[Urinary tract infections in patients with type 2 diabetes mellitus with pharmacological glucosuria].

Selective inhibitors of sodium-glucose cotransporter belong to a new class of drugs for the treatment of type 2 diabetes mellitus. The mechanism of their action is based on insulin-independent reduction of glucose reabsorption in the proximal renal tubules, which leads to stimulation of its excretion in the urine and, accordingly, to a decrease in the concentration of glucose in the blood plasma. Drugs of this group demonstrate effectiveness in the treatment of type 2 diabetes, but their use may be associated with an increased frequency of urinary tract infections. Pharmacological glucosuria, which leads to a decrease in the concentration of glucose in the blood, creates the preconditions for the occurrence of urinary tract infections. Urinary tract and genital infections are the most common adverse events associated with the use of sodium-glucose cotransporter inhibitors. In the presented literature review for 20162019, the relationship between urinary tract infections in patients with type 2 diabetes mellitus and therapy with sodium-glucose cotransporter inhibitors was analyzed.

[Recurrent vomiting and headaches in a 26-year-old male patient]. / Rezidivierendes Erbrechen und Kopfschmerzen bei einem 26-jährigen Patienten.

This article reports the case of a 26-year-old male patient with recurrent emesis and headache due to central nervous system tuberculosis. The thoracic computed tomography showed bilateral disseminated pulmonary micronodular infiltrates and a cavern connecting to the bronchial system. The cranial magnetic resonance imaging showed multiple supratentorial and infratentorial microabscesses with concomitant meningitis. Mycobacterium tuberculosis was detected in sputum, bronchoalveolar lavage and cerebrospinal fluid. The patient received first-line antituberculous drug treatment, including streptomycin (instead of ethambutol) and adjuvant prednisolone.

Effect of High Dose Statin Pretreatment on Endothelial Progenitor Cells After Percutaneous Coronary Intervention (HIPOCRATES Study).

BACKGROUND: Pretreatment with high-dose statins given before percutaneous coronary intervention (PCI) has been shown to have beneficial effects, in particular by reducing peri-procedural myocardial infarction. The mechanism of these lipid-independent beneficial statin effects is unclear. Circulating endothelial progenitor cells (EPCs) have an important role in the process of vascular repair, by promoting re-endothelization following injury. We hypothesized that statins can limit the extent of endothelial injury induced by PCI and promote re-endothelization by a positive effect on EPCs. We, therefore, aimed to examine the effect of high-dose statins given prior to PCI on EPCs profile. METHODS: Included were patients, either statin naïve or treated chronically with low-dose statins, with stable or unstable angina who underwent PCI. Patients were randomized to receive either high-dose atorvastatin (80 mg the day before PCI and 40 mg 2-4 h before PCI) or low- dose statin. EPCs profile was examined before PCI and 24 h after it. Circulating EPCs levels were assessed by flow cytometry as the proportion of peripheral mononuclear cells co-expressing VEGFR-2+ CD133+ and VEGFR-2+ CD34+. The capacity of the cells to form colony forming units (CFUs) was quantified after 7 days of culture. RESULTS: Twenty three patients (mean age 61.4 ± 7.4 years, 87.0% men) were included in the study, of which 12 received high-dose atorvastatin prior to PCI. The mean number of EPC-CFUs before PCI was higher in patients treated with high-dose atorvastatin vs. low-dose statins (165.8 ± 58.8 vs. 111.7 ± 38.2 CFUs/plate, respectively, p < 0.001). However, 24 h after the PCI, the number of EPC-CFUs was similar (188.0 ± 85.3 vs. 192.9 ± 66.5 CFUs/plate in patients treated with high-dose atorvastatin vs. low- dose statins, respectively, p = 0.15). There were no statistical significant differences in FACS analyses between the 2 groups. CONCLUSIONS: The current study showed higher EPC- CFUs levels in patients treated with high-dose atorvastatin before PCI and a lower increment in EPC-CFUs after PCI. These findings could account for the beneficial effects of statins given prior to PCI, yet further investigation is required.

Influence of the rate of contrast change on the quality of contrast sensitivity assessment: a comparison of three psychophysical methods.

