Nasal disease and quality of life in athletes.

OBJECTIVES: Nasal disease imposes a significant disease burden upon the individual in the general population, but is relatively under studied in athletes. This study sought to define the frequency of nasal symptoms in the active population, and to quantify the impact of these symptoms on quality of life and on the frequency of upper respiratory tract infections. RESULTS: A total of 296 participants completed the study (246 athletes and 50 sedentary controls). Nasal symptoms were significantly more frequent in the active group than in the sedentary controls (70 per cent vs 52 per cent). Upper respiratory tract infections were significantly more common in athletes with regular nasal symptoms than in athletes without nasal symptoms. Quality-of-life scores, as measured by the 22-item Sino-Nasal Outcome Test, were significantly worse in athletes with regular nasal symptoms. CONCLUSION: This study suggests that regular exercise is associated with a significant increase in the prevalence of troubling nasal symptoms, and nasal symptoms in athletes are associated with increased susceptibility to upper respiratory tract infections. Quality of life was negatively affected, confirming the importance of nasal health to athlete welfare.

Characterizing problematic hypoglycaemia: iterative design and preliminary psychometric validation of the Hypoglycaemia Awareness Questionnaire (HypoA-Q).

AIMS: To design and conduct preliminary validation of a measure of hypoglycaemia awareness and problematic hypoglycaemia, the Hypoglycaemia Awareness Questionnaire. METHODS: Exploratory and cognitive debriefing interviews were conducted with 17 adults (nine of whom were women) with Type 1 diabetes (mean ± sd age 48 ± 10 years). Questionnaire items were modified in consultation with diabetologists/psychologists. Psychometric validation was undertaken using data from 120 adults (53 women) with Type 1 diabetes (mean ± sd age 44 ± 16 years; 50% with clinically diagnosed impaired awareness of hypoglycaemia), who completed the following questionnaires: the Hypoglycaemia Awareness Questionnaire, the Gold score, the Clarke questionnaire and the Problem Areas in Diabetes questionnaire. RESULTS: Iterative design resulted in 33 items eliciting responses about awareness of hypoglycaemia when awake/asleep and hypoglycaemia frequency, severity and impact (healthcare utilization). Psychometric analysis identified three subscales reflecting 'impaired awareness', 'symptom level' and 'symptom frequency'. Convergent validity was indicated by strong correlations between the 'impaired awareness' subscale and existing measures of awareness: (Gold: rs =0.75, P < 0.01; Clarke: rs =0.76, P < 0.01). Divergent validity was indicated by weaker correlations with diabetes-related distress (Problem Areas in Diabetes: rs =0.25, P < 0.01) and HbA1c (rs =-0.05, non-significant). The 'impaired awareness' subscale and other items discriminated between those with impaired and intact awareness (Gold score). The 'impaired awareness' subscale and other items contributed significantly to models explaining the occurrence of severe hypoglycaemia and hypoglycaemia when asleep. CONCLUSIONS: This preliminary validation shows the Hypoglycaemia Awareness Questionnaire has robust face and content validity; satisfactory structure; internal reliability; convergent, divergent and known groups validity. The impaired awareness subscale and other items contribute significantly to models explaining recall of severe and nocturnal hypoglycaemia. Prospective validation, including determination of a threshold to identify impaired awareness, is now warranted.

Severe hypoglycaemia in type 1 diabetes mellitus: underlying drivers and potential strategies for successful prevention.

Hypoglycaemia remains an over-riding factor limiting optimal glycaemic control in type 1 diabetes. Severe hypoglycaemia is prevalent in almost half of those with long-duration diabetes and is one of the most feared diabetes-related complications. In this review, we present an overview of the increasing body of literature seeking to elucidate the underlying pathophysiology of severe hypoglycaemia and the limited evidence behind the strategies employed to prevent episodes. Drivers of severe hypoglycaemia including impaired counter-regulation, hypoglycaemia-associated autonomic failure, psychosocial and behavioural factors and neuroimaging correlates are discussed. Treatment strategies encompassing structured education, insulin analogue regimens, continuous subcutaneous insulin infusion pumps, continuous glucose sensing and beta-cell replacement therapies have been employed, yet there is little randomized controlled trial evidence demonstrating effectiveness of new technologies in reducing severe hypoglycaemia. Optimally designed interventional trials evaluating these existing technologies and using modern methods of teaching patients flexible insulin use within structured education programmes with the specific goal of preventing severe hypoglycaemia are required. Individuals at high risk need to be monitored with meticulous collection of data on awareness, as well as frequency and severity of all hypoglycaemic episodes.

