Risk factors for oral hairy leukoplakia in HIV-infected adults of Brazil

BACKGROUND: Oral hairy leukoplakia (OHL) may be an indicator of the progression of Human Immunodeficiency Virus (HIV)-induced immuno-depression, and the evaluation of risk factors leading to OHL is important in the management of these HIV-infected patients. However, there are few studies that analyze risk factors leading to OHL in the Brazilian population. The aim of this case-control study is to present data about prevalence rates and risk factors leading to OHL in a sample of HIV-infected adults in Brazil. METHODS: This case-control study included 111 HIV-infected patients treated at a clinic for sexually transmitted diseases and HIV. In the initial examinations with dentists, variables were collected from all patients. Diagnosis of OHL was performed in accordance with the International Classification System and cytological features. The Fisher and the chi-squared tests were used for statistical analysis. The proportional prevalence and odds ratio were estimated. RESULTS: Outcome presented a positive, statistically significant association among the presence of OHL and viral load of 3000 copies/mul or greater (P = 0.0001; odds ratio (OR) = 5.8), presence of oral candidiasis (P = 0.0000; OR = 11.1), previous use of fluconazole (P = 0.0000; OR = 24.6), and use of systemic acyclovir (P = 0.032; OR = 4.3). Antiretroviral medication presented a negative, statistically significant association with the presence of OHL (P = 0.002; OR = 8.4). CONCLUSIONS: Prevalence of OHL was 28.8%. Viral load, oral candidiasis, previous use of fluconazole, and systemic acyclovir were determined to be risk factors for OHL. Antiretroviral medication proved to be protective against the development of OHL.     

Electrophysiologic effects of halothane and quinidine on canine Purkinje fibers: evidence for a synergistic interaction

The authors studied possible interactions between halothane and quinidine on the action potentials of canine Purkinje fibers superfused with Tyrode's solution. Using standard microelectrode techniques and a physiologic pacing rate (2 Hz), halothane in concentrations from 0.5% to 2% decreased the action potential duration to 50% repolarization (ADP50). Total ADP (APD100), in contrast, increased after 1% and 2% halothane. Resting membrane potential (RMP) and action potential amplitude (APamp) increased after 0.5% halothane, but returned to control with higher halothane levels. Conduction time (CT) increased at each halothane level. Pacing at faster (3 Hz) or slower (1 Hz) rates did not markedly alter the effects of halothane. Quinidine 1 X 10(-5)M decreased the phase O upstroke (Vmax) and prolonged APD100 and CT. When halothane was added, RMP and APamp decreased, Vmax decreased further, and APD100 and CT were markedly prolonged. This resulted in conduction block or inexcitability, especially at faster pacing rates (3 Hz). Synergistic interactions between halothane and quinidine were found on RMP, APamp, APD100, and CT. Effects on Vmax, APD50, and action potential duration to 90% repolarization (APD90) were additive. It is concluded that quinidine and halothane act synergistically to decrease action potential amplitude, lower RMP, and prolong conduction. Severe depression of conduction often progressed to conduction block or inexcitability when halothane, 2%, was administered during superfusion with therapeutic concentrations of quinidine.     

Autologous rosette-forming T cells and their relationship to OKT4+ and OKT8+ cells in chronic HBV infection

A percentage of human T lymphocytes forms rosettes with autologous erythrocytes and this property has been considered as a marker for post-thymic precursor suppressor cells capable of providing suppression under the influence of inducer cells. We quantitated autologous rosette-forming T cells (ARFC) in the peripheral blood of 37 patients with chronic HBV infection: 8 healthy carriers, 9 chronic persistent hepatitis (CPH-B) and 20 chronic active hepatitis (CAH-B). Two control groups were studied, one consisting of 26 healthy individuals and the other of 8 individuals with non-HBV-associated CAH. Patients with non-HBV-associated CAH had a significant reduction in the proportion of ARFC, whereas CAH-B patients fell into 2 distinct patterns, one with increased and the other with decreased proportions of ARFC. This was unrelated to the degree of biochemical activity of the disease or to degree of viral replication as defined by HBeAg status and HBV-DNA in the serum. Healthy carriers and CPH-B had no changes in ARFC. Simultaneous quantitation of OKT4 and OKT8+ cells was done and a positive correlation was found between the proportions of ARFC and the proportions of OKT8+ cells. The possible significance of this correlation and the relevance of the bimodal distribution of autologous rosette-forming cells in CAH-B are discussed.     

Rupture of a submitral ventricular aneurysm into the left atrium diagnosed by transesophageal echocardiography.

Submitral ventricular aneurysm is a thoroughly studied pathology but is not well known due to its rarity. Clinically, it is manifested by symptoms and signs of heart failure, mitral regurgitation and/or ventricular arrhythmias, and may be associated with thromboembolic phenomena and myocardial ischemia due to compression of the coronary arteries by the aneurysm. A rare complication of this type of aneurysm is rupture into the left atrium. Transthoracic echocardiography plays an important role in the definitive diagnosis of this pathology, although the role of transesophageal echocardiography in the evaluation of these patients is less known. We report a case of a submitral ventricular aneurysm complicated by rupture into the left atrium, which was diagnosed by transesophageal echocardiography.     

Pulmonary embolism.

Pulmonary embolism (PE) is an important health problem and often a major clinical challenge, not only because of the low specificity of its clinical manifestations but also because of the increasing number of medical circumstances that are risk factors for this illness and the importance of early identification, since prompt and appropriate treatment can decrease mortality from this disease by about 25%. In recent years research on PE has been extensive, directed mainly at trying to determine and characterize its risk factors, establish new clinical probability algorithms, develop new diagnostic methods and put existing ones into perspective, seek new therapeutic approaches (pharmacological and non-pharmacological), and above all establish protocols that can guide the clinician from the stage of clinical suspicion to measures to prevent recurrence. It was the authors' aim to review the most significant literature on this subject, in order to produce a text that reflects the state of the art concerning PE and that can be used as a guide in the clinical approach to this pathology.     

Type 2 diabetes: assessment of endothelial lesion and fibrinolytic system markers.

This study aimed to investigate whether endothelial cells are damaged and to evaluate fibrinolytic system function in patients with type 2 diabetes. For this proposal, plasma levels of von Willebrand factor (an endothelial marker of injury), homocysteine (an inductor of endothelial injury), D-dimer (a marker of coagulation cascade activation) and plasminogen activator inhibitor-1 (a fibrinolysis marker) were measured in individuals with both type 2 diabetes and high blood pressure, with type 2 diabetes, with high blood pressure and in healthy control individuals. No significant differences among groups were observed for von Willebrand factor and homocysteine plasma levels. The type 2 diabetes and high blood pressure group presented a significant difference to the other groups for D-dimer and also presented high values for plasminogen activator inhibitor-1. The high blood pressure group and type 2 diabetes group presented separately higher values of plasminogen activator inhibitor-1 compared with the control group. High levels of D-dimer and plasminogen activator inhibitor-1 in patients with type 2 diabetes and high blood pressure with normoalbuminuria therefore indicate a state of hypercoagulability and hypofibrinolysis, despite no evident microvascular injury supported by normal levels of von Willebrand factor and homocysteine.