Prognostic Significance of Pulmonary Artery to Aorta Ratio and Other CT Markers in Pulmonary Fibrosis With and Without Emphysema.

Pulmonary hypertension (PH) is associated with decreased survival in patients with pulmonary fibrosis and combined pulmonary fibrosis and emphysema. Main pulmonary artery (PA) diameter and PA diameter/ascending aortic diameter (PA/AA) ratio, as measured on CT, have recently emerged as specific markers for PH. Our single-center retrospective study found that PA/AA ratio > 1 is associated with decreased survival in individuals with pulmonary fibrosis, with or without emphysema. Our study also describes markers of cardiac remodeling, and the echocardiographic diagnosis of PH in this patient population.

Compliance with CPAP therapy in older men with obstructive sleep apnea.

OBJECTIVES: Factors specifically affecting compliance with continuous positive airway pressure (CPAP) in older patients with obstructive sleep apnea (OSA) have not been described. The purpose of this study is to determine which factors are associated with compliance and noncompliance in older patients, a growing segment of the population. DESIGN: A retrospective chart review of older male patients prescribed CPAP therapy for OSA over an 8-year period. SETTING: Veterans Affairs Medical Center. PARTICIPANTS: All patients age 65 and older for whom CPAP therapy had been prescribed for treatment of OSA in the past 8 years. MEASUREMENTS: Records of all older male patients prescribed CPAP therapy for OSA over the last 8 years were reviewed. Compliance was defined by time-counter readings averaging 5 or more hours of machine run-time per night. RESULTS: Of 33 older male patients with OSA studied, 20 were found to be compliant and 13 noncompliant with nasal CPAP therapy. The mean age (+/- SEM) at the time of diagnosis of OSA in the compliant group was 68 (+/-1) years, whereas that of the noncompliant group was 72 (+/-1) years (P <.05). Of the compliant patients, 95% attended a CPAP patient education and support group, whereas only 54% of noncompliant patients attended (P =.006). Resolution of initial symptoms of OSA with CPAP therapy was significantly associated with compliance. Symptom resolution occurred in 90% of compliant patients and in only 18% of noncompliant patients (P <.0002). Factors that were significantly associated with noncompliance with CPAP were cigarette smoking, nocturia, and benign prostatic hypertrophy (BPH). Of noncompliant patients, 82% complained of nocturia, whereas only 33% of compliant patients complained of nocturia (P =.02). BPH was diagnosed in 62% of noncompliant patients and in only 15% of compliant patients (P =.004). Diuretic use was more common in the compliant group and, therefore, was not a cause of increased nocturia in noncompliant patients. CONCLUSION: In older male patients with OSA, compliance with CPAP therapy is associated with attendance at a patient CPAP education and support group. Resolution of symptoms with therapy also appears to be associated with enhanced compliance. In addition, we found an association between nocturia and the existence of BPH in older men with OSA who are not compliant with nasal CPAP. Larger observational studies should be performed to confirm these findings, and, if so confirmed, then further studies to determine whether treatment of BPH in older men with OSA improves compliance with CPAP.

Effects of withdrawal of inhaled steroids in men with severe irreversible airflow obstruction.

Inhaled corticosteroid therapy has proven efficacy for asthmatics, but the benefit for patients with chronic obstructive pulmonary disease (COPD) is less well supported. We hypothesized that withdrawal of inhaled steroids in elderly patients with severe irreversible airway obstruction would not lead to a deterioration in respiratory function. We designed a prospective, double-blind, randomized, placebo-controlled, crossover study to follow spirometry, quality of life questionnaire, six-minute (6-min) walk test, and sputum markers of inflammation during a 6-wk placebo treatment period and a 6-wk treatment period with beclomethasone dipropionate (BDP), 336 microg/d. There were 24 men receiving BDP who entered the study; 15 completed the study. Their mean age was 66.9 +/- 1.9 yr, and mean FEV(1) was 1.61 +/- 0.1 L (47% of predicted). There was a significant decrease in the mean FEV(1 )while using the placebo inhaler (1.70 L versus 1.60 L, baseline versus placebo: 95% CI, 0.002 to 0.195; p < 0.05). There was a decrease in the mean percentage change in FEV(1) for the study subjects during the placebo treatment period as compared with the BDP treatment period (-6.28 versus 5.03%, placebo versus BDP: 95% CI, -23.38 to 0.76; p = 0.06). Six-minute walk test results and sputum analysis for cell count and differential were not significantly different during placebo and BDP treatment periods. Borg scale assessment of dyspnea after exercise was increased while using the placebo inhaler as compared with baseline, and decreased during the BDP treatment period. Chronic Respiratory Disease Questionnaire (CRQ) scores revealed no significant difference between placebo and BDP. This study has demonstrated that in elderly patients with severe irreversible airway obstruction, withdrawal of inhaled corticosteroid therapy leads to a deterioration in ventilatory function and increased exercise-induced dyspnea.