An evidence-based approach to the child who drools saliva.

BACKGROUND: Drooling is a common dysfunction in children with cerebral palsy and may also affect neurologically unimpaired children. It causes significant social handicap to both children and their families. METHODS: The data in this article are supported by a Medline search (November 2008) utilising the keywords drooling, sialorrhea, botulinum toxin, salivary duct ligation and also by the use of the personal bibliographies of the senior authors. RESULTS: The majority of the published literature for drooling is of level III/IV evidence. CONCLUSION: Multiple therapeutic interventions are available for paediatric drooling. These are most appropriately introduced in a stepwise progression from behaviour therapy, to pharmacotherapy to surgical procedures.

Use of complementary and alternative medicine in pediatric otolaryngology patients attending a tertiary hospital in the UK.

OBJECTIVE: Little data is available on complementary and alternative medicine (CAM) use in children attending otolaryngology services. We investigated the prevalence and pattern of CAM use among children attending the pediatric otolaryngology department in a tertiary pediatric teaching hospital in Scotland. DESIGN: A cross-sectional survey conducted by administering an anonymous questionnaire to the parents accompanying patients attending the pediatric otolaryngology department. Elective admissions and clinic attendees were included over a 3-month period in 2005/2006. SETTING: Academic tertiary care referral centre in North-East Scotland. PATIENTS: Five hundred and fifty-four consecutive patients aged less than 16 years were eligible. The response rate was 59% (n=327). MAIN OUTCOME MEASURES: Prevalence of CAM use in children. Secondary measures include types of CAM used, indications for use and communication with family physicians. RESULTS: Based on 327 responses, 93 patients (29%) had ever used CAM, 20% within the last year. Commonly used CAM preparations were cod-liver oil, echinacea, aloe vera, cranberry, primrose oil and herbal vitamin supplements. The popular non-herbal CAM included homeopathy, massage, aromatherapy, chiropractic, yoga and reiki. Nineteen percent used CAM for their admission illness. Sixty-one percent of parents thought that CAM was effective and 65% would recommend it to others. Fifty-one percent of parents stated that the family physician was unaware of CAM use by the child. CONCLUSIONS: Despite concerns regarding the efficacy, safety and cost effectiveness of complementary and alternative medicine, its use among the pediatric otolaryngology population is more common than many providers may realize. This has implications for all healthcare workers involved in their care.

Teratogen-induced activation of caspase-6 and caspase-7 in early postimplantation mouse embryos.

BACKGROUND: Previous work has shown that teratogens such as hyperthermia (HS), 4-hydroperoxycyclophosphamide (4CP), and staurosporine (ST) induce cell death in day 9 mouse embryos by activating the mitochondrial apoptotic pathway. Key to the activation of this pathway is the activation of a caspase cascade involving the cleavage-induced activation of an initiator procaspase, caspase-9, and the downstream effector procaspase, caspase-3. For example, procaspase-3, an inactive proenzyme of 32 kDa is cleaved by activated caspase-9 to generate a large subunit of approximately 17 kDa and a small subunit of approximately 10 kDa. In turn, caspase-3 is known to target a variety of cellular proteins for proteolytic cleavage as part of the process by which dying cells are eliminated. Previous work has also shown that neuroepithelial cells are sensitive to teratogen-induced activation of this pathway and subsequent cell death whereas cells of the heart are resistant. Although caspase-3 is a key effector caspase activated by teratogens, two other effector caspases, caspase-6 and caspase-7, are known; however, their role in teratogen-induced cell death is unknown. METHODS: Because cleavage-induced generation of specific subunits is the most specific assay for activation of caspases, we have used antibodies that recognize the procaspase and one of its active subunits and a Western blot approach to assess the activation of caspase-6 and caspase-7 in day 9 mouse embryos (or heads, hearts and trunks isolated from whole embryos) exposed to HS, 4CP, and ST. To probe the relationship between teratogen-induced activation of caspase-9/caspase-3 and the activation of caspase-6/caspase-7, we used a mitochondrial-free embryo lysate with or without the addition of cytochrome c, recombinant active caspase-3, or recombinant active caspase-9. RESULTS: Western blot analyses show that these three teratogens, HS, 4CP, and ST, induce the activation of procaspase-6 (appearance of the 13 kDa subunit, p13) and caspase-7 (appearance of the 19 kDa subunit, p19) in day 9 mouse embryos. In vitro studies showed that both caspase-6 and caspase-7 could be activated by the addition of cytochrome c to a lysate prepared from untreated embryos. In addition, caspase-6 could be activated by the addition of either recombinant caspase-3 or caspase-9 to a lysate prepared from untreated embryos. In contrast, caspase-7 could be activated by addition of recombinant caspase-3 but only minimally by recombinant caspase-9. Like caspase-9/caspase-3, caspase-6 and caspase-7 were not activated in hearts isolated from embryos exposed to these three teratogens. CONCLUSIONS: HS, 4CP and ST induce the cleavage-dependent activation of caspase-6 and caspase-7 in day 9 mouse embryos. Results using DEVD-CHO, a caspase-3 inhibitor, suggest that teratogen-induced activation of caspase-6 is mediated by caspase-3. In addition, our data suggest that caspase-7 is activated primarily by caspase-3; however, we cannot rule out the possibility that this caspase is also activated by caspase-9. Finally, we also show that teratogen-induced activation of caspase-6 and caspase-7 are blocked in the heart, a tissue resistant to teratogen-induced cell death.

