V348I mutation in UL23 gene of human herpesvirus 1 in a case of herpetic hepatitis and haemophagocytic lymphohistiocytosis.

We herein report the case of a young immunocompetent adult patient with a rapidly fatal haemophagocytic lymphohistiocytosis syndrome related to human herpesvirus 1 (HHV-1) infection, with herpetic hepatitis and persistent high-level viraemia despite treatment with acyclovir. Haemophagocytic lymphohistiocytosis was confirmed in the patient's spleen and bone marrow. HHV-1 DNA was extracted from whole blood and liver biopsy and the UL23 gene was sequenced. A V348I natural polymorphism of the TK protein was found in blood and liver specimens. Further studies are needed to investigate the role of this polymorphism in the development of systemic immune dysregulation.

Non-invasive ventilation as a first-line treatment for acute respiratory failure: "real life" experience in the emergency department.

OBJECTIVE: To describe our experience with non-invasive ventilation (NIV) for patients with acute respiratory failure (ARF) in the emergency department (ED). METHODS: A prospective/retrospective, observational study on 190 patients with ARF (mean +/-SD age 72.2+/-12.9 years, mean APACHE II score 18.9+/-5.9), who received 200 NIV trials in an ED. We analysed the NIV register data (prospectively collected) and medical records (retrospective data abstraction) and evaluated clinical indications for NIV, patient outcomes, and predictive factors for success and death. NIV success was defined as tolerance of the procedure and no need for endotracheal intubation (ETI). RESULTS: Main indications to NIV were cardiogenic pulmonary oedema (CPE) (70 trials), acute exacerbation of COPD (39), both CPE and acute exacerbation of COPD (11), pneumonia (48), decompensation of obesity/hypoventilation (6), other conditions (26). The procedure was successful in 60.5% of trials. Global mortality was 34.5%, similar to the APACHE II predicted mortality of 32%. ETI rates were 6.5% and tracheostomy rates 1%. The improvement of pH within six hours after NIV initiation was predictive of survival in the hypercapnic group. CONCLUSIONS: Our results confirm the global efficacy of NIV in an ED setting, and show that, in spite of lower success rate in "real practice" in comparison with RCTs, an intermediate care unit can represent an appropriate and less expensive setting to perform this technique. The low rate of ETI seems to be because of the high number of patients for whom NIV was used as "ceiling" treatment.

Nicotine effects on alveolar bone changes induced by occlusal trauma: a histometric study in rats.

BACKGROUND: The aim of the present study was to verify nicotine effects on alveolar bone changes induced by occlusal trauma during a periodontitis experimental model in rats. METHODS: Thirty adult male rats were used. The animals were randomly assigned to one of three groups receiving daily intraperitoneal injections: A, nicotine solution (0.44 mg/ml) and occlusal overload; B, saline solution and occlusal overload; or C, saline solution. Rats from groups A and B underwent bilateral amputation of the second and third molar cusps to simulate an occlusal overload. The first molars were then randomly assigned to receive a cotton ligature in the sulcular area, while the contralateral tooth was left unligated. The animals were sacrificed 30 days later. The resected mandibles were processed, and histomorphometric measurements were performed in the alveolar bone adjacent to the furcation area of the first molars. RESULTS: Nicotine enhanced the bone loss induced by occlusal trauma (P<0.001) on the ligated teeth of group A (12.27 +/- 4.4 mm2), when compared to groups B (8.43 +/- 3.51 mm2) and C (4.43 +/- 2.17 mm2). Alveolar bone loss (P<0.01) was also observed in the contralateral teeth of groups A (nicotine + trauma) and B (saline + trauma), when compared to group C (saline only). CONCLUSION: Within the limits of the study, it is concluded that nicotine may influence the alveolar bone changes induced by occlusal trauma by enhancing bone loss.

Urinary protein excretion induced by exercise: effect of a mountain agonistic footrace in healthy subjects. Renal function and mountain footrace.

The increase in albuminuria induced by exercise in healthy subjects is variably dependent on an increased glomerular filtration and/or to a decreased tubular reabsorption of albumin, in relation to the intensity of muscular work. Membrane anionic charges and haemodynamic changes have been implicated in exercise-induced albuminuria. We evaluated in 12 healthy subjects albumin and beta-2-microglobulin excretion rate and the presence in urine of cationic compounds before and after an agonistic mountain footrace. Albumin excretion rate increased significantly (3.7 +/- 1.3 vs 43.7 +/- 10.0 micrograms/min) (p less than 0.001) and beta-2-microglobulin excretion rate (16.5 +/- 4.4 vs 37.9 +/- 7.4 micrograms/min) (p less than 0.025), too. In 3/4 subjects, urines revealed a peak of highly cationic proteins, sharing antigenic and biological characteristics with platelet-derived cationic proteins. The increase in albuminuria induced by strenuous exercise of an agonistic mountain footrace is of mixed type (both glomerular and tubular) and is associated to the urinary excretion of cationic proteins.

The increase in albuminuria induced by exercise is not associated with preferential excretion of glycated albumin in type 1 (insulin-dependent) diabetic patients.

The increase in urinary albumin excretion induced by acute exercise in Type 1 (insulin-dependent) diabetic patients is associated with the urinary excretion of cationic proteins. To test whether the renal excretion of glycated albumin (more anionic than non-glycated albumin) is affected by exercise, we submitted seven normoalbuminuric (albumin excretion rate less than 30 mg/24 h) Type 1 diabetic patients and six well-matched healthy subjects to an exercise test (600 kpm/min for 20 min) on a bicycle ergometer, preceded and followed by a 1-h resting period. The selectivity index (renal clearance of non-glycated/glycated albumin) was not significantly different among the pre-exercise, exercise and post-exercise periods, either in the normal subjects (1.01 +/- 0.03 vs 1.08 +/- 0.06 vs 1.08 +/- 0.05) or in the diabetic patients (1.25 +/- 0.09 vs 1.20 +/- 0.07 vs 1.20 +/- 0.06), whereas it was significantly higher (p less than 0.05) in diabetic patients compared to healthy subjects during pre-exercise. These results are not consistent with the hypothesis that acute exercise may induce a preferential excretion of glycated albumin.