Cutaneous leucocytoclastic vasculitis associated with oxacillin.

A 67-year-old man who was treated with oxacillin for one week because of Staphylococcus aureus bacteremia, developed renal failure and diffuse, symmetric, palpable purpuric lesions on his feet. Necrotic blisters were noted on his fingers. Skin biopsies showed findings diagnostic of leucocytoclastic vasculitis. Oxacillin was discontinued and patient was treated with corticosteroids. The rash disappeared after three weeks and renal function returned to normal. Leucocytoclastic vasculitis presents as palpable purpura of the lower extremities often accompanied by abdominal pain, arthralgia, and renal involvement. Etiologic factors or associated disorders include infections, medications, collagen vascular disease and neoplasia. However, in half of the cases no etiologic factor is identified. Usually it is a self-limited disorder, but corticosteroid therapy may be needed in life-threatening cases since early treatment with corticosteroids in severe cases can prevent complications. Oxacillin should be included among the drugs that can cause leucocytoclastic vasculitis.

Protein tyrosine phosphatase-dependent proteolysis of focal adhesion complexes in endothelial cell apoptosis.

Adenosine and/or homocysteine causes endothelial cell apoptosis, a mechanism requiring protein tyrosine phosphatase (PTPase) activity. We investigated the role of focal adhesion contact disruption in adenosine-homocysteine endothelial cell apoptosis. Analysis of focal adhesion kinase (FAK), paxillin, and vinculin demonstrated disruption of focal adhesion complexes after 4 h of treatment with adenosine-homocysteine followed by caspase-induced proteolysis of FAK, paxillin, and p130(CAS). No significant changes were noted in tyrosine phosphorylation of FAK or paxillin. Pretreatment with the caspase inhibitor Z-Val-Ala-Asp-fluoromethylketone prevented adenosine-homocysteine-induced DNA fragmentation and FAK, paxillin, and p130(CAS) proteolysis. Asp-Glu-Val-Asp-ase activity was detectable in endothelial cells after 4 h of treatment with adenosine-homocysteine. The PTPase inhibitor sodium orthovanadate did not prevent endothelial cell retraction or FAK, paxillin, or vinculin redistribution. Sodium orthovanadate did block adenosine-homocysteine-induced FAK, paxillin, and p130(CAS) proteolysis and Asp-Glu-Val-Asp-ase activity. Thus disruption of focal adhesion contacts and caspase-induced degradation of focal adhesion contact proteins occurs in adenosine-homocysteine endothelial cell apoptosis. Focal adhesion contact disruption induced by adenosine-homocysteine is independent of PTPase or caspase activation. These studies demonstrate that disruption of focal adhesion contacts is an early, but not an irrevocable, event in endothelial cell apoptosis.

Leucocytoclastic vasculitis: an update for the clinician.

Leucocytoclastic vasculitis is a small vessel inflammatory disease mediated mostly by deposition of immune complexes. Infections, medications, chemicals, bacteria, viruses, and diseases associated with immune complexes have been accused in the pathogenesis. Cutaneous leucocytoclastic vasculitis presents as palpable purpura most often localized in the lower extremities, often accompanied by abdominal pain, arthralgia and renal involvement. The clinical diagnosis of leucocytoclastic vasculitis is confirmed histopathologically by skin biopsy. In order to determine the cause of the disease, depending on the patient's history, complete blood cell count, blood cultures, cryoglobulins, serum protein electrophoresis, rheumatoid factor, antinuclear antibody, and autoantibodies to neutrophilic cytoplasmic antigens and complement should be checked. Once the diagnosis of leucocytoclastic vasculitis is made, emphasis should be on the search for an etiological factor and the identification of the involved organs. If possible, the underlying cause should be treated or removed, for example discontinuation of drugs. The prognosis depends on the disease that has the cutaneous leucocytoclastic angiitis as a component, as well as the severity of internal organ involvement. For example, a patient with cutaneous leucocytoclastic angiitis and moderate nephritis as component of Henoch-Schonlein purpura has a much better prognosis than a patient with these same findings as a component of Wegener's granulomatosis. Only if physicians recognize and report severe reactions to regulatory authorities and manufacturers, new drugs associated with a risk of such reactions can be identified.

