Dental implants in patients seropositive for HIV: A 12-year follow-up study.

BACKGROUND AND OVERVIEW: Patients seropositive HIV and AIDS represent a group of patients who experience longer longevity at the expense of effective therapies for infection control and related opportunistic diseases. However, the prolonged use of these drugs is often associated with adverse events, which theoretically may influence dental management and the long-term stability of dental implants. The objective of this study was to prospectively evaluate a group of HIV-positive people from a previous study who had received dental implants for 12 years after oral rehabilitation and functional loading. CASE DESCRIPTION: Nine patients with a total of 18 implants participated in this study. Viral load was undetectable in 8 patients, with 1 who had 48 copies/milliliter. The cluster of differentiation 4 T lymphocyte count ranged from 227 through 1,000 cells/cubic millimeter, mean (standard deviation [SD]) 564 (271.13) cells/mm3. Five of the 9 (55.5%) patients had visible plaque, and 5 (55.5%) had bleeding on probing with no implant mobility. Radiographs obtained at 6 months, 12 months, and 12 years of functional loading showed mean (SD) marginal bone losses of 0.32 (0.23) mm, 0.37 (0.23) mm, and 2.43 (1.48), respectively. CONCLUSION AND PRACTICAL IMPLICATIONS: These results suggest that dental implant treatment in HIV-positive patients achieved long-term survival, with a success rate comparable with that observed in healthy patients, indicating that implant rehabilitation is not a contraindication for HIV-positive patients.

Mechanical determinants of early acute ventilatory failure in COPD patients: a physiologic study.

OBJECTIVE: The purpose of this study is to investigate the respiratory mechanics, breathing pattern, and pressure-generating capacity of respiratory muscles during the early phases of an acute exacerbation of COPD. DESIGN: Prospective study. SETTING: Division of Emergency Critical Care and Chronic Ventilator Unit. PATIENTS: A total of 24 COPD patients: nine patients requiring ventilatory support because of acute respiratory acidosis due to COPD exacerbation (NPPV group, pH 7.28 +/- 0.02); seven patients successfully managed with medical therapy only (SB group, pH 7.39 +/- 0.04); eight clinically stable, long term mechanically ventilated, COPD patients (IPPV group). MEASUREMENTS: Respiratory mechanics during a period of unsupported breathing. RESULTS: A rapid shallow breathing, in the presence of a high drive to breath and a high diaphragmatic tension-time index (TT(di)), was found in NPPV and IPPV groups compared to the SB group (f/V (T) ratio: 118 +/- 43 and 137 +/- 65, respectively, versus 37 +/- 12 breaths/min/L; P (0.1): 5.0 +/- 1.0 and 5.4 +/- 1.4, respectively, versus 2.2 +/- 0.2 cmH(2)O, TT(di): 0.168 +/- 0.035 and 0.161 +/- 0.039, respectively, versus 0.057 +/- 0.033); at variance, PEEPi(dyn) was greater in IPPV compared to the other two groups. A significant relationship was observed between TT(di) ratio and f/V (T) (Rho 0.756). CONCLUSION: During the early phases of an acute exacerbation, patients with COPD and acute respiratory failure had an imbalance between the decreased capacity of the respiratory muscles to generate pressure and the increased respiratory load. This imbalance was similar to that recorded in patients with COPD and chronic ventilatory failure. In both groups, the imbalance was associated with rapid shallow breathing. Among the mechanical constraints to ventilation, only PEEPi,dyn was different between acute and chronic patients with ventilatory failure.

Autonomic neuropathy and QT interval in hemodialysed patients.

