losartan-potassium and Sleep-Apnea-Syndromes

Currently available data regarding the blood levels of erythropoietin (EPO) in sleep apnea (SA) patients are contradictory. The aim of the present meta-analysis was to evaluate the EPO levels in SA patients via quantitative analysis. A systematic search of Pubmed, Embase, and Web of Science were performed. EPO levels in SA group and control group were extracted from each eligible study. Weight mean difference (WMD) or Standard mean difference (SMD) with 95% confidence interval (CI) was calculated by using fixed-effects or random effect model analysis according to the degree of heterogeneity between studies. A total of 9 studies involving 407 participants were enrolled. The results indicated that EPO levels in SA group were significantly higher than that in control group (SMD 0.61, 95% CI 0.11-1.11, p = 0.016). Significantly higher EPO levels were found in patients with body mass index <30 kg/m

Topics: Erythropoietin; Humans; Sleep Apnea Syndromes; Statistics as Topic

Topics: Angiotensin II; Angiotensin Receptor Antagonists; Antihypertensive Agents; Calcium Channel Blockers; Erythropoietin; Humans; Hypertension; Kidney Failure, Chronic; Renal Circulation; Renal Dialysis; Renin-Angiotensin System; Sleep Apnea Syndromes; Sympathetic Nervous System; Vascular Resistance

The failure to lower systolic blood pressure at night (called non-dipping) and sleep apnea are both associated with adverse cardiovascular outcomes. Sleep apnea is a common cause of non-dipping blood pressure.. Sleep apnea increases night time blood pressure through enhanced cardiac pre-load, sleep disturbance and hypoxia. Hypoxia elicits increased levels of norepinephrine, endothelin and erythropoetin. Patients with sleep apnea tend to be elderly and obese, so they have poor endothelial nitric oxide release and blunted baroreflexes. They thus have several stimuli for high blood pressure and poor compensatory mechanisms to lower blood pressure.. Non-dipping patients without sleep apnea have evidence of volume overload and correct their blood pressure pattern in response to diuretics. Individuals with sleep apnea have evidence of increased cardiac pre-load from episodes of negative intrathoracic pressure. Their daytime blood pressure responds poorly to many drugs, but beta blockers may be effective. Their night time blood pressure responds only slightly to therapy of their sleep apnea with continuous positive airway pressure, even though continuous positive airway pressure decreases their norepinephrine, erythropoetin and endothelin levels.

Topics: Blood Pressure; Blood Volume; Cardiovascular Diseases; Circadian Rhythm; Endothelins; Erythropoietin; Humans; Hypertension; Kidney Diseases; Nitric Oxide; Racial Groups; Respiration, Artificial; Sleep Apnea Syndromes; Sleep Wake Disorders

Chronic renal failure, dialysis and transplantation have major effects on male reproductive health because of the impairment of spermatogenesis, steroidogenesis and sexual function. Hypothalamo-pituitary testicular dysfunction in uraemia is manifest clinically as delayed growth and puberty, sexual dysfunction, androgen deficiency, impaired spermatogenesis and infertility. Apart from renal anaemia, there are at present no proven indications for androgen therapy in chronic renal failure. This chapter reviews the basis and scope for various clinical applications of gonadotropin and androgen therapy as an adjunct to the standard medical care of chronic renal failure. The therapeutic possibilities implied by experimental and clinical findings suggesting that uraemic hypogonadism may be a functional state of gonadotropin deficiency are emphasized.

Topics: Anemia; Clinical Trials as Topic; Enuresis; Erythropoietin; Gonadotropins; Growth Disorders; Humans; Infertility, Male; Kidney Failure, Chronic; Male; Puberty, Delayed; Sleep Apnea Syndromes; Testosterone

Tissue hypoxia stimulates the production of erythropoietin (EPO), the main effect of which is, in turn, to stimulate erythropoiesis. Sleep apnea-hypopnea syndrome (SAHS) is an entity characterized by repeated episodes of hypoxemia during sleep.. To analyze whether hypoxemia stimulated increased urinary excretion of EPO, and if so, to evaluate if treatment with continuous positive airway pressure (CPAP) can inhibit this phenomenon.. We studied 25 subjects with suspected SAHS who underwent a polysomnography study (PSG). EPO levels in first morning urine (uEPO) and blood creatinine and hemoglobin were determined in all patients. Patients with severe SAHS repeated the same determinations after CPAP treatment.. Twelve subjects were diagnosed with severe SAHS (mean ± SD, AHI 53.1 ± 22.7). Creatinine and hemoglobin levels were normal in all subjects. uEPO was 4 times higher in the SAHS group than in the control group (1.32 ± 0.83 vs. 0.32 ± 0.35 UI/l, p <.002). CPAP treatment reduced uEPO to 0.61 ± 0.9 UI/l (p <.02), levels close to those observed in healthy subjects. No dose-response relationship was observed between severity of PSG changes and uEPO values.. Patients with severe SAHS show increased uEPO excretion, but this normalizes after treatment with CPAP.