Pulmonary hypertension update.

Research into the causes and treatment of primary pulmonary hypertension (PPH) has provided new hope for this disease. This article reviews recent developments in its pathogenesis, classification, and treatment. An approach to diagnosing the patient with pulmonary hypertension also is outlined.

Adenosine induces endothelial apoptosis by activating protein tyrosine phosphatase: a possible role of p38alpha.

Endothelial cell (EC) apoptosis is important in vascular injury, repair, and angiogenesis. Homocysteine and/or adenosine exposure of ECs causes apoptosis. Elevated homocysteine or adenosine occurs in disease states such as homocysteinuria and tissue necrosis, respectively. We examined the intracellular signaling mechanisms involved in this pathway of EC apoptosis. Inhibition of protein tyrosine phosphatase (PTPase) attenuated homocysteine- and/or adenosine-induced apoptosis and completely blocked apoptosis induced by the inhibition of S-adenosylhomocysteine hydrolase with MDL-28842. Consistent with this finding, the tyrosine kinase inhibitor genistein enhanced apoptosis in adenosine-treated ECs. Adenosine significantly elevated the PTPase activity in the ECs. Mitogen-activated protein kinase activities were examined to identify possible downstream targets for the upregulated PTPase(s). Extracellular signal-regulated kinase (ERK) 1 activity was slightly elevated in adenosine-treated ECs, whereas ERK2, c-Jun NH(2)-terminal kinase-1, or p38beta activities differed little. The mitogen-activated protein kinase-1 inhibitor PD-98059 enhanced DNA fragmentation, suggesting that increased ERK1 activity is a result but not a cause of apoptosis in adenosine-treated ECs. Adenosine-treated ECs had diminished p38alpha activity compared with control cells; this effect was blunted on PTPase inhibition. These results indicate that PTPase(s) plays an integral role in the induction of EC apoptosis upon exposure to homocysteine and/or adenosine, possibly by the attenuation of p38alpha activity.

Role of the Na/H antiport in pH-dependent cell death in pulmonary artery endothelial cells.

We investigated the role of intracellular pH (pH(i)) and Na/H exchange in cell death in human pulmonary artery endothelial cells (HPAEC) following a metabolic insult (inhibition-oxidative phosphorylation, glycolysis). Metabolic inhibition in medium at pH 7. 4 decreased viability (0-15% live cells) over 6 h. Cell death was attenuated by maneuvers that decreased pH(i) and inhibited Na/H exchange (acidosis, Na/H antiport inhibitors). In contrast, cell death was potentiated by maneuvers that elevated pH(i) or increased Na/H exchange (monensin, phorbol ester treatment) before the insult. HPAEC demonstrated a biphasic pH(i) response following a metabolic insult. An initial decrease in pH(i) was followed by a return to baseline over 60 min. Maneuvers that protected HPAEC and inhibited Na/H exchange (acidosis, Na(+)-free medium, antiport inhibitors) altered this pattern. pH(i) decreased, but no recovery was observed, suggesting that the return of pH(i) to normal was mediated by antiport activation. Although Na/H antiport activity was reduced (55-60% of control) following a metabolic insult, the cells still demonstrated active Na/H exchange despite significant ATP depletion. Phorbol ester pretreatment, which potentiated cell death, increased Na/H antiport activity above the level observed in monolayers subjected to a metabolic insult alone. These results demonstrate that HPAEC undergo a pH-dependent loss of viability linked to active Na/H exchange following a metabolic insult. Potentiation of cell death with phorbol ester treatment suggests that this cell death pathway involves protein kinase C-mediated phosphorylation events.

Nucleotide-induced PMN adhesion to cultured epithelial cells: possible role of MUC1 mucin.