Criterion-free forced-choice procedures for measuring contrast sensitivity with a cathode ray tube (CRT) have low within-subject, intersubject, and test-retest variabilities, but a long test time compared with psychophysical methods that rely on the subject's criterion to determine threshold. Test time and variability of criterion-dependent methods depend on the rate at which the contrast changes on the CRT display. This study compared two criterion-dependent psychophysical methods for measuring contrast sensitivity (the method of increasing contrast and the von Békésy tracking method) with a criterion-free two-alternative forced-choice procedure. A range of rates of contrast change was studied: 0.1, 0.3, 0.5, 0.7 and 1.0 log unit s-1. Contrast sensitivity, within-subject variability, intersubject variability, test-retest variability, and test time of the three methods were compared. The 2-AFC procedure performed best with regard to within-subject, intersubject, and test-retest variabilities. A time-efficient alternative was the von Békésy tracking method at rates between 0.1 and 0.5 log unit s-1.

Acute left ventricular failure after large volume pericardiocentesis.

This paper reports on two cases of large volume pericardiocentesis followed by transient severe acute left ventricular (LV) systolic failure in the absence of any prior history of LV dysfunction. Acute LV volume overload due to interventricular volume mismatch is believed by most authors to be the cause for this phenomenon. Another plausible physiopathologic explanation is the acute increase in "wall stress" (Laplace's law) due to acute distention of the cardiac chambers secondary to a sudden increase in venous return at high filling pressures, combined with a "vacuum" effect of the evacuated pericardial space.

The importance of the level of the lip line and resting lip pressure in Class II, Division 2 malocclusion.

Many clinicians hypothesize that retroclination of the maxillary central incisors in Class II, Division 2 malocclusion is caused by increased resting lip pressure against these teeth. The purpose of this study was (1) to verify this assumption by means of simultaneous lip-pressure measurements at two different levels on the maxillary central incisor crowns, and (2) to examine factors that could possibly contribute to the increased resting lip pressure. This is the first study to prove that individuals with Class II, Division 2 malocclusion (n = 21) have the upper central incisors exposed to significantly higher lip pressure than those with Class I malocclusion (n = 21). Our statistical evaluation revealed that this is primarily attributed to a high lip line and not to a hypertonic peri-oral musculature. We concluded that orthodontic treatment of Class II, Division 2 cases should include intrusion of the maxillary incisors, to eliminate the non-physiologically high pressure exerted by the lower lip on these teeth and, consequently, to reduce the high risk of a post-orthodontic relapse.

Prediction of the extent and severity of left ventricular dysfunction in anterior acute myocardial infarction by the admission electrocardiogram.

BACKGROUND: The grade of ischemia, as detected by the relation between the QRS complex and ST segment on the admission electrocardiogram, is associated with larger infarct size and increased mortality rates in acute myocardial infarction. METHODS: We assessed the correlation between left ventricular function and the admission electrocardiogram in 151 patients with first anterior acute myocardial infarction who received thrombolytic therapy and underwent cardiac catheterization at 90 minutes and before hospital discharge. The number of leads with ST elevation, sum of ST elevation, maximal Selvester score, and the presence of severe (grade 3) ischemia were determined in each electrocardiogram. Left ventricular ejection fraction, the number of chords with wall motion abnormalities, and the severity of dysfunction (SD/chord) were determined. RESULTS: At 90 minutes, the 39 ischemia grade 3 patients had lower ejection fraction than the 112 grade 2 patients. Both at 90 minutes and at hospital discharge, the grade 3 group had more chords with wall motion abnormalities and more severe regional dysfunction (SD/chord). However, the number of leads with ST elevation, sum of ST elevation, and maximal Selvester score had no correlation with ejection fraction at 90 minutes and only mild correlation with the extent of dysfunction (number of chords) at 90 minutes. There was no correlation between either the number of leads with ST elevation or the sum of ST elevation and the severity of regional dysfunction. CONCLUSIONS: The number of leads with ST elevation, sum of ST elevation, and maximal Selvester score had only mild correlation with the extent of myocardial dysfunction but not with the severity of dysfunction. Grade 3 ischemia is predictive of more extensive myocardial involvement and greater severity of regional dysfunction.

Value of the initial electrocardiogram in patients with inferior-wall acute myocardial infarction for prediction of multivessel coronary artery disease.

