Diagnosis of Bexler Apnea Syndrome in newborn. What is this?This is a 3&1/2 month old baby with numerous problems;
Cranial Facial, Hypothyroidism,Hypocalcium, Bilateral ear anomalies, Bilateral hip dislocation , Colostomy, Perferated Anus, Trach, MicKey Button, GERD,
-tll
I dunno what it is try googling it.....
I am sorry sounds like the baby is have a rough time!!
-debrasearch
Inflammation and Obstructive Sleep Apnea Syndrome
How Many Ways Do I Look at Thee?
Umur Hatipolu, MD and Israel Rubinstein, MD, FCCP
Chicago, IL
Dr. Hatipolu is Clinical Assistant Professor of Medicine, Section of Respiratory and Critical Care Medicine, Department of Medicine, University of Illinois at Chicago; Dr. Rubinstein is Professor of Medicine, Section of Respiratory and Critical Care Medicine, Department of Medicine, University of Illinois at Chicago and VA Chicago Health Care System.
Correspondence to: Israel Rubinstein, MD, FCCP, Department of Medicine (M/C 719), University of Illinois at Chicago, 840 South Wood St, Room 173, Chicago, IL 60616-7323; e-mail:IRubinst@uic.edu
Obstructive sleep apnea syndrome (OSAS) is characterized by repeated episodes of upper airway occlusion during sleep that are associated with excessive daytime sleepiness and abnormalities in cardiopulmonary and metabolic function. Anatomic narrowing of the airway, increased collapsibility of upper airway tissue, abnormal upper airway reflexes, and pharyngeal inspiratory muscle dysfunction contribute to the occurrence of airway occlusion.
Studies have implicated local and systemic inflammation in the pathophysiology of this seemingly all-mechanical problem. Histologic analysis of tissues obtained from patients undergoing uvulopalatopharyngoplasty for obstructive sleep apnea reveals marked subepithelial edema,1 excessive plasma cell infiltration,2 and reduction in surface area of connective tissue papillae that provide anchorage for epithelium.3 In the nasal lavage fluid of patients with obstructive sleep apnea, polymorphonuclear leukocytes and concentrations of bradykinin and vasoactive intestinal peptide are increased.45 These inflammatory changes are postulated to occur, in part, due to snoring that evokes vibration frequencies associated with soft-tissue damage.6 In addition to local inflammation, evidence of systemic inflammation is present in patients with OSAS.
Tumor necrosis factor (TNF)- and interleukin-6 levels are elevated in patients with OSAS when compared with patients with hypersomnia7 and subjects with nonapneic obesity.8 Importantly, the circadian rhythm of TNF- secretion in patients with OSAS is markedly different compared with healthy volunteers.9 Application of nasal continuous positive airway pressure (CPAP) for 3 months does not change the abnormal circadian pattern, implying a role for inflammation independent of mechanical obstruction in pathogenesis of obstructive sleep apnea. Given that TNF- is thought to modulate somnolence and fatigue, this cytokine may play a role in mediating the constitutional symptoms of obstructive sleep apnea.
C-reactive protein, a sensitive marker for systemic inflammation, is increased in patients with obstructive sleep apnea when compared with control subjects matched for age and body mass index.10 After 1 month of nasal CPAP therapy, there is a marked reduction in serum levels of C-reactive protein and monocyte production of interleukin-6 without a change in body mass index.11 Reactive oxygen species such as superoxide anion and hydroxyl radical are injurious to cells, and are implicated in ischemia reperfusion injury that is operant in conditions such as myocardial infarction and stroke. There is increased production of reactive oxygen species from inflammatory cells in patients with OSAS.1213 Following treatment with nasal CPAP, oxidative metabolism returns to normal levels.13 Whether ongoing inflammation, including in the CNS, plays a role in residual cognitive and behavioral abnormalities observed after successful nasal CPAP therapy in patients with OSAS remains to be determined.
