Lung volumes and mean apnea duration in obstructive sleep apnea.

Former studies suggested that lung volumes might play a role in pathomechanisms of obstructive sleep apnea (OSA). Mean apnea duration (MAD) is a rarely investigated parameter in OSA but is possibly a surrogate of arousal threshold. The aim of this study was to evaluate the influence of lung volumes to MAD in OSA. In 69 patients with obstructive sleep apnea (51 male und 18 female, BMI 34.2+/-6.0 kg/m(2), age 53.6+/-9.7 years, AHI 43.1+/-21.1/h) we performed a polysomnography and pulmonary function testing in daytime. There was a significant correlation between MAD and residual volume (RV) (r=0.51; p<0.001), which was the highest correlation we found. In linear regression analysis RV remained the only independent variable with significant influence on MAD (p<0.001). We could show that RV seems to play a role in the mechanisms of apnea termination in terms of MAD. MAD reflects the time until a specific negative intrathoracic pressure is reached to induce an arousal. In this process dependency on RV could explain our results. Despite some limitations these results provide some new aspects in understanding pathophysiology of OSA.

Night eating, binge eating and related features in patients with obstructive sleep apnea syndrome.

The aim of the study was to explore the nature and extent of the association between night eating, other forms of disordered eating and obstructive sleep apnea (OSAS).Eighty-one participants (20 women and 61 men), mean age 53.7 years diagnosed with OSAS were assessed prior to starting treatment. Using a cut-off of > or =25 on the Night Eating Questionnaire (NEQ), 8.6% of the participants screened positive for night eating syndrome (NES). In addition, 7.5% met criteria for a daytime eating disorder. NES was significantly associated with diagnoses of depression, anxiety and eating disorders and was significantly correlated with an impairment of mental quality of life. No associations were found between NES and gender, BMI and the severity of the OSAS. NES does not appear to be closely linked to OSAS; however, in patients with OSAS and NES a significant co-morbidity with psychiatric disorders can be expected which might require additional treatment.

Long-term improvement of insulin sensitivity during CPAP therapy in the obstructive sleep apnoea syndrome.

BACKGROUND: We recently demonstrated that continuous positive airway pressure (CPAP) therapy rapidly improves insulin sensitivity within 2 days in non-diabetic patients with obstructive sleep apnea syndrome. In these very patients we investigated whether this improvement of insulin sensitivity is maintained during long-term CPAP therapy. MATERIAL/METHODS: After a mean of 2.9 years (963+/-98 days) of CPAP treatment, these patients were reevaluated and hyperinsulinemic euglycemic clamp studies were performed in those with regular and effective CPAP treatment. RESULTS: From the initial 31 patients 16 could be reevaluated. 4 patients did not use their devices regularly (CPAP usage <2.5 h/night), 2 patients had insufficient CPAP treatment (AHI > or =10/h). One patient had developed type 2 diabetes mellitus. In the remaining 9 patients who used their devices regularly and effective (mean CPAP usage 5.2+/-1.6 h/night, mean AHI 3.3+/-2.6/h), mean insulin sensitivity index (ISI) was significantly higher than the baseline ISI established 2.9 years before (10.6+/-7.0 vs. 6.3+/-5.6 micromol/kg x min; p=0.008). At baseline 7 out of 9 patients had an impaired fasting glucose, after 2.9 years of treatment 3 out of 9 patients still had an impaired fasting glucose. The mean body mass index (BMI) had remained unchanged (31.4+/-7.8 vs. 31.4+/-7.6 kg/m2; mean individual difference -0.02+/-1.9 kg/m2). CONCLUSIONS: OSA is a risk factor for impaired insulin sensitivity. CPAP treatment, when used regularly and with effective pressure, may improve insulin sensitivity over long time.

Resistin levels in patients with obstructive sleep apnoea syndrome--the link to subclinical inflammation?

BACKGROUND: The role of resistin, a "new" white adipose tissue hormone, still needs to be established. Its linkage to insulin sensitivity and body mass was controversial in previous studies. MATERIAL/METHODS: Twenty obese patients (BMI: 32.1+/-6.9 kg/m2 ) with obstructive sleep apnoea syndrome (OSAS) (Apnoea-Hypopnoea Index: 48.6+/-19.1, underwent measurements of resistin, interleukin-6 (IL-6), intracellular adhesion molecule-1 (ICAM-1), CRP and the insulin sensitivity index (ISI) by hyperinsulinaemic euglycaemic clamp before, 2 days and 2 months after onset of CPAP treatment. RESULTS: Resistin remained unchanged during CPAP-therapy and was negatively correlated to ISI (r=-0.359; p=0.006), the latter was significantly improved by CPAP (p<0.001). In a correlation matrix, IL-6 and ICAM-1 were significantly (p=0.001) correlated to resistin (p=0.614 and 0.427). Changes of inflammatory markers under CPAP treatment were related to AHI, as well as resistin changes. CONCLUSIONS: In agreement with previous investigations, we could only demonstrate a weak linkage between ISI and resistin. However, at least in obese patients with OSAS, there is a close relation to subclinical inflammation (IL-6) and endothelial activation (ICAM-1).

The effect of continuous positive airway pressure treatment on insulin sensitivity in patients with obstructive sleep apnoea syndrome and type 2 diabetes.

