the patient group.When the known risk factors of coronary heart disease were compared in the patients carrying these genotypes with the non-carrying group, no significant differences were encountered. CONCLUSIONS: HLA-DR B1*13, DR16, DQ2 and DQ5 may be associated with the pathogenesis and increase the risk of CAE.     

Hepatic apoptosis and proliferation in male and female rats fed alcohol: role of cytokines

Background: The female liver is more sensitive to the toxic effect of chronic alcohol intake than the male liver. The aim of the study was to compare the influence of gender and sex hormonal status on apoptosis and cell proliferation following chronic ethanol intake.
Methods: Male and female rats were pair fed for 8 weeks a liquid diet containing 36% of their total daily calories as ethanol (ETOH group) or sucrose (control group). Liver samples were analyzed for apoptosis and hepatocyte proliferation by immunohistochemistry. The hepatic production of factors able to influence cell death and proliferation, such as tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6) were determined.
Results: In both male and female rats, ethanol intake promoted apoptosis in the liver. This effect of ethanol was more evident in female than male rat livers. Hepatic TNFα levels, which promote apoptosis, are significantly more elevated in female than in male livers. Hepatic IL-6 production, which promotes hepatocyte proliferation, was induced by ethanol only in males, but not female animals.
Conclusion: This observed difference in cytokine responses may contribute to the enhanced sensitivity of female liver to EtOH-induced injury.