BACKGROUND: Patients with inferior-wall acute myocardial infarction (AMI) who have ST-segment depression in the left precordial leads (LSTD+) on the initial electrocardiogram were reported to have more diffuse coronary artery disease (CAD) than had those without this finding (LSTD-). This suggests that LSTD+ patients may need extensive revascularization interventions more often than do LSTD- patients. However, this has not yet been confirmed. OBJECTIVE: To compare the coronary angiographic findings and treatment strategies for patients with inferior-wall AMI according to the LSTD pattern. METHODS: The clinical outcomes and the angiographic findings for 238 consecutive patients aged < or = 75 years who had been admitted to our hospital between 1 February 1995 and 1 February 1997 with inferior-wall AMI were retrospectively analyzed. The patients were divided into two groups according to the pattern of precordial ST-segment depression: LSTD+, ST-segment depression in leads V4-V6; and LSTD-, absence of this finding. All patients were treated according to current practice guidelines including with thrombolysis and revascularization interventions. RESULTS: The final study population included 217 patients; 83 were LSTD+ and 134 were LSTD-. All underwent coronary angiography within 30 days of the infarction. Compared with LSTD- patients, LSTD+ patients tended to be older (mean age 62.7 +/- 11.7 versus 58.3 +/- 9.6 years, P = 0.004), and had higher incidences of hypertension (39.8 versus 24.6%, P = 0.019) previous myocardial infarction (45.8 versus 20.1%, P = 0.0001) and congestive heart failure (21.7 versus 3.7%, P = 0.00008). Three-vessel CAD was much more common, and single-vessel CAD much less common, in the LSTD+ than in LSTD- group (62.7 versus 13.4% and 8.4 versus 50.7%, P < 0.00001 for both). Coronary-artery-bypass surgery and multivessel percutaneous coronary interventions (PCI) were used in treating 65.1% of the LSTD+ versus only 6.0% of the LSTD- patients (P < 0.00001), whereas single-vessel PCI was used in treating 71.6% of the LSTD- patients versus only 24.1% of the LSTD+ patients (P < 0.00001). Thus, the LSTD- pattern predicted single-vessel disease and single-vessel PCI only, whereas the LSTD+ pattern was predictive of multivessel CAD and of use of coronary-artery-bypass surgery or multivessel PCI (predictive values of 94.0 and 65.1%, respectively). CONCLUSIONS: Among patients with inferior-wall AMI, left precordial ST-segment depression predicts a very high prevalence of multivessel CAD and use of extensive revascularization interventions. The absence of this finding predicts nondiffuse CAD and lack of a need for extensive revascularization.

Relation between evolutionary ST segment and T-wave direction and electrocardiographic prediction of mycardial infarct size and left ventricular function among patients with anterior wall Q-wave acute myocardial infarction who received reperfusion therapy.

In the prethrombolytic era it was found that infarct size and left ventricular ejection fraction could be predicted using the Selvester QRS score. We evaluated whether infarct size and left ventricular ejection fraction could be predicted by the predischarge QRS score in patients who had received reperfusion therapy and whether considering the configuration of the ST segments and T waves would increase the accuracy of these predictions. We evaluated 51 patients with first anterior wall myocardial infarction who had received reperfusion therapy and predischarge resting technetium-99m-sestamibi scan. The electrocardiograms recorded on the same day of the scan were analyzed for the QRS score and were divided into 3 groups: A, isoelectric ST and negative T waves; B, ST elevation (> or =0.1 mV) and negative T waves; and C, ST elevation (> or =0.1 mV) and positive T waves. Groups A, B, and C included 12, 23, and 16 patients, respectively. The myocardial perfusion defect extent increased from groups A to C (median 21%, 37%, and 43.5% in groups A, B, and C, respectively; p = 0.023). Similarly, left ventricular ejection fraction decreased (44%, 38%, and 34%, respectively; p = 0.042) from groups A to C. Overall, the correlation between the QRS score and the myocardial perfusion defect extent (rho 0.249; p = 0.08) and ejection fraction (rho -0.229; p = 0.11) was poor. A statistically significant correlation between myocardial perfusion defect size and QRS score was found only in group A (rho 0.599, p = 0.04). Among patients with anterior myocardial infarction who received reperfusion therapy, the predischarge QRS score was predictive of infarct size only in those in whom ST elevation resolved completely. In patients with residual ST elevation there was no correlation between QRS score and infarct size.

Methylenetetrahydrofolate reductase genotypes and early-onset coronary artery disease.