Influence of cigarette smoking on inhaled corticosteroid treatment in mild asthma.

BACKGROUND: Although inhaled corticosteroids have an established role in the treatment of asthma, studies have tended to concentrate on non-smokers and little is known about the possible effect of cigarette smoking on the efficacy of treatment with inhaled steroids in asthma. A study was undertaken to investigate the effect of active cigarette smoking on responses to treatment with inhaled corticosteroids in patients with mild asthma. METHODS: The effect of treatment with inhaled fluticasone propionate (1000 microg daily) or placebo for 3 weeks was studied in a double blind, prospective, randomised, placebo controlled study of 38 steroid naïve adult asthmatic patients (21 non-smokers). Efficacy was assessed using morning and evening peak expiratory flow (PEF) readings, spirometric parameters, bronchial hyperreactivity, and sputum eosinophil counts. Comparison was made between responses to treatment in non-smoking and smoking asthmatic patients. RESULTS: There was a significantly greater increase in mean morning PEF in non-smokers than in smokers following inhaled fluticasone (27 l/min v -5 l/min). Non-smokers had a statistically significant increase in mean morning PEF (27 l/min), mean forced expiratory volume in 1 second (0.17 l), and geometric mean PC20 (2.6 doubling doses), and a significant decrease in the proportion of sputum eosinophils (-1.75%) after fluticasone compared with placebo. No significant changes were observed in the smoking asthmatic patients for any of these parameters. CONCLUSIONS: Active cigarette smoking impairs the efficacy of short term inhaled corticosteroid treatment in mild asthma. This finding has important implications for the management of patients with mild asthma who smoke.

High resolution computed tomographic assessment of airway wall thickness in chronic asthma: reproducibility and relationship with lung function and severity.

BACKGROUND: In some patients chronic asthma results in irreversible airflow obstruction. High resolution computed tomography (HRCT) has been advocated for assessing the structural changes in the asthmatic lung and permits investigation of the relationships between airway wall thickening and clinical parameters in this condition. METHODS: High resolution CT scanning was performed in 49 optimally controlled asthmatic patients and measurements of total airway and lumen diameter were made by two independent radiologists using electronic callipers. Wall area as % total airway cross sectional area (WA%) and wall thickness to airway diameter ratio (T/D) were calculated for all airways clearly visualised with a transverse diameter of more than 1.5 mm, with a mean value derived for each patient. Intra- and inter-observer variability was assessed for scope of agreement in a subgroup of patients. Measurements were related to optimum forced expiratory volume in 1 second (FEV1), forced mid expiratory flow, carbon monoxide gas transfer, two scores of asthma severity, airway inflammation as assessed with induced sputum, and exhaled nitric oxide. RESULTS: Neither observer produced a statistically significant difference between measurements performed on two occasions but there was a significant difference between observers (limits of agreement -2.6 to 6.8 for WA%, p<0.0001). However, mean WA% measured on two occasions differed by no more than 5.4% (limits of agreement -4.0 to 5.4; mean (SD) 0.7 (2.4)). Statistically significant positive associations were observed between both WA% and T/D ratio and asthma severity (r(S)=0.29 and 0.30, respectively, for ATS score), and an inverse association with gas transfer coefficient was observed (r(S)=-0.43 for WA% and r(S)=-0.41 for T/D). No association was identified with FEV1 or airway inflammation. CONCLUSIONS: The airway wall is thickened in more severe asthma and is associated with gas transfer coefficient. This thickening does not relate directly to irreversible airflow obstruction as measured with FEV1.