Accumulation of intraluminal polymorphonuclear leukocytes (PMN) is a hallmark of inflammatory diseases of the airways. Extracellular nucleotides stimulate PMN adhesion to human main pulmonary artery endothelial cells (HPAEC) by a purinoceptor-mediated mechanism. We investigated the effects of nucleotides on adhesion of freshly isolated human PMN to cultured human tracheobronchial epithelial cells (HBEC). We found that extracellular ATP and UTP were much less effective in stimulating PMN adhesion to HBEC compared with HPAEC, whereas the bacterial chemotactic peptide N-formyl-Met-Leu-Phe stimulated PMN adhesion to both cell types to an equal degree. We investigated several mechanisms that might account for decreased nucleotide-induced PMN adhesion to HBEC. The ectonucleotidase-resistant ATP analog adenosine 5'-O-(3-thiotriphosphate) was also ineffective in stimulating PMN adhesion to HBEC, indicating that degradation of ATP by ectonucleotidase(s) was not responsible for altered PMN adhesion. HBEC responded to ATP and UTP with increased intracellular calcium, indicating that these cells are capable of purinoceptor-mediated responses. We found that ATP and UTP also did not stimulate PMN adhesion to Chinese hamster ovary (CHO) cells, which had been stably transfected with the gene for hamster Muc1, a cell-associated mucin. However, ATP and UTP did stimulate adhesion of PMN to nontransfected CHO cells. These results suggested that MUC1 mucin modulates PMN adhesion to epithelium. We found that cultured HBEC expressed more mRNA and protein for MUC1 mucin than did HPAEC. We conclude that extracellular nucleotides are less effective in stimulating PMN adhesion to epithelial cells than to endothelial cells and that overexpression of hamster Muc1 mucin inhibits nucleotide-induced PMN adhesion to CHO cells.

Lamotrigine overdose presenting as anticonvulsant hypersensitivity syndrome.

OBJECTIVE: To describe the laboratory and physical manifestations of lamotrigine toxicity presenting as anticonvulsant hypersensitivity syndrome. CASE SUMMARY: A 49-year-old white man presented to our institution with a two-day history of low-grade fever, erythema, and edema involving the periorbital area. Five days earlier, he had been placed on lamotrigine treatment for bipolar disorder. He inadvertently received four daily doses of lamotrigine 2700 mg each. Physical examination was significant for periorbital edema and discrete and confluent blanching red macules and papules involving the face, trunk, and extremities. Laboratory tests revealed leukocytosis, hepatitis, and acute renal failure. With normalization of the laboratory results, the eruptions and edema gradually resolved. DISCUSSION: Lamotrigine toxicity can lead to periorbital edema, rash, and multiorgan system abnormalities. This presentation has clinical and laboratory similarities with anticonvulsant hypersensitivity syndrome, which suggests that at some threshold concentration the amount of lamotrigine may overwhelm the body's ability to metabolize the drug, leading to a similar hypersensitivity reaction. Lamotrigine is a relatively new agent, and this report may provide useful insights on evaluating the clinical toxicology of this agent. CONCLUSIONS: Healthcare providers should be aware that lamotrigine overdose may present with multiorgan involvement, similar to anticonvulsant hypersensitivity syndrome.

Effect of hypoxic exposure on Na+/H+ antiport activity, isoform expression, and localization in endothelial cells.

Little is known about the effects of prolonged hypoxic exposure on membrane ion transport activity. The Na+/H+ antiport is an ion transport site that regulates intracellular pH in mammalian cells. We determined the effect of prolonged hypoxic exposure on human pulmonary arterial endothelial cell antiport activity, gene expression, and localization. Monolayers were incubated under hypoxic or normoxic conditions for 72 h. Antiport activity was determined as the rate of recovery from intracellular acidosis. Antiport isoform identification and gene expression were determined with RT-PCR and Northern and Western blots. Antiport localization and F-actin cytoskeleton organization were defined with immunofluorescent staining. Prolonged hypoxic exposure decreased antiport activity, with no change in cell viability compared with normoxic control cells. One antiport isoform [Na+/H+ exchanger isoform (NHE) 1] that was localized to the basolateral cell surface was present in human pulmonary arterial endothelial cells. Hypoxic exposure had no effect on NHE1 mRNA transcript expression, but NHE1 protein expression was upregulated. Immunofluorescent staining demonstrated a significant alteration of the F-actin cytoskeleton after hypoxic exposure but no change in NHE1 localization. These results demonstrate that the decrease in NHE1 activity after prolonged hypoxic exposure is not related to altered gene expression. The change in NHE1 activity may have important consequences for vascular function.