BACKGROUND: Homozygosity for the common (677C-->T) mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is associated with hyperhomocysteinemia, but there is uncertainty as to the association between this mutation and coronary artery disease (CAD). This study examined the association between MTHFR genotypes and age at onset of CAD. METHODS AND RESULTS: Patients (n=169) with documented myocardial infarction or angiographically documented CAD who were aged < or = 55 years at onset of CAD symptoms and DNA samples from control subjects (n=313) were studied. The prevalence of homozygosity among patients with early CAD onset (aged < or = 45 years) was 28%, which was significantly higher than that in patients with later onset (13%) and in control subjects (14%) (odds ratio 2.4, 95% CI 1.24 to 4.69, P=0.006, and odds ratio 2.7, 95% CI 1.15 to 6.42, P=0.01, respectively). Plasma folate was lower in TT homozygotes who had early CAD onset than in those with later onset (P=0.005). Among patients with plasma folate in the lowest quintile (< or = 12.6 nmol/L), 31% were homozygotes, as were 45% of those with low plasma folate and early CAD onset. There was no difference in the prevalence of traditional risk factors among genotypes. The frequency of homozygosity in patients with < or = 1 risk factor was higher than in those with > or = 2 risk factors (30% versus 12%, P<0.05). In multiple regression analysis, TT homozygosity and plasma folate were independently associated with CAD, but the impact of folate was small. CONCLUSIONS: Homozygosity for the 677C-->T mutation of MTHFR is common and is associated with an increased risk of premature CAD in this population.

Acute myocardial infarction following sildenafil citrate (Viagra) intake in a nitrate-free patient.

Since its introduction to the market in March 1997, sildenafil acetate (Viagra) has been prescribed to 1.7 million people. Sixteen men who were taking the drug have died, 7 of them during or soon after sexual activity. Most of these data have been derived from the media and not from the scientific literature. There is a general impression that cardiovascular complications of sildenafil occur mainly when the drug is taken concomitantly with nitrates. We describe a 65-year-old man with known coronary artery disease who had an acute myocardial infarction shortly after taking sildenafil and engaging an sexual activity. The patient had not been using nitrates. We suggest that the emotional arousal induced by Viagra, followed by the heavy physical exertion during sexual activity, triggers plaque rupture that leads to acute myocardial infarction.

Terminal QRS distortion on admission is better than ST-segment measurements in predicting final infarct size and assessing the Potential effect of thrombolytic therapy in anterior wall acute myocardial infarction.

We assessed predicting final infarct size (using predischarge Selvester score) by 3 electrocardiographic variables in 267 patients with first anterior wall acute myocardial infarction (AMI) undergoing (n = 86) or not undergoing (n = 181) thrombolysis. Patients with previous AMI or inverted T waves in leads with ST elevation were excluded. The sum (sigma) of ST elevation, the number of leads with ST elevation, and the initial electrocardiographic pattern were determined on the admission electrocardiogram (absence (QRS-) or presence (QRS+) of distortion of the terminal portion of the QRS in > or =2 leads (J point > or =0.5 of the R-wave amplitude in leads I, aVL, V4 to V6, or presence of ST elevation without S waves in leads V1 to V3). There was no association between sigmaST elevation and final infarct size in patients who did or did not receive thrombolytic therapy. Analysis of covariance showed that the number of leads with ST elevation (F = 19.6), thrombolysis (F = 25.2), and QRS+ initial pattern (F = 19.5) were all associated with final infarct size (p <0.0001 for all). Among patients who did not receive thrombolytic therapy, the average Selvester score was 19.7+/-9.9 for the QRS- patients and 26.1+/-10.4 for the QRS+ patients (p = 0.02). Among patients who received thrombolytic therapy, the average Selvester score was 11.7+/-9.8 for the QRS- patients and 24.2+/-10.1 for the QRS+ patients (p <0.0001). Thrombolysis reduced final Selvester score only in the QRS- group (p <0.00001), but not in the QRS+ group (p = 0.45). It is concluded that (1) final Selvester score in anterior wall AMI can be predicted by the number of leads with ST elevation, the initial electrocardiographic pattern, and thrombolysis, and (2) thrombolysis reduces final Selvester score only in patients with QRS- pattern.

The avian fli gene is specifically expressed during embryogenesis in a subset of neural crest cells giving rise to mesenchyme.