Smoking and airway inflammation in patients with mild asthma.

STUDY OBJECTIVES: Cigarette smoking is common in asthmatic patients, and we investigated the impact of cigarette smoking on airway inflammation in asthma. DESIGN: Single-center observational study of airway inflammation in asthmatic and healthy smokers and nonsmokers. SETTING: Asthma research unit in a university hospital. PATIENTS OR PARTICIPANTS: Sixty-seven asthmatic and 30 nonasthmatic subjects classified as smokers or nonsmokers. Asthmatics had chronic, stable asthma and were not receiving inhaled or oral steroids at the time of the study. INTERVENTIONS: We examined induced-sputum cell counts and levels of interleukin (IL)-8 and eosinophilic cationic protein (ECP). Bronchial hyperreactivity was assessed using methacholine challenge. MEASUREMENTS AND RESULTS: Asthmatic smokers had higher total sputum cell counts than nonsmoking asthmatics and both smoking and nonsmoking healthy subjects. Smoking was associated with sputum neutrophilia in both asthmatics and nonasthmatics (median, 47% and 41%, respectively) compared with nonsmokers (median, 23% and 22%, respectively), and sputum IL-8 was increased in smokers compared with nonsmokers, both in subjects with asthma (median, 945 pg/mL vs 660 pg/mL, respectively) and in healthy subjects (median, 1,310 pg/mL vs 561 pg/mL, respectively). Sputum eosinophils and ECP levels were higher in both nonsmoking and smoking asthmatics than in healthy nonsmokers. In smoking asthmatics, lung function (FEV(1) percent predicted) was negatively related to both sputum IL-8 (r = - 0.52) and sputum neutrophil proportion (r = - 0.38), and sputum IL-8 correlated positively with smoking pack-years (r = 0.57) and percent neutrophil count (r = 0.51). CONCLUSIONS: In addition to the eosinophilic airway inflammation observed in patients with asthma, smoking induces neutrophilic airway inflammation; a relationship is apparent between smoking history, airway inflammation, and lung function in smoking asthmatics.

Hepatocellular carcinoma: current surgical management.

At present the only potentially curative treatment for hepatocellular carcinoma (HCC) is either partial hepatectomy or total hepatectomy with orthotopic liver transplantation (OLT). Underlying liver reserve and regenerative capacity are the most important determinants of the risk of postoperative hepatic failure after partial hepatectomy; thus, careful preoperative assessment of liver function is mandatory. In specialized centers perioperative mortality is less than 5%, although cirrhotic patients are at increased risk. Various neoadjuvant and adjuvant therapies are under investigation, but as yet there are no data that demonstrate benefit from adjuvant systemic chemotherapy. The use of OLT is limited by the difficulty of obtaining donor livers. Patients selected for transplantation and partial hepatectomy represent two distinct subgroups, but their survival after treatment is comparable. Despite the progress in the management of HCC by surgical resection, the fact remains that the majority of these patients will experience local recurrences. This has led to the development of a variety of novel new treatments that require further evaluation.

Co-localization of active caspase-3 and DNA fragmentation (TUNEL) in normal and hyperthermia-induced abnormal mouse development.