Mechanism of extracellular ATP- and adenosine-induced apoptosis of cultured pulmonary artery endothelial cells.

Apoptosis may be important in the exacerbation of endothelial cell injury or limitation of endothelial cell proliferation. We have found that extracellular ATP (exATP) and adenosine cause endothelial apoptosis and that the development of apoptosis is linked to intracellular metabolism of adenosine [Dawicki, D. D., D. Chatterjee, J. Wyche, and S. Rounds. Am. J. Physiol. 273 (Lung Cell Mol. Physiol. 17): L485-L494, 1997]. In the present study, we investigated the mechanism of this effect. We found that exATP, adenosine, and the S-adenosyl-L-homocysteine (SAH) hydrolase inhibitor MDL-28842 caused apoptosis and decreased the ratio of S-adenosyl-L-methionine to SAH compared with untreated control cells. Using release of soluble [3H]thymidine as a measure of DNA fragmentation, we found that the effect of adenosine on soluble DNA release was potentiated by coincubation with homocysteine. These results suggest that the mechanism of exATP- and adenosine-induced endothelial cell apoptosis involves inhibition of SAH hydrolase. exATP-induced apoptosis was enhanced by an inhibitor of adenosine deaminase, whereas exogenous adenosine-induced apoptosis was partially inhibited by an adenosine deaminase inhibitor. These results suggest that adenosine deaminase may also be involved in the mechanism of adenosine-induced endothelial cell apoptosis. Adenosine and MDL-28842 caused intracellular acidosis as assessed with the fluorescent probe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. The cell-permeant base chloroquine prevented adenosine-induced acidosis but not apoptosis. Thus, although intracellular acidosis is associated with adenosine-induced apoptosis, it is not necessary for this effect. We speculate that exATP- and adenosine-induced endothelial cell apoptosis may be due to an inhibition of methyltransferase(s) activity. Purine-induced endothelial cell apoptosis may be important in limiting endothelial cell proliferation after vascular injury.

Differences in nucleotide effects on intracellular pH, Na+/H+ antiport activity, and ATP-binding proteins in endothelial cells.

Bovine (BPAEC) and human (HPAEC) pulmonary artery endothelial cell monolayers were incubated with either ATP, ATP analogues, or UTP, followed by measurement of intracellular pH (pHi) and the rate of recovery from acidosis. ATP increased baseline pHi and the rate of acid recovery in BPAEC. This response was inhibited by the amiloride analogue, methyisobutylamiloride, demonstrating that activation of the Na+/H+ antiport was responsible for the increase in baseline pHi and the recovery from acidosis. This response had the features of both a P2Y and P2U purinergic receptor, based on the responses to a series of ATP analogues and UTP. In contrast, none of the nucleotides had any significant effect on pHi and Na+/H+ antiport activity in HPAEC. This difference in the response to extracellular nucleotides was not due to a difference in ATP metabolism between cell types, since the ectonucleotidase-resistant analogue. ATP gamma S, also had no effect on HPAEC. Analogues of cAMP had no effect on pHi or acid recovery in either cell type. Incubation of BPAEC and HPAEC with the photoaffinity ligand [32P] 8-AzATP indicated that both BPAEC and HPAEC possess an ATP-binding protein of 48 kDa. However, BPAEC exhibited an additional binding protein of 87 kDa. Thus, the contrasting response to extracellular ATP between bovine and human pulmonary artery endothelial cells may be related to differences in the signal transduction pathway leading to antiport activation, including different ATP-binding sites on the cell membrane.

Studies on the mechanism of short-term regulation of pulmonary artery endothelial cell Na/K pump activity.