BACKGROUND: QT interval prolongation increases the risk of ventricular arrhythmias and sudden death in diabetic autonomic neuropathy and ischemic heart disease. In end-stage renal disease (ESRD), the effects of hemodialysis on QT interval are diverse and the influence of autonomic neuropathy has yet to be clearly defined. METHODS: Sixty-nine ERSD patients (age 64 +/- 14) were studied. Prior to the dialysis session, patients underwent four standard autonomic cardiovascular tests; before and after the dialysis session, a 12-lead ECG was recorded. Corrected QT intervals (QTc) were measured and QT dispersion (QTd) was calculated. Twelve subjects (age 59 +/- 6) with normal renal function served as control group. RESULTS: Compared to controls, ESRD patients showed a longer QTc (434 +/- 26 vs 414 +/- 28 ms; p = 0.016) and a similar QTd (35 +/- 13 vs 37 +/- 14 ms; p = 0.54).QTc was > 440 ms in 33.3% of the patients. No difference in the prevalence or score of autonomic neuropathy was observed between the subgroups with and without a prolonged QTc. After the hemodialysis session, QTc increased in 56% and decreased in 43% of the patients, and QTd increased in 45 % and decreased in 55% of the patients. QTc and QTd changes were not related to the presence of autonomic neuropathy. CONCLUSIONS: A large variability in QTc and QTd response was observed after hemodialysis. Autonomic neuropathy did not contribute to QTc and QTd length, nor to QTc and QTd change after dialysis.

Helicobacter pylori infection and gastric function in primary autonomic neuropathy.

Helicobacter pylori (Hp) infection in diabetic patients has been related to impaired gastric clearance of bacteria due to autonomic neuropathy. Gastrointestinal dysfunction has been described in primary autonomic failure (AF). The aim of the study was to evaluate, for the first time, the presence of Hp infection and gastric function in patients with primary AF Twelve patients with primary AF (aged 58-78), 31 healthy controls (aged 48-75) and 31 patients affected by type 2 diabetes (aged 46-75) were studied. A 13C-urea breath test was performed to assess the presence of Hp infection. To evaluate gastric function, AF patients underwent two non-invasive tests: 1) 13C-octanoic acid breath test (OBT) to evaluate gastric emptying, and 2) electrogastrogram (EGG) to evaluate gastric electrical activity. Hp infection was found in 100% of AF patients, in 48% of controls and in 71% of diabetic patients (p = 0.02 between groups). Electrical or mechanical gastric function was altered in 50% of AF patients. In particular, 1) after OBT, half-time gastric emptying was delayed in 6 out of 12 patients, and 2) EGG showed the presence of gastric dysrhythmias in 6 out of 12 patients. In conclusion, Hp infection was detected in all AF patients studied; as previously demonstrated in diabetes, such a finding might be related to autonomic neuropathy causing mechanical or electrical gastric dysfunction. Hp detection might be important for the gastrointestinal and extradigestive complications of such infection.

Nonalcoholic steatohepatitis, insulin resistance, and metabolic syndrome: further evidence for an etiologic association.

This study aims to determine the presence of the components of the metabolic syndrome in primary nonalcoholic steatohepatitis (NASH) and to assess the role of liver disease in the genesis of peripheral hyperinsulinemia. Nineteen patients (18 men and 1 woman; mean age, +/- SD, 38 +/- 10 years; body mass index [BMI], 26 +/- 2 kg/m(2)) with histologic evidence of NASH were enrolled; 19 age- and sex-matched normal subjects were investigated as controls. Plasma glucose, insulin, and C-peptide levels were measured during an oral glucose tolerance test, and a frequently sampled intravenous glucose tolerance test (FSIGT), analyzed by minimal modeling technique, was performed. Compared with controls, the NASH group had lower insulin sensitivity (3.84 +/- 2.44 vs. 7.48 +/- 3.01 10(-4) x min(-1)/microU/mL; P =.0003) and higher total insulin secretion (21 +/- 13 vs. 10 +/- 3 nmol/L in 240 minutes; P =.001). Hepatic insulin extraction was similar in both groups (69.8% +/- 16.1% vs. 70.2% +/- 18.3%; P =.854). According to the results of the oral glucose tolerance test, no patient was classified as diabetic, 5 were classified as glucose intolerant, and 1 was classified as having impaired fasting glycemia. Nine patients (47%) had at least the 2 minimum criteria required to define the metabolic syndrome according to the European Group for the Study of Insulin Resistance (EGIR). In conclusion, hyperinsulinemia and insulin resistance occur frequently in patients with NASH; these conditions do not stem from a reduced hepatic insulin extraction but from an enhanced pancreatic insulin secretion compensatory to reduced insulin sensitivity. The derangement of insulin regulation, often associated with the metabolic syndrome, may play a causal role in the pathogenesis of NASH.