BACKGROUND: Previous work has shown that caspase-3 activation and DNA fragmentation, two hallmarks of apoptosis, are induced in day 9 mouse embryos exposed to hyperthermia (43 degrees C); however, the methods used to assess caspase-3 activation (Western blot) and DNA fragmentation (gel electrophoresis) did not allow these apoptotic events to be localized to specific cells within the embryo. METHODS: To co-localize active caspase-3 and DNA fragmentation to specific cells, we used paraffin sections of day 13 mouse limb buds, sections of control and hyperthermia-treated day 9 mouse embryos, and sequential immunohistochemical staining for caspase-3 and TUNEL staining for DNA fragmentation. We used a primary rabbit antibody specific for the active, p17 subunit of caspase-3 and a goat anti-rabbit secondary antibody conjugated to Alexa 594 fluorochrome (red fluorescence) to localize active caspase-3. To co-localize DNA fragmentation, we subsequently processed the same sections by the TUNEL method using fluorescein-labeled dUTP (green fluorescence). RESULTS: Using this dual labeling approach, we show that active caspase-3 (caspase-3 positive) and DNA fragmentation (TUNEL positive) occur in a sub-population of interdigital mesenchyme cells of day 13 mouse limb buds. Using the same approach, we detected a small number of caspase-3 positive and TUNEL-positive cells in the central nervous system and in the mesenchyme of the first branchial arch of untreated day 9 mouse embryos. The number of caspase-3 and TUNEL-positive cells are greatly increased 5 hr after a brief exposure to hyperthermia (43 degrees C, 13 min). Caspase-3 and TUNEL-positive cells were most abundant in the neuroepithelium of the developing central nervous system, mesenchyme of the first pharyngeal arch, and somitic mesoderm. In contrast, the heart, mesencephalic mesenchyme, and the visceral yolk sac contained few, if any, caspase-3 and TUNEL-positive cells. CONCLUSIONS: This is the first demonstration that activation of caspase-3 and DNA fragmentation co-localize in cells programmed to die in the interdigital mesenchyme of day 13 limb buds and in the neuroepithelium and branchial arch mesenchyme of day 9 mouse embryos. Similarly, our results represent the first co-localization of teratogen-induced activation of caspase-3 and DNA fragmentation in specific cells of early postimplantation mouse embryos, and confirm that cells of the developing central nervous system are acutely sensitive to the cell death-inducing potential of hyperthermia, whereas cells of the heart are resistant. Finally, we show for the first time that, like cells of the heart, cells of the mesencephalic mesenchyme and the visceral yolk sac are also resistant to hyperthermia-induced apoptosis.

Adding group psychotherapy to medication treatment in dysthymia: a randomized prospective pilot study.

Patients with dysthymia have been shown to respond to treatment with antidepressant medications, and to some degree to psychotherapy. Even patients successfully treated with medication often have residual symptoms and impaired psychosocial functioning. The authors describe a prospective randomized 36-week study of dysthymic patients, comparing continued treatment with antidepressant medication (fluoxetine) alone and medication with the addition of group therapy treatment. After an 8-week trial of fluoxetine, medication-responsive subjects were randomly assigned to receive either continued medication only or medication plus 16 sessions of manualized group psychotherapy. Results provide preliminary evidence that group therapy may provide additional benefit to medication-responding dysthymic patients, particularly in interpersonal and psychosocial functioning.

Non-invasive markers of airway inflammation as predictors of oral steroid responsiveness in asthma.

BACKGROUND: Sputum eosinophil counts and exhaled nitric oxide (NO) levels are increased in asthma and both measurements fall in response to corticosteroids. METHODS: Exhaled NO levels and sputum eosinophil counts were assessed as non-invasive markers of the response to an oral steroid in 37 patients (19 women) with stable chronic asthma (mean (SD) age 48.6 (12.2) years, asthma duration 25. 9 (17.3) years, and baseline forced expiratory volume in one second (FEV(1)) 76.3 (21.9)% predicted). Spirometric tests, with reversibility to a beta agonist (2.5 mg nebulised salbutamol), and induced sputum (using nebulised 3% saline) were performed at recruitment and following treatment with 30 mg prednisolone/day for 14 days. RESULTS: Baseline NO levels correlated with the percentage improvement in FEV(1) from baseline to the post-steroid, post-bronchodilator value (r(s) = 0.47, p = 0.003), with an NO level of >10 ppb at baseline having a positive predictive value of 83% for an improvement in FEV(1) of > or =15% (sensitivity 59%, specificity 90%). Sputum eosinophilia (> or =4%) had a positive predictive value of 68% (sensitivity 54%, specificity 76%) for an increase in FEV(1) of > or =15%. A combination of sputum eosinophilia and increased NO levels resulted in a positive predictive value of 72% and a negative predictive value of 79% (sensitivity 76%, specificity 75%). CONCLUSION: Exhaled NO levels and sputum eosinophilia may be useful in predicting the response to a trial of oral steroid in asthma.

Cytochrome c release from mitochondria of early postimplantation murine embryos exposed to 4-hydroperoxycyclophosphamide, heat shock, and staurosporine.