In this issue of CHEST (see page 13), Goldbart and his colleagues report on the presence of a differential upregulation of cysteinyl leukotriene receptor (LTR)-1 and LTR-2 in tonsils of children undergoing tonsillectomy for OSAS. Expressions of both receptors were predominantly in the epithelial layer and extra follicular area within the tonsillar parenchyma, which presumably reflects the area affected by vibration trauma. The expression of both receptors was detected, albeit to a significantly lesser extent, in the tonsils of children who underwent tonsillectomy for recurrent infections.
Cysteinyl leukotrienes are major mediators of inflammation, particularly in asthma and allergic rhinitis. They have potent contractile activity on human bronchi, and also increase microvasculature permeability, mucus secretion, and eosinophil recruitment. LTR-1 and LTR-2 have been localized in bronchial smooth-muscle cells, interstitial macrophages, eosinophils, peripheral monocytes and macrophages, and mast cells. LTR-2 is also present in the heart, brain, and adrenal gland.14 To our knowledge, this is the first report of their presence in human tonsillar tissue. Furthermore, the leukotriene pathway is implicated in association with the inflammatory state of OSAS in children, again for the first time. Given that the regulation of LTRs is poorly understood and that specific receptor antagonists for LTR-2 are not yet available, additional research is warranted to elucidate the significance of these findings. Irrespective, Goldbart et al have unraveled an intriguing putative venue in the pathophysiology of OSAS in children and perhaps also in adults. Whether their observations are confined to the tonsils or could represent a more widespread phenomenon, including CNS involvement, in patients with OSAS is uncertain.
References
Saul, S, Kimmelman, CP, Brooks, JS, et al (1988) Histopathology of sleep apnea. Trans Am Laryngol Assoc 109,222-225
Sekosan, M, Zakkar, M, Wenig, B, et al Inflammation in the uvula mucosa of patients with obstructive sleep apnea. Laryngoscope 1996;106,1018-1020[CrossRef][ISI][Medline]
Paulsen, FP, Steven, P, Tsokos, M, et al Upper airway epithelial structural changes in obstructive sleep disordered breathing. Am J Respir Crit Care Med 2002;166,501-509[Abstract/Free Full Text]
Rubinstein, I Nasal inflammation in patients with obstructive sleep apnea. Laryngoscope 1995;105,175-177[ISI][Medline]
Müns, G, Rubinstein, I, Singer, P Phagocytosis and oxidative burst of granulocytes in the upper respiratory tract in chronic and acute inflammation. J Otolaryngol 1995;24,105-110[ISI][Medline]
Cohn, M, Hesla, PE, Kiel, M, et al Vibration frequency of snoring in obstructive sleep apnea syndrome. Chest 1986;89,529S
Vgontzas, AN, Papanicolaou, DA, Bixler, EO Elevation of plasma cytokines in disorders of excessive daytime sleepiness: role of sleep disturbance and obesity. J Clin Endocrinol Metab 1997;82,1313-1316[Abstract/Free Full Text]
Vgontzas, AN, Papanicolaou, DA, Bixler, EO Sleep apnea and daytime sleepiness and fatigue: relation to visceral obesity, insulin resistance, and hypercytokinemia. J Clin Endocrinol Metab 2000;85,1151-1158[Abstract/Free Full Text]
Entzian, P, Linnemann, K, Schlaak, M, et al Obstructive sleep apnea and circadian rhythms of hormones and cytokines. Am J Respir Crit Care Med 1996;153,1080-1086[Abstract]
Shamsuzzaman, AS, Winnicki, M, Lanfranchi, P, et al Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation 2002;105,2462-2464[Abstract/Free Full Text]
Yokoe, T, Minoguchi, K, Matsuo, H, et al Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation 2003;107,1129-1134[Abstract/Free Full Text]
Schulz, R, Mahmoudi, S, Hattar, K, et al Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Am J Respir Crit Care Med 2000;162,566-570[Abstract/Free Full Text]
Dyugovskaya, L, Lavie, P, Lavie, L Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients. Am J Respir Crit Care Med 2002;165,934-939[Abstract/Free Full Text]
Hui, Y, Funk, CD Cysteinyl leukotriene receptors. Biochem Pharmacol 2002;64,1549-1557[CrossRef][ISI][Medline]
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