Topics: Adult; Aged; Cell Hypoxia; Continuous Positive Airway Pressure; Creatinine; Erythropoietin; Female; Hemoglobins; Humans; Hypoxia; Male; Middle Aged; Polysomnography; Sleep Apnea Syndromes

The effect of nasal continuous positive pressure (CPAP) treatment on erythropoietin (EPO) was examined by measuring diurnal serum EPO levels before and twice (over the 3rd day and over 1 day on recall after > or = 1 mo of therapy) after initiation of treatment in 12 obstructive sleep apnea syndrome patients with normal hemoglobin, hematocrit, creatinine, blood urea nitrogen, and albumin levels. Over each study day, oxygen saturation was measured by an ambulatory pulse oximetry system. Patients spent 27 +/- 9% (SE) of time below oxygen saturation of 88% vs. 2.1 +/- 0.6% after initiation of nasal CPAP treatment (P < 0.01). The number of desaturation events per hour of sleep before nasal CPAP treatment was 62 +/- 6 vs. 9 +/- 2 with nasal CPAP (P < 0.01). EPO levels measured by radioimmunoassay were drawn every hour before and at 3 days (n = 9) and before and at recall (n = 0) after initiation of CPAP therapy. The mean serum EPO level was higher before treatment (61 +/- 14 mU/ml) than that at 3 days (38 +/- 10 mU/ml, P < 0.01) or at recall (32 +/- 7 mU/ml, P < 0.01). We conclude that nasal CPAP treatment of sleep-disordered breathing will reduce diurnal levels of EPO.

Topics: Adult; Aged; Blood Gas Monitoring, Transcutaneous; Circadian Rhythm; Erythropoietin; Female; Humans; Hypoxia; Male; Middle Aged; Oxygen; Positive-Pressure Respiration; Sleep Apnea Syndromes

Chronic intermittent hypoxia (CIH), one of the main features of obstructive sleep apnea (OSA), enhances carotid body-mediated chemoreflex and induces hypertension and breathing disorders. The carbamylated form of erythropoietin (cEpo) may have beneficial effects as it retains its antioxidant/anti-inflammatory and neuroprotective profile without increasing red blood cells number. However, no studies have evaluated the potential therapeutic effect of cEpo on CIH-related cardiorespiratory disorders. We aimed to determine whether cEpo normalized the CIH-enhanced carotid body ventilatory chemoreflex, the hypertension and ventilatory disorders in rats.. Male Sprague-Dawley rats (250 g) were exposed to CIH (5% O2, 12/h, 8 h/day) for 28 days. cEPO (20 μg/kg, i.p) was administrated from day 21 every other day for one more week. Cardiovascular and respiratory function were assessed in freely moving animals.. Twenty-one days of CIH increased carotid body-mediated chemoreflex responses as evidenced by a significant increase in the hypoxic ventilatory response (FiO2 10%) and triggered irregular eupneic breathing, active expiration, and produced hypertension. cEpo treatment significantly reduced the carotid body--chemoreflex responses, normalizes breathing patterns and the hypertension in CIH. In addition, cEpo treatment effectively normalized carotid body chemosensory responses evoked by acute hypoxic stimulation in CIH rats.. Present results strongly support beneficial cardiorespiratory therapeutic effects of cEpo during CIH exposure.

Topics: Animals; Erythropoietin; Humans; Hypoxia; Male; Rats; Rats, Sprague-Dawley; Respiration; Sleep Apnea Syndromes