Cell death is an early and common event in the pathogenesis associated with the abnormal development induced by a variety of teratogens. Previously, we showed that the cell death induced in day 9 mouse embryos by three teratogens, hyperthermia (HS), 4-hydroperoxycyclophosphamide (4-CP), and sodium arsenite (As), is apoptotic in nature involving the activation of caspase-3, cleavage of poly(ADP-ribose) polymerase (PARP), and DNA fragmentation. We now show that HS, 4-CP, and staurosporine (ST) induce the release of cytochrome c from mitochondria with kinetics suggesting a causal relationship with the activation of caspase-3 and caspase-2. This causal relationship is supported by data showing that procaspase-3 and -2 can be activated in vitro by the addition of cytochrome c to a S-100 fraction prepared from control day 9 embryos. Together, these data support the notion that these three teratogens induce changes in embryonic mitochondria resulting in the release of cytochrome c and the subsequent activation of caspase-9, the upstream activator of caspase-3. Previously, we also showed that cells within the day 9 mouse embryo are differentially sensitive/resistant to the cell death-inducing potential of HS, 4-CP, and As. The most dramatic example of this differential sensitivity is the complete resistance of heart cells, characterized by the lack of caspase-3 activation, PARP cleavage, and DNA fragmentation. We now show that this block in the terminal phase of the apoptotic pathway in heart cells is associated with a lack of teratogen-induced release of cytochrome c. Together, our data indicate that mitochondria play a pivotal role in cell death during the early phases of teratogenesis.

Sputum cellular and cytokine responses to inhaled endothelin-1 in asthma.

BACKGROUND: Endothelin (ET)-1 is a 21-amino acid peptide which has potent bronchoconstrictor activity. Animal studies show elevation of ET-1 during experimental airway inflammation, and inhibition of inflammation by endothelin-antagonists, suggesting pro-inflammatory activity for ET-1. OBJECTIVE: We wanted to assess any acute influence that bronchoconstrictor doses of inhaled ET-1 might have on cells, tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, nitrite (NO2) and albumin in induced sputum in asthma. METHODS: Bronchial challenge was performed using nebulized ET-1 (nebulized dose range 0.96-15.36 nmol) and placebo in 10 adult asthmatic subjects in a randomized double-blind placebo-controlled cross-over study. Sputum induction was performed 30 min and 4 h after placebo or ET-1 bronchial challenge. RESULTS: All subjects experienced dose-dependent bronchoconstriction to inhaled ET-1 with a mean (range) PC15 forced expiratory volume in 1 s (FEV1) to ET-1 of 9.45 (1.2-21.7) nmol. Comparing ET-1 with placebo inhalation, there was no change in sputum differential cell counts, TNFalpha, IL-1beta, NO2 or albumin at 30 min or 4 h after inhalation, nor was there a difference in these parameters at 4 h compared with 30 min after ET-1 inhalation. There was no fall in FEV1 at 4 h after ET-1 inhalation, suggesting that ET-1 inhalation is not associated with a late bronchoconstrictor response. CONCLUSIONS: We conclude that inhaled ET-1 does not appear to stimulate an acute inflammatory response in asthma as assessed by differential cell count, TNFalpha, IL-1beta, NO2 and albumin concentrations in induced sputum.

Predictors of nocturnal oxygen desaturation in patients with COPD.

The aim of this study was to identify factors which might predict nocturnal desaturation (defined as a fall of > 4% from awake baseline level for > or = 5 min) in normoxic or mildly hypoxic patients with stable COPD [arterial O2 saturation (SaO2) > or = 91%]. The study was prospective in nature, had full ethical approval and was performed in the Respiratory Department of a city teaching hospital. Thirty-three patients [mean (SD) age 67.2 (9) years] with stable COPD [mean (SD) FEV1 36.8 (11.0)% pred.] were recruited via the respiratory outpatient clinics and through the respiratory wards. The following parameters were measured: daytime arterial blood gases; spirometry; lung volumes (helium dilution); single breath CO transfer factor (TLCO and KCO); maximum inspiratory (IMP) and expiratory mouth pressures; pulse oximetry (SpO2) across a 6-min walk test, and SpO2 during sleep. Seventeen patients who experienced nocturnal desaturation had significantly lower mean PaO2 and SaO2, and higher PaCO2 values compared to non-desaturators. There was a positive correlation between mean nocturnal SpO2 and daytime PaO2, SaO2, and minimum exercise SpO2, and a negative correlation between mean nocturnal SpO2 and PaCO2, and FRC. Regression analysis revealed that daytime SaO2 was the only independent predictor of mean nocturnal saturation (accounting for 61% of the variability in the mean nocturnal SpO2). We observed nocturnal desaturation in all patients with a daytime SaO2 < or = 93% but in no patient with SaO2 > or = 95%. We conclude that daytime SaO2 can be used to predict nocturnal desaturation in normoxic or mildly hypoxic patients with stable COPD. Nocturnal desaturation is likely in patients with COPD where daytime SaO2 < or = 93%, and unlikely where daytime SaO2 > or = 95%.