BACKGROUND: The obstructive sleep apnoea syndrome (OSA) is a frequent condition, as well as type 2 diabetes mellitus. Both diseases are characterized by insulin resistance. OBJECTIVES: The aim of this study was to establish whether OSA is an independent risk factor for increased insulin resistance in diabetics. For this purpose, we tested the hypothesis that the insulin sensitivity in patients with type 2 diabetes and OSA can be improved by 2 days or 3 months of continuous positive airway pressure (CPAP) treatment. METHODS: In 9 obese patients with type 2 diabetes and OSA [apnoea/hypopnoea index 43.1 +/- 21.3; body mass index (BMI) 37.3 +/- 5.6 kg/m2] and good glycaemic control on oral antidiabetics or on diet alone (HbA1c 6.4 +/- 0.7%), the insulin sensitivity index (ISI) was established by euglycaemic hyperinsulinaemic clamp tests at baseline, after 2 days and after 3 months of effective CPAP treatment. RESULTS: ISI was unchanged after 2 days of CPAP treatment, but was significantly improved after 3 months (4.38 +/- 2.94 vs. 2.74 +/- 2.25 at baseline; p = 0.021), without any significant changes in BMI. Glycaemic control was unaffected after 3 months (HbA1c 6.3 +/- 0.6%; not significant). Fasting leptin levels showed no significant changes. CONCLUSIONS: These results indicate that OSA itself is an independent risk factor for insulin resistance. This effect may be explained by the elevated sympathetic activity in OSA.

Continuous positive airway pressure treatment rapidly improves insulin sensitivity in patients with obstructive sleep apnea syndrome.

The obstructive sleep apnea syndrome is typically associated with conditions known to increase insulin resistance as hypertension, obesity, and diabetes. We investigated whether obstructive sleep apnea itself is an independent risk factor for increased insulin resistance and whether continuous positive airway pressure (CPAP) treatment improves insulin sensitivity. Forty patients (apnea-hypopnea index > 20) were treated with CPAP. Before, 2 days after, and after 3 months of effective CPAP treatment, hyperinsulinemic euglycemic clamp studies were performed. Insulin sensitivity significantly increased after 2 days (5.75 +/- 4.20 baseline versus 6.79 +/- 4.91 micromol/kg.min; p = 0.003) and remained stable after 3 months of treatment. The improvement in insulin sensitivity after 2 days was much greater in patients with a body mass index less than 30 kg/m2 than in more obese patients. The improved insulin sensitivity after 2 nights of treatment may reflect a decreasing sympathetic activity, indicating that sleep apnea is an independent risk factor for increased insulin resistance. The effect of CPAP on insulin sensitivity is smaller in obese patients than in nonobese patients, suggesting that in obese individuals insulin sensitivity is mainly determined by obesity and, to a smaller extent, by sleep apnea.

Insulin resistance, hyperleptinemia, and obstructive sleep apnea in Launois-Bensaude syndrome.

OBJECTIVE: Launois-Bensaude Syndrome (LBS) is a very rare cause of obesity, characterized by a symmetrical accumulation of a very large number of lipomata in different regions of the body, excluding the face, the forearms, and the shanks. Obesity is known to be closely associated with insulin resistance, hyperleptinemia, and obstructive sleep apnea (OSA). We were interested in studying whether these conditions are also present in patients with obesity due to LBS with a similar frequency as in patients with "simple" truncal obesity. RESEARCH METHODS AND PROCEDURES: We performed polysomnography and hyperinsulinemic euglycemic clamp studies and measured serum leptin in three patients with LBS and in six patients with "simple" truncal obesity, matched for sex and body mass index (LBS group, 36.39 kg/m(2); controls, 35.82 kg/m(2)). RESULTS: Polysomnography revealed severe OSA in one LBS patient with marked "horsecollar lipomata." In the other LBS patients, no OSA could be demonstrated. The leptin levels of the two groups were comparable (LBS group, 36.39 microg/liter; controls, 37.18 microg/liter) and the insulin responsiveness index was also comparable in the two groups (LBS group, 3.47 micromol/kg. minute; controls, 3.79 micromol/kg. minute). DISCUSSION: Patients with LBS demonstrated similar metabolic features in terms of insulin sensitivity and hyperleptinemia as patients with "simple" truncal obesity. LBS is not strictly associated with OSA.

Cat-scratch disease in an immunocompromised host.

BACKGROUND: The main causative agents of cat-scratch disease are Bartonella henselae, tiny, gram-negative bacilli. The disease usually has a benign course with the development of a papule at the inoculation site, followed by regional lymphadenopathy. In most cases, complete resolution occurs, but in immunocompromised hosts, the course of the disease can be aggravated. CASE REPORT: A patient received methotrexate and corticosteroids for 3 months due to rheumatoid arthritis. He developed fever, exanthema and leukopenia under methotrexate therapy. Dark red indurations with central ulcerations at his right thigh revealed a further problem apart from the methotrexate-induced leucopenia and immunosuppression. The ulcerations were the remainders of recurrent scratches from the patient's cat. The patient's antibody titers against Bartonella henselae remained low and inguinal lymph node swelling was only for a short time to be observed, this reaction obviously weakened as a result of the immunosuppression. However, the typical course, the exclusion of other reasons for the exanthema and the rapid improvement of the patient's condition after antibiotic treatment ascertained the diagnosis. CONCLUSIONS: In immunocompromised hosts, diseases with a typically benign course can become severe and life-threatening illnesses. Ownership of pets should be taken into consideration before onset of an immunosuppressive therapy.