Based on the fact that erythropoietin (Epo) administration in rodents protects against spatial learning and cognitive deficits induced by chronic intermittent hypoxia (CIH)-mediated oxidative damage, here we tested the hypothesis that Epo in the brain protects against cardiorespiratory disorders and oxidative stress induced by CIH in adult mice.. Adult control and transgenic mice overexpressing Epo in the brain only (Tg21) were exposed to CIH (21%-10% O2-10 cycles/hour-8 hours/day-7 days) or room air. After CIH exposure, we used the tail cuff method to measure arterial pressure, and whole-body plethysmography to assess the frequency of apneic episodes at rest, minute ventilation, and ventilatory responses to hypoxia and hypercapnia. Finally, the activity of pro-oxidant (XO-xanthine oxidase, and NADPH) and antioxidant (super oxide dismutase) enzymes was evaluated in the cerebral cortex and brainstem.. Exposure of control mice to CIH significantly increased the heart rate and arterial pressure, the number of apneic events, and the ventilatory response to hypoxia and hypercapnia. Furthermore, CIH increased the ratio of pro-oxidant to antioxidant enzymes in cortex and brainstem tissues. Both physiological and molecular changes induced by CIH were prevented in transgenic Tg21 mice.. We conclude that the neuroprotective effect of Epo prevents oxidative damage in the brain and cardiorespiratory disorders induced by CIH. Considering that Epo is used in clinics to treat chronic kidney disease and stroke, our data show convincing evidence suggesting that Epo may be a promising alternative drug to treat sleep-disorder breathing.

Topics: Animals; Apnea; Arterial Pressure; Brain; Brain Stem; Cerebral Cortex; Erythropoietin; Heart Rate; Hypercapnia; Hypoxia; Male; Mice; Mice, Transgenic; NADP; Oxidative Stress; Plethysmography, Whole Body; Pulmonary Ventilation; Reactive Oxygen Species; Rest; Sleep Apnea Syndromes; Superoxide Dismutase; Xanthine Oxidase

In rodents, exposure to intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA), is associated with neurobehavioral impairments, increased apoptosis in the hippocampus and cortex, as well as increased oxidant stress and inflammation. Such findings are markedly attenuated in rodents exposed to sustained hypoxia 9SH) of similar magnitude. The hypoxia-sensitive gene erythropoietin (EPO) has emerged as a major endogenous neuroprotectant, and could be involved in IH-induced neuronal dysfunction.. IH induced only transiently increased expression of EPO mRNA in hippocampus, which was continued in (SH)-exposed mice. IH, but not SH, adversely affected two forms of spatial learning in the water maze, and increased markers of oxidative stress. However, on a standard place training task, mice treated with exogenously administered EPO displayed normal learning, and were protected from the spatial learning deficits observed in vehicle-treated (C) littermates exposed to IH. Moreover, anxiety levels were increased in IH as compared to normoxia, while no changes in anxiety emerged in EPO-treated mice. Additionally, C mice, but not EPO-treated IH-exposed mice had significantly elevated levels of NADPH oxidase expression, as well as increased MDA and 8-OHDG levels in cortical and hippocampal lysates.. The oxidative stress responses and neurobehavioral impairments induced by IH during sleep are mediated, at least in part, by imbalances between EPO expression and increased NADPH oxidase activity, and thus pharmacological agents targeting EPO expression in CNS may provide a therapeutic strategy in sleep-disordered breathing.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Analysis of Variance; Animals; Cells, Cultured; Cerebral Cortex; Cognition Disorders; Deoxyguanosine; Disease Models, Animal; Embryo, Mammalian; Erythropoietin; Escape Reaction; Gene Expression Regulation; Humans; Hypoxia; Injections, Intraperitoneal; Lipid Peroxidation; Male; Malondialdehyde; Maze Learning; Memory; Mice; Mice, Inbred C57BL; NADPH Oxidases; Neurons; Phosphopyruvate Hydratase; Sleep Apnea Syndromes; Swimming; Time Factors

Snoring is common among pregnant women and early reports suggest that it may bear a risk to the fetus. Increased fetal erythropoiesis manifested by elevated circulating nucleated red blood cells (nRBCs) has been found in complicated pregnancies involving fetal hypoxia. Both erythropoietin (EPO) and interleukin-6 (IL-6) mediate elevation of circulating nRBCs. The intermittent hypoxia and systemic inflammation elicited by sleep-disordered breathing (SDB) could affect fetal erythropoiesis during pregnancy. We hypothesized that maternal snoring will result in increased levels of fetal circulating nRBCs via increased concentrations of EPO, IL-6, or both.. Women of singleton uncomplicated full-term pregnancies were recruited during labor and completed a designated questionnaire. Umbilical cord blood was collected immediately after birth and analyzed for nRBCs, plasma EPO and plasma IL-6 concentrations. Newborn data were retrieved from medical records.. One hundred and twenty-two women were recruited. Thirty-nine percent of women reported habitual snoring during pregnancy. Cord blood levels of circulating nRBCs, EPO and IL-6 were significantly elevated in habitual snorers compared with non-snorers (p = 0.03, 0.005 and 0.01; respectively). No differences in maternal characteristics or newborn crude outcomes were found.. Maternal snoring during pregnancy is associated with enhanced fetal erythropoiesis manifested by increased cord blood levels of nRBCs, EPO and IL-6. This provides preliminary evidence that maternal snoring is associated with subtle alterations in markers of fetal well being.

