Weight loss induced alleviation of sleep-disordered breathing is associated with improvement of non-alcoholic fatty liver disease.

INTRODUCTION: Sleep-disordered breathing (SDB) and non-alcoholic fatty liver disease (NAFLD) are both common comorbidities in obese patients. Structured weight loss programs are effective and can reduce the incidence and severity of obesity-related comorbidities. The objective of the present analysis is to test whether weight loss induced alleviation of SDB is a predictor for improvement of NAFLD. METHODS: Obese participants underwent a standardized non-surgical 3 months weight reduction program (800 kilocalories per day with low carbohydrate and fat content). Abdominal sonography for NAFLD (grade 0 to 3) and monitoring for SDB (defined as apnea-hypopnea index [AHI] ≥ 15/h) were performed at baseline and after 3 months. Alleviation of SDB was defined as a shift from AHI≥ 15/h to <15/h. RESULTS: 48 patients (48% female, age 42 ± 12 years, body-mass index 40.3 ± 8.1 kg/m2, AHI 14 ± 17/h, 85% NAFLD grade ≥1) participated in the weight loss program. In contrast to the no SDB group, in patients with SDB weight loss of 27.1 ±0 .9 kg (8.4 ± 2.8 kg/m2) after three months was paralleled by a reduction in AHI (-22 ± 17/h), prevalence of SDB (from 31% to 13%), and oxidized low-density lipoprotein (-13 ± 11 U/l). In individuals with preexisting SDB NAFLD grade improved more (2 versus 1, p<0.001) and was at a lower degree at 3 months than in those without SDB (0 versus 1, p = 0.015). In multivariable analysis models, SDB at baseline was associated with improvement of NAFLD grade (B 0.908; 95% CI 0.125, 1.691; p = 0.024), independently of age, sex, and BMI (each p>0.05, respectively). Decreasing BMI (B 0.16 [95%-CI 0.08; 0.23], p<0.001) and alleviation of SDB (B 0.90 [95%-CI 0.21; 1.58], p = 0.012) were independently associated with improvement of NAFLD grade. CONCLUSION: Preexisting SDB and weight loss induced alleviation of SDB are predictors for improvement in NAFLD grade, independent of the extent of weight loss. SDB may contribute to the pathogenesis of NAFLD via SDB-induced oxidative stress and inflammation, but the causal mechanism remains unclear.

Adipocyte fatty acid-binding protein levels are associated with left ventricular diastolic dysfunction in morbidly obese subjects.

OBJECTIVES: This study aimed to examine the association of adipocyte fatty acid-binding protein (FABP4) levels with left ventricular diastolic dysfunction (LVDD) in obese subjects with varying degrees of the metabolic syndrome (MetS). METHODS: Fifty morbidly obese subjects with LVDD were selected at random and matched by age (±5 years) and sex with 50 morbidly obese with normal left ventricular (LV) function. In addition, 24 healthy lean subjects were included as controls. RESULTS: Median FABP4 levels (interquartile range) in obese subjects with LVDD were significantly higher (42 ng ml(-1) (32-53)) than in obese with normal LV function (24 ng ml(-1) (36-43), P=0.036), and in normal weight controls (13 ng ml(-1) (10-20), P<0.0001). Increasing FABP4 tertiles were significantly associated with parameters of LVDD, the number of LVDD components, physical performance and epicardial fat thickness. In multivariate regression analysis adjusting for age, sex and adiposity, FABP4 levels remained significantly associated with parameters of diastolic function. The association of FABP4 levels with LVDD was mainly observed in subjects with metabolic complications, but not in metabolically healthy obese. CONCLUSIONS: FABP4 levels are significantly associated with LVDD in obese subjects, when the MetS is present. Thus, FABP4 may be a link between obesity and cardiometabolic disorders.

Comparison of the Nidek EAS 1000 system and the Topcon SL-45 in clinical application.

Some years ago, Nidek developed a new imaging system for the anterior eye segment, which offers the possibility of recording Scheimpflug and retroillumination images. The system consists of 2 different technical units, a camera unit for image recording and a computer unit for storage, system operation and image analysis. To evaluate the clinical use of the system and its reproducibility, a study with 31 volunteers/patients was performed that were photographed with the Nidek EAS 1000 at the meridians 0 degree, 45 degrees and 180 degrees. Two examinations with a 1-week interval were performed. In addition, a direct comparison of the EAS 1000 with the Topcon SL-45 was carried out with 32 volunteers that were photographed at 0 degree and 45 degrees; a retroillumination photo was additionally recorded. The video images were evaluated with the computer software, the SL-45 negatives were standardly measured with a Joyce-Loebl densitometer. The handling of the EAS 1000 in clinical use was found to be easy and comfortable for the patient, as the alignment is done with infrared light. Difficulties occur only with the retroillumination photography in that the infrared light for imaging may outshine the red fixation light during exposure. However, shadowing problems due to the eyelashes occur in oblique slit positions, especially in those patients with a pronounced front head. In studying the reproducibility, the mean values of the individual coefficients of variation for light scattering (density) were in a range between 3.6 and 5.06%, but more than 35% of the single values show a variation coefficient above 5% (maximum 20.3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral perfusion deficits in dysbaric illness.

Decompression sickness (DCS) is usually categorised as type I (mild; peripheral pain, non-neurological) or type II (serious; neurological). Type II is regarded as predominantly a spinal cord disease with infrequent cerebral involvement. Cerebral perfusion was studied by injection of 99Tcm-hexamethylpropyleneamine oxime and single photon emission tomography in 28 divers with confirmed incidents of DCS and cerebral arterial gas embolism (CAGE). Cerebral perfusion deficits were present in all 23 cases of type II DCS and in all 4 cases of CAGE. No deficits were present in the single case of type I DCS. Type II DCS should be recognised as a diffuse, multifocal, central nervous system disease.