M. Bosch

Free fatty acids and the metabolic syndrome in patients with obstructive sleep apnoea

Obesity and metabolic syndrome (MS) occur frequently in patients with obstructive sleep apnoea syndrome (OSAS). We hypothesised that circulating free fatty acids (FFAs) are elevated in OSAS patients independently of obesity. This elevation may contribute to the development of MS in these patients. We studied 119 OSAS patients and 119 controls. Participants were recruited and studied at sleep unit of our institution (Hospital Universitari Son Dureta, Palma de Mallorca, Spain) and were matched for sex, age and body mass index (BMI). The occurrence of MS was analysed by clinical criteria. Serum levels of FFAs, glucose, triglycerides, cholesterol, high-density lipoprotein–cholesterol, aspartate aminotransferase, alanine aminotransferase, &ggr;-glutamyltransferase, C-reactive protein and 8-isoprostanes were determined. Prevalence of MS was higher in OSAS than in the control group (38 versus 21%; p = 0.006). OSAS patients had higher FFAs levels than controls (mean±sd 12.2±4.9 versus 10.5±5.0 mg·dL−1; p = 0.015). Among subjects without MS, OSAS patients (OSAS+ MS-) showed higher levels of FFAs than controls (OSAS- MS-) (11.6±4.7 versus 10.0±4.4 mg·dL−1; p = 0.04). In a multiple regression model, after adjustment for age, sex, BMI and the presence of MS, FFAs were significantly associated with apnoea/hypopnoea index (p = 0.04). This study shows that FFAs are elevated in OSAS and could be one of the mechanisms involved in the metabolic complications of OSAS.

The measurement of exhaled carbon monoxide is influenced by airflow obstruction

The concentration of carboxyhaemoglobin (COHb) is often estimated from measurements of carbon monoxide in the exhaled air (COexh). This study investigates whether the presence of airflow obstruction significantly alters the relationship between COexh and COHb. Eighty-one regular smokers were prospectively studied and divided in four groups according to the presence and severity of airflow obstruction (none, mild, moderate, severe). In each subject, the authors measured in this order: 1) arterial blood gases; 2) haemoglobin concentration and COHb (by co-oxymetry); 3) COexh; 4) lung volumes; and 5) forced spirometry. The size of the measurement error (deltaCO) was calculated from the difference between COHb and COexh. Neither the smoking history nor COexh were different in the four groups of subjects studied. In contrast, deltaCO increased in parallel to the degree of airflow obstruction. DeltaCO was >2% (a threshold value normally used in the clinic to separate smokers from nonsmokers) only in patients with severe airflow obstruction. A stepwise multivariate analysis showed that both forced expiratory volume in one second (FEV1) (percentage reference) and COHb contributed significantly (p<0.0001) to predict deltaCO. This study shows that the estimation of carboxyhaemoglobin from exhaled carbon monoxide measurements can be inaccurate in patients with severe airflow obstruction. In these patients, the direct measurement of carboxyhaemoglobin seems advisable in clinical practice.

Recuperación de la función pulmonar tras colecistectomía laparoscópica: papel del dolor postoperatorio

OBJECTIVES: Lung function has been shown to deteriorate after laparoscopic cholecystectomy (LC). The present study evaluated 1) the rate of recovery after LC, and 2) the pathogenic role of postoperative pain in functional deterioration. DESIGN: Lung function was measured 24 hours before LC, upon hospital discharge (48-72 h after LC), and 10 days later. All patients received metamizol after LC until discharge (2 g every 6 h i.v.). Half the patients (analgesia group) received tramadol (150 mg i.m.) 30 minutes before lung function testing on the day of hospital discharge. The remaining patients constituted the control group. PATIENTS: Twenty healthy subjects (53 4 years old) undergoing LC for gall bladder removal. All signed informed consent forms. Measures and outcomes: Patient characteristics and preoperative lung function results were similar in both groups. LC duration and postoperative course were also similar in both groups. All were discharged without complications within 72 hours after LC. Lung function upon discharge (FVC, FEV1, TLC, PaO2 and AaPO2) had deteriorated in both groups (p<0.001). Deterioration was less marked in the analgesia group (p < 0.05). Ten days later, lung function had normalized for all subjects. CONCLUSIONS: These results indicate that after LC, 1) lung function is still abnormal when the patient is discharged from hospital, 2) lung function has fully recovered within 10 days, and 3) postoperative pain contributes significantly to temporary deterioration in lung function.