Topics: Adult; Biomarkers; Erythroblastosis, Fetal; Erythroblasts; Erythropoiesis; Erythropoietin; Female; Fetal Blood; Humans; Infant, Newborn; Interleukin-6; Pilot Projects; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Sleep Apnea Syndromes; Snoring; Young Adult

Topics: Anemia, Iron-Deficiency; Erythropoietin; Heart Failure; Humans; Iron Compounds; Length of Stay; Prevalence; Prognosis; Sleep Apnea Syndromes; Survival Rate

Central sleep apnea (CSA) (with or without Cheyne-Stokes breathing) or obstructive sleep apnea (OSA) are common in congestive heart failure (CHF). Correction of anemia may improve CHF. We hypothesized that correction of anemia might also improve sleep-related breathing disorders (SRBDs) in CHF.. Thirty-eight patients with CHF and anemia (hemoglobin level < 12 g/dL) were treated with erythropoietin and intravenous iron to a target hemoglobin level of 13 g/dL. Home sleep recordings were done before and after 3 months of treatment.. Thirty-seven patients had SRBD (Apnea Hypopnea Index [AHI] of > or = 10). Hemoglobin level increased from 10.4 +/- 0.8 to 12.3 +/- 1.2 g/dL (P < .001). Total AHI values decreased from 35.9 +/- 12.2 to 24.9 +/- 12.2 (P < .001). The AHI of CSA, OSA and Cheyne-Stokes breathing decreased from 26.5 +/- 14.6 to 18.6 +/- 7.7, from 9.4 +/- 10.9 to 6.9 +/- 9.8, and from 13.1 +/- 16.4 to 9.0 +/- 12.2, respectively (all P < .05). Sleep minimal oxygen saturation (SaO2) increased from 62% +/- 12% to 71% +/- 11%; Epworth Sleepiness Scale score improved from 9.4 +/- 6.2 to 6.0 +/- 5.0 and New York Heart Association class improved from 2.9 +/- 0.4 to 1.7 +/- 0.7, all P < .001. Hemoglobin level improvement correlated with improvement in OSA+CSA, CSA, minimal SaO2, Epworth Sleepiness Scale score, and New York Heart Association class (all P < .001).. Improvement of anemia in CHF is associated with a reduction in SRBD and an improvement in daytime sleepiness.

Topics: Aged; Anemia, Iron-Deficiency; Dose-Response Relationship, Drug; Drug Therapy, Combination; Erythropoietin; Female; Ferric Compounds; Ferritins; Follow-Up Studies; Heart Failure; Hematinics; Humans; Injections, Intravenous; Injections, Subcutaneous; Male; Polysomnography; Retrospective Studies; Sleep; Sleep Apnea Syndromes; Treatment Outcome

To better understand how humans adapt to hypoxia, the levels of hemoglobin (Hb), serum erythropoietin (Epo), and vascular endothelial growth factor (VEGF) were measured in 106 patients with severe obstructive sleep apnea-hypopnea syndrome. The results indicated that temporal hypoxic stimulation increases Hb. Furthermore, a minor increase in Epo and a substantial increase in VEGF were found. The induction in patients with severe sleep apnea was greater than that reported in other types of hypoxia. (Blood. 2001;98:1255-1257)

Topics: Case-Control Studies; Endothelial Growth Factors; Erythropoietin; Hemoglobins; Humans; Hypoxia; Lymphokines; Sleep Apnea Syndromes; Sleep Apnea, Obstructive; Syndrome; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors

A 58 year old male heavy smoker presented with intracranial haemorrhage and erythrocytosis. Four aetiologies of polycythaemia--polycythaemia rubra vera (PRV), renal cell carcinoma, sleep apnoea syndrome, and relative polycythaemia--were found to be associated with the underlying causes of erythrocytosis. He did not fulfill the diagnostic criteria for PRV at initial presentation, but an erythropoietin independent erythroid progenitor assay identified the masked PRV, and the low post-phlebotomy erythropoietin concentration also suggested the likelihood of PRV evolution. This case demonstrates that a search for all the possible causes of erythrocytosis is warranted in patients who already have one aetiology of polycythaemia.