The Na/K pump is critically important in maintenance of cell homeostasis in the face of injury. Little is known about the regulation of endothelial cell Na/K-pump activity. We previously reported that short-term (30-minute) oxidant-induced endothelial cell perturbation increased Na/K-pump activity in intact monolayers of bovine pulmonary artery endothelial cells (BPAECs). In this study we investigated the mechanism of oxidant-induced increases in endothelial Na/K-pump activity, focusing on short-term modulation of alpha1-pump subunit. By using immunofluorescence microscopy and confocal scanning laser microscopy, we found alpha1 subunit on both apical and basal aspects of BPAECs without polarized distribution. Short-term (30-minute) incubation of PAEC monolayers with H2O2 (1 mmol/L) did not change the relative amounts of alpha1 subunit in membrane fractions, as assessed by immunoblotting. Phosphorylation of the alpha1 subunit also was not affected by H2O2 treatment. Because protein kinases have been reported to alter Na/K-pump activity in several tissues and because H2O2 has been reported to increase PKC activity of endothelial cells, we determined the effects of inhibition and activation of protein kinase C (PKC) on Na/K-pump activity quantitated as ouabain-inhibitable uptake of 86Rb. We also determined the effects of PKC activation and inhibition on H2O2-induced increases in Na/K-pump activity. Inhibitors of PKC increased Na/K-pump activity over a 30-minute period in intact monolayers. Inhibition or depletion of PKC did not prevent H2O2-induced increases in pump activity. These results indicate that PKC is an endogenous regulator of pulmonary artery endothelial cell Na/K-pump activity but that the effects of H2O2 are not mediated by activation of PKC or by changes in the expression or phosphorylation of alpha1 subunit.

Extracellular ATP and adenosine cause apoptosis of pulmonary artery endothelial cells.

ATP acts as an intracellular energy source and an extracellular signaling molecule. We report that extracellular ATP causes apoptosis in pulmonary artery endothelial cells, as assessed by morphological changes and internucleosomal DNA degradation. We investigated the mechanism of this effect using release of tritiated soluble DNA as a marker for apoptosis. We conclude that the metabolite adenosine is responsible for the apoptotic effect of ATP, since nucleotides that can be degraded to adenosine, as well as adenosine itself, cause DNA damage, whereas nonmetabolizable ATP analogs and uridine 5'-triphosphate are inactive. Furthermore, the ecto-5'-nucleotidase inhibitor alpha, beta-methylene-ADP blocks ATP-induced DNA fragmentation. The adenosine receptor agonist 5'-N-ethylcarboxamide adenosine does not cause DNA fragmentation, and adenosine receptor antagonists do not block adenosine-induced apoptosis. However, the nucleoside transport inhibitor dipyridamole prevents extracellular ATP-induced DNA cleavage. These findings indicate that ATP- and adenosine-mediated apoptosis are mediated via intracellular events rather than through cell surface receptor(s). The adenosine metabolites inosine, hypoxanthine, and xanthine do not cause apoptosis. The adenosine analogs 3-deazaadenosine and MDL-28842, which are not metabolized and are S-adenosylhomocysteine hydrolase inhibitors, also cause DNA fragmentation. Therefore, we speculate that extracellular ATP and adenosine cause apoptosis of pulmonary artery endothelial cells by altering methylation reactions that require S-adenosylmethionine as the methyl donor. We speculate that ATP released from cells undergoing cytolysis or degranulation may cause endothelial cell death. Endothelial cell apoptosis may be important in acute vascular injury or in limiting angiogenesis.

Group education sessions and compliance with nasal CPAP therapy.

STUDY OBJECTIVES: To determine an effective means of improving compliance with nasal continuous positive airway pressure (CPAP) for obstructive sleep apnea (OSA). DESIGN: Retrospective chart review. SETTING: An outpatient clinic at a Veterans Affairs Medical Center. PATIENTS: Seventy-three patients with OSA. INTERVENTIONS: Hour meters on CPAP machines provided documentation of nightly machine use. A 2-h group CPAP clinic, scheduled every 6 months, provided education, support, symptom treatment, and equipment monitoring for all CPAP patients. RESULTS: Twenty-five patients had hour meter readings taken at their first CPAP clinic. In these patients, nightly CPAP use increased from 5.2 +/- 0.6 to 6.3 +/- 0.6 h per night after attendance at one CPAP clinic (p < 0.05). CPAP use increased from 5.2 +/- 0.5 before CPAP clinic to 6.3 +/- 0.6 h per night after attendance at all subsequent CPAP clinics for 34 patients (p < 0.05), an improvement that was sustained over 605 +/- 34 days. Twenty-nine percent of patients increased nightly CPAP use by at least 2 h, while only 6% decreased by > or = 2 h (p < 0.025). Patients receiving supplemental oxygen had higher CPAP use prior to CPAP clinic compared to patients not receiving oxygen (p < 0.05). CONCLUSIONS: Attendance in a group clinic designed to encourage patient compliance with CPAP therapy provided a simple and effective means of improving treatment of OSA.