The ets-family of transcription factors is involved in the development of endothelial and hematopoietic cells. Among these genes, fliwas shown to be responsible for erythroblastomas and Ewing's sarcomas. Its involvement in Ewing's sarcoma, a putative neurectodermal tumor, as well as the in situ hybridization studies performed in mice and Xenopus suggested a role in neural crest development. We cloned quail fli cDNA in order to analyze in more detail its expression in neural crest cells, which have been extensively studied in avian species. Fli gene maps on chicken chromosome 1 to band q31->q33. Two RNAs are transcribed, most likely arising from two different promoters. The analysis of its expression in neural crest cells reveals that it is expressed rather late, when the neural crest cells reach their target. Among the various lineages derived from the crest, it is restricted to the mesenchymal one. It is maintained at later stages in the cartilage of neural crest but also of mesodermal origin. In addition, fli is expressed in several mesoderm-derived cells: endothelial cells as well as intermediate and splanchnopleural mesoderm.

QRS complex distortion predicts no reflow after emergency angioplasty in patients with anterior wall acute myocardial infarction.

BACKGROUND: In patients with acute myocardial infarction, distortion of the terminal portion of the QRS complex on the electrocardiogram (ECG) at the time of their admission to hospital is associated with larger final infarct size and greater mortality. This study assessed the results of emergency coronary angioplasty in patients with anterior acute myocardial infarction with and without distortion of the terminal portion of the QRS complex on the admission ECG. METHODS: We assessed the Thrombolysis in Myocardial Infarction (TIMI) trial flow grade, resolution of ischemic ECG changes, and clinical outcome after emergency angioplasty for acute anterior wall myocardial infarction in patients with (n = 21) and without (n = 21) distortion of the terminal portion of the QRS complex on the admission ECG. RESULTS: Compared with patients without distortion of the terminal portion of the QRS complex on the admission ECG, those with distortion had a significantly lower incidence of TIMI flow grade 3 (52% compared with 84%, P < 0.05), lower rate of resolution of the ischemic ECG changes (33% compared with 84%, P < 0.005), and greater rate of mortality during their stay in hospital despite successful balloon angioplasty (19% compared with 0%, P < 0.05). CONCLUSIONS: In patients with anterior wall acute myocardial infarction, distortion of the terminal portion of the QRS complex on the admission ECG predicts a greater mortality rate and a greater incidence of reflow impairment after emergency angioplasty.

Overexpression of the Xenopus Xl-fli gene during early embryogenesis leads to anomalies in head and heart development and erythroid differentiation.

The product of the Xl-fli gene, a Xenopus laevis transcription factor of the ets family, specifically expressed in several lineage of migratory cells during Xenopus development (Meyer et al., Int. J. Dev. Biol. 39: 909-919, 1995) was overproduced during Xenopus embryogenesis, upon microinjection of a synthetic transcript in the fertilized egg or in the early embryo. This results in anomalies of the antero-posterior and dorso-ventral polarities, and in tissue differentiation, particularly in the eye- and head cartilage development, as well as erythroid differentiation (absence of erythrocyte differentiation in the circulating blood, often accompanied by ectopic localization of mature erythrocytes, leading to important hemangiomas). Cytological examination reveals at gastrulation the existence of abnormal cells separating the different embryonic layers, suggesting modifications of the cellular adhesion properties. The possible involvement of the fli gene in controlling the dissemination of migratory cells is discussed.

Whole-mount in situ hybridization reveals the expression of the Xl-Fli gene in several lineages of migrating cells in Xenopus embryos.

The expression of the Xl-Fli gene, which belongs to the ets family of transcription factors, was studied by whole-mount in situ hybridization during Xenopus embryogenesis. Digoxigenin-labeled antisense RNA probes were synthesized by in vitro transcription and used in the hybridization reaction. In addition to expression in territories invaded by neural crest cells reported earlier (Meyer et al., 1993), we observed Xl-Fli gene expression in a number of regions affected by important cellular migrations and/or epithelium<==>mesenchyme transitions: in the endothelial cells of the heart, in blood vessels, along the pronephric duct migration pathway and at the level of hypophysis. The possibility that the FLI protein is involved in the expression of guidance cues and/or modification of the cellular adhesion properties is discussed. A screening of a promoter library with a consensus sequence, bound by the FLI protein with a high affinity, revealed the presence of putative FLI response elements in a number of genes encoding adhesion molecules or components of the extra-cellular matrix.