Topics: Carcinoma, Renal Cell; Erythroid Precursor Cells; Erythropoietin; Humans; Intracranial Hemorrhages; Kidney Neoplasms; Male; Middle Aged; Polycythemia; Polycythemia Vera; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sleep Apnea Syndromes; Smoking

We measured nocturnal plasma erythropoietin concentration (EPO) in eight subjects with obstructive sleep apnea syndrome (OSAS) and eight healthy overweight subjects while they were undergoing nocturnal polysomnography. We also measured EPO (radioimmunoassay) after 120 min of exposure to 10.5% O2. The subjects with OSAS had a respiratory disturbance index (RDI) of 50.8 +/- 41.9 and a maximal O2 desaturation of 65 +/- 13.3%, and they spent 104.5 +/- 89.3 min out of a total sleep time of 356 +/- 54 min below 90% oxygen saturation (T90). Nocturnal EPO concentrations were normal and did not differ between the two groups. We found no correlation between the T90, T80, or RDI and either the mean or maximal EPO concentrations. After the exposure to 10.5% oxygen, during which oxygen saturations were between 80 and 85%, the healthy subjects and those with OSAS developed increases in EPO of 34 and 49%, respectively, 240 min after the initiation of exposure (p < 0.05). We conclude that the nocturnal hypoxemia occurring in these subjects with OSAS may not have been sufficiently severe to stimulate an increased EPO production. The lack of EPO response was not due to down-regulation of EPO production.

Topics: Adaptation, Physiological; Adult; Case-Control Studies; Down-Regulation; Erythropoietin; Female; Humans; Hypoxia; Male; Obesity; Polysomnography; Radioimmunoassay; Sleep Apnea Syndromes; Time Factors

Hypoxia causes an increased production of erythropoietin (EPO), but the time course of the EPO response in humans has not been well characterized. This study examines the relationship between the duration of normobaric hypoxic exposure and plasma EPO levels in healthy human subjects. Six volunteers breathed a gas mixture of 10.5% O2-89.5% N2 continuously for 5, 60, and 120 or intermittently for 240 min. O2 saturations were maintained between 75 and 85% during the exposure. Arterial pH was 7.467 +/- 0.019, PO2 37.05 +/- 2.43 Torr, and PCO2 36.69 +/- 2.05 Torr. O2 half-saturation pressures of hemoglobin were normal for all subjects. Plasma EPO was measured every 30 min for 360 min by radioimmunoassay. No increase in EPO was seen after the 5- and 60-min exposures. However, a 50% increase was seen 240 min after the initiation of the 120-min hypoxic exposure (P less than 0.01). Intermittent exposure resulted in an increase of EPO by 52% 360 min after the onset of exposure (P less than 0.05). Therefore, exposing humans continuously to an inspiratory O2 fraction of 0.105 for 120 min or intermittently for 240 min provides a sufficient stimulus to increase production of EPO.

Topics: Adult; Altitude; Erythropoietin; Humans; Hypoxia; Kinetics; Male; Polycythemia; Sleep Apnea Syndromes

A polysomnographic study was undertaken in nine patients with unexplained polycythaemia and nine age- and sex-matched controls. Circulating plasma levels of immunoreactive erythropoietin (IrEPO) were analysed before and after sleep. Seven out of nine polycythaemia patients were found to have sleep-disordered breathing and fulfilled the criteria for the sleep apnoea syndrome. Erythrocyte volume fraction was by definition higher among polycythaemia patients, and showed a weak positive correlation with minimum oxygen saturation during sleep (P less than 0.05). However, plasma IrEPO did not differ between the two groups or between morning and evening samples within the respective groups. In a separate study, IrEPO was repeatedly analysed during sleep in a group of six patients with severe obstructive sleep apnoea and six matched controls. No correlation with severity of sleep-disordered breathing was found. None of these patients had polycythaemia, and there was no obvious diurnal variation in IrEPO levels. A nocturnal sleep study may be warranted in patients with unexplained polycythaemia. Obstructive sleep apnoea does not appear to be related to increased IrEPO levels, although polycythaemia has been reported as a relatively common finding in this disease.

