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Background : 2006 2009 : Doctoral Program, Faculty of Medicine Universitas Indonesia, Jakarta 1994 1998 : Physical Medicine and Rehabilitation Specialist, Faculty of Medicine Universitas Indonesia, Jakarta 1983 1989 : General Practitioner, North Sumatera University, Medan Position : Januari 2002 Now : Head Division of Sport Injury and Obesity Clinic, Physical Medicine and Rehabilitation Department, RSUPN Cipto Mangunkusumo, Jakarta November 2007 2013 : Secretary of Specialist Program Physical Medicine and Rehabilitation RSUPN Cipto Mangunkusumo, Jakarta / Faculty of Medicine Universitas Indonesia, Jakarta
Organization
IDI PERDOSRI
In Elderly Patients
Sarcopenic Obesity (SO) A combination of excess weight, reduced muscle mass and / or strength and endurance Maximize their effects on physical disability, morbidity and mortality
With comorbidities
Surgery
With comorbidities
Bessesen DH, Medical evaluation of the overwight & obese patients In: Bessesen DH, Kussner R, evaluation & management of obesity. Philadelphia, Hanley and Belfus Inc, 2002, p85
Epidemiology of OSA
Approximately 25% of adults with a BMI 25 kg/m2 - 28 kg/m2 have at least mild OSA ( [AHI] > 5) The prevalence varies according to gender (~30% in men and ~15% in women), age, and body weight. Mens risk for OSA is 2x -higher than women. Postmenopausal women >>risk than premenopausal OSA prevalence increases until age 65 years
Obesity may worsen OSA fat deposition in the tissues surrounding the upper airway smaller lumen and increased collapsibility of the upper airway, predisposing to apnea. Fat deposits around the thorax chest compliance and functional residual capacity, and may O2 demand. Visceral obesity is common in subjects with OSA.
OSA patients have been shown to have increased triglycerides, total cholesterol HDL ratio and LDL and lower HDL values. Intermittent hypoxia, a key feature of OSA, causes an increase in the liver content of triglycerides in mice. OSA patients may also have reduced HDL-mediated inhibition of low density lipoprotein oxidation ex vivo . The independent roles of OSA and obesity in these abnormalities remain unclear
Leptin is a hormone produced by adipose tissue and binds to the ventral medial nucleus of hypothalamus Binding of leptin to this nucleus sensation of satiety. Sleep deprivation inhibits leptin production, suggesting a potential mechanism for the early development of obesity. Paradoxically, subjects with obesity have higher levels of leptin, likely due to increase fat mass
This hyperleptinemia is believed to be accompanied by desensitized cellular responses to leptin so that the effect of leptin is not achieved. Leptin also modulates ventilatory control, and may therefore be implicated in abnormal breathing patterns in obesity. adipokines, TNF-a and IL-6, are also elevated in obesity and may be linked to depression of CNS activity and airway neuromuscular control,perhaps increasing OSA severity
Leptin in OSA is higher than would be expected because of the obesity alone, and leptin after as little as days of CPAP Serum adiponectin have been shown to improve glucose and lipid metabolism and prevent inflammation and atherosclerosis. Adiponectin is low in obesity and also in OSA. Adiponectin levels have been shown to increase with CPAP Ghrelin, a hormone produced by cells lining the stomach, stimulates appetite a counter-regulator to leptin. Ghrelin is increased during the night in obese subjects, and reduced sleep has been shown to increase of ghrelin, stimulates appetite, and obesity and worsening of OSA.
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