Topics: Circadian Rhythm; Erythropoietin; Humans; Hypoxia; Middle Aged; Monitoring, Physiologic; Polycythemia; Sleep Apnea Syndromes

We measured arterial oxygen saturation (SaO2) and serum erythropoietin (EPO) levels in patients with obstructive sleep apnea syndrome (OSAS) and in healthy subjects. SaO2 profile was analyzed as the cumulative distribution of SaO2 over time. OSAS patients spent 25.5 +/- 30.9% (SD) of the time at SaO2 of less than 88% vs. 0.64 +/- 1.6% in healthy subjects (P less than 0.05) and had 59 +/- 25 desaturations (greater than 4%) per hour vs. less than 5 per hour in healthy subjects (P less than 0.05). EPO measurements (radioimmunoassay) were made in blood samples withdrawn every 1 or 2 h over a 24-h period. The mean EPO concentration was higher (P less than 0.05) for OSAS patients (45 +/- 33 mU/ml) than for normal subjects (17 +/- 8 mU/ml). There was a significant variability in EPO values over the 24-h period. To analyze the EPO pattern over 24 h, EPO time series were fit to a general cosine function. Data from normal subjects conformed to a cosine function with an amplitude of 3.5 +/- 2.1 (CV of 60%) and an acrophase of 1,000 +/- 184 min after 0800 (CV of 18%), indicating a zenith about 1 A.M. and a nadir around 1 P.M. Data from OSAS subjects fit a similar cosine function with an amplitude of 19.9 +/- 41.0 (CV of 206%) and acrophase of 582 +/- 408 min (CV of 70%), indicating a greater variability in the magnitude and the timing of peak serum EPO levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Circadian Rhythm; Erythropoietin; Humans; Hypoxia; Male; Middle Aged; Oxygen; Sleep Apnea Syndromes

Eight patients with obstructive sleep apnoea and a normal haemoglobin concentration underwent nocturnal studies during which oxyhaemoglobin saturation was recorded continuously with an ear oximeter and serum erythropoietin concentration was measured hourly by means of a radioimmunoassay. Serum erythropoietin concentrations remained within the normal range throughout the study despite falls in oxyhaemaglobin saturation in individuals to 33-78%. There was no relation between the degree of nocturnal hypoxaemia and serum erythropoietin concentrations. The brief cyclical episodes of hypoxaemia typical of obstructive sleep apnoea may not be a sufficient stimulus for erythropoietin secretion.

Topics: Adult; Aged; Erythropoietin; Humans; Hypoxia; Male; Middle Aged; Oxyhemoglobins; Sleep Apnea Syndromes

A noninvasive, inexpensive method of excluding significant sleep-associated hypoxemia would be desirable for patients being investigated and treated for obstructive sleep apnea (OSA). Sixty-eight such patients provided specimens before and after sleep studies for estimation of urinary uric acid:creatinine ratio (UA:Cr), serum erythropoietin (EPO), and blood 2,3-diphosphoglycerate (2,3-DPG). Mean (SD) morning 2,3-DPG was higher in 26 patients with overnight hypoxemia than in 42 normoxemic patients (2.54 [0.46] versus 2.24 [0.44] mmol/L; p = 0.01). Neither overnight change nor absolute values of serum EPO or urinary UA:Cr were significantly different between hypoxemic and normoxemic groups. There was a diurnal variation in serum EPO in normoxemic patients (P.M. EPO = 14.8 [7.1] mU/ml; A.M. EPO = 10.7 [7.1] mU/ml; p less than 0.05) but not in hypoxemic patients. Eighteen hypoxemic patients were restudied after using nasal continuous positive airway pressure (nCPAP) for at least 4 wk. Seven normoxemic patients not using nCPAP were restudied after a similar time. There were no significant differences between pretreatment and posttreatment nights in absolute values or percentage overnight change of blood 2,3-DPG or serum EPO in either group. In the hypoxemic (nCPAP) group, overnight change in urinary UA:Cr was lower on the second night (p = 0.04); there was no significant change in the control group. We conclude that although urinary UA:Cr, serum EPO, and 2,3-DPG may be physiologically related to hypoxemia, none of these measures can be used to predict accurately the presence of moderate nocturnal hypoxemia in patients with OSA or in monitoring the effect of their therapy.

Topics: 2,3-Diphosphoglycerate; Circadian Rhythm; Creatinine; Diphosphoglyceric Acids; Erythropoietin; Female; Humans; Hypoxia; Male; Middle Aged; Positive-Pressure Respiration; Sleep Apnea Syndromes; Uric Acid

Topics: Animals; Erythropoietin; Humans; Hypoxia; Male; Oxygen; Rats; Rats, Inbred Strains; Sleep Apnea Syndromes