Exercise in severe COPD: Is walking different from stair-climbing?

BACKGROUND: It remains unclear whether the 6-min walking test can predict performance during stair-climbing in severe COPD patients. The present study aimed to assess different pathophysiological changes between walking and stair-climbing in these patients. METHODS: Sixteen COPD patients (mean FEV1 33+/-13% predicted) underwent a 6-min walking test and performed stair-climbing (44 steps) in a randomized, cross-over design. Blood gases, blood lactate, lung function parameters, maximal inspiratory mouth, sniff nasal and twitch mouth pressures, blood pressure, heart rate, and Borg Dyspnea Scale (BDS) were measured before and after exercise. RESULTS: The median drop of PaO2 during walking (2.6 mmHg) and stair-climbing (2.4 mmHg) was comparable (p=0.93). However, stair-climbing caused more dyspnea (median BDS 6.5 vs. 5.5, p=0.01), a higher median blood lactate (1.1 vs. 0.3 mmol/l p<0.001), a more pronounced drop in mean pH (-0.05+/-0.02 vs. -0.03+/-0.03, p=0.02) and a higher increase in mean systolic blood pressure (27+/-11 vs. 13+/-16 mmHg; p=0.009). Stair-climbing, but not walking, caused prolonged lung hyperinflation (mean TLC difference 4.4+/-4.7% predicted, p=0.003). There was no relationship between the 6-min walking distance (314+/-104 m) and the time needed for stair-climbing (55+/-33 s), nor were there any differences in inspiratory muscle strength and heart rate. CONCLUSION: Although the drop of PaO2 was comparable, stair-climbing resulted in more prolonged hyperinflation of the lungs, higher blood lactate production and more dyspnea than walking. The walking distance was not related to the time needed to manage stair-climbing. Therefore, pathophysiological changes during the 6-min walking test do not anticipate those during stair-climbing in patients with severe COPD.     

Ultrasonography versus nerve conduction study in patients with carpal tunnel syndrome: substantive or complementary tests?

OBJECTIVE: Our aim is to assess the optimal discriminatory sonographic criteria and relevant threshold values in patients with carpal tunnel syndrome (CTS) and to evaluate quantitative ultrasonography (US) as a tool for diagnosis and treatment of patients suffering from carpal tunnel syndrome in comparison with electrophysiological study. METHODS: Seventy-eight patients with CTS and 78 asymptomatic controls were assessed and underwent ultrasonography of the wrists. All patients and controls completed a self-administered questionnaire. Electrophysiological testing was done for all patients and control subjects. Data from the patient and the control groups were compared to determine the diagnostic relations in patients with CTS and the grade of severity. RESULTS: There was a high degree of correlation between the conduction abnormalities of the median nerve as detected by electrodiagnostic tests, self-administered assessment and the measurement of the cross-sectional area of the nerve by US (P<0.05). Various levels of disease severity could also be illustrated by US, giving confident results for diagnosis, treatment planning and following the patients with CTS. In 16 patients (17%) tenosynovitis/localized swelling in the tendons in the carpal tunnel was the primary cause of CTS. A cut-off point of 10 mm(2) for the mean cross-sectional area of the median nerve was found to be the upper limit for normal values. Based on the results of this study, an algorithm for evaluation and management of CTS has been suggested. CONCLUSION: High-frequency US examination of the median nerve and measurement of its cross-sectional area should be strongly considered as a new alternative diagnostic modality for the evaluation of CTS. In addition to being of high diagnostic accuracy it is able to define the cause of nerve compression and aids treatment planning; US also provides a reliable method for following the response to therapy.     

Maintenance pharmacotherapy of mild and moderate COPD: what is the evidence?

Chronic obstructive pulmonary disease (COPD) affects more than 24 million individuals in the United States, although at least half of the cases are not diagnosed. Proactive diagnosis and limitation of risk exposure from smoking or pollutants are important to improve prognosis. Pharmacologic treatments are prescribed according to COPD stage and symptoms. Mild COPD is symptomatically treated 'as needed' with short-acting bronchodilators; major guidelines recommend starting maintenance treatment at the moderate COPD stage with long-acting bronchodilators; inhaled corticosteroids may be added for patients with more severe disease and frequent exacerbations. Maintenance therapy preserves 24-h airway patency, reduces exacerbations, and improves activity tolerance and health-related quality of life. Recent post-hoc analyses of large clinical trials that contain subgroups of patients with less severe COPD suggest that, similar to those with advanced disease, patients with moderate disease benefit from long-term maintenance therapies. Studies suggest symptomatic mild patients may also benefit. This concept needs to be prospectively tested in studies specific to these COPD disease stages. Proactive identification and pharmacologic intervention in early COPD has the potential to alter clinical outcomes throughout the disease course.     

Anti-neutrophil cytoplasmic antibodies tests: which tests should be used in practice?

Serological testing for anti-neutrophil cytoplasmic antibodies (ANCA) has become an important tool for supporting a diagnosis of systemic necrotizing small vessel vasculitis: Wegener's granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome and oligo-symptomatic forms of these. These so-called ANCA-associated vasculitides most often necessitate the institution of therapies with cytotoxic as well as anti-inflammatory agents, and hence, a firmly established diagnosis is mandatory to avoid unnecessary and risky treatment. In the laboratory of today the most appropriate way to detect the presence of vasculitis-associated ANCA is by using both indirect immunofluorescence and direct enzyme immuno-assay for antibodies to proteinase 3 and myeloperoxidase. The diagnostic specificity of these latter assays towards systemic vasculitis can only be secured by setting a suitably high cut-off value, chosen in collaboration with clinicians after testing carefully selected disease control sera. When classical cytoplasmic ANCA as well as a significant level of proteinase 3-ANCA are found in a given serum this combined result strongly indicates vasculitis. Similarly, the combination of perinuclear ANCA and a significant level of myeloperoxidase-ANCA is close to 100% specific for vasculitis.     

Laboratory tests for identification or exclusion of heparin induced thrombocytopenia: HIT or miss?

Heparin induced thrombocytopenia (HIT) is a potentially fatal condition that arises subsequent to formation of antibodies against complexes containing heparin, usually platelet‐factor 4‐heparin (“anti‐PF4‐heparin”). Assessment for HIT involves both clinical evaluation and, if indicated, laboratory testing for confirmation or exclusion, typically using an initial immunological assay (“screening”), and only if positive, a secondary functional assay for confirmation. Many different immunological and functional assays have been developed. The most common contemporary immunological assays comprise enzyme‐linked immunosorbent assay [ELISA], chemiluminescence, lateral flow, and particle gel techniques. The most common functional assays measure platelet aggregation or platelet activation events (e.g., serotonin release assay; heparin‐induced platelet activation (HIPA); flow cytometry). All assays have some sensitivity and specificity to HIT antibodies, but differ in terms of relative sensitivity and specificity for pathological HIT, as well as false negative and false positive error rate. This brief article overviews the different available laboratory methods, as well as providing a suggested approach to diagnosis or exclusion of HIT.     

Laboratory tests for coagulation system monitoring in a patient with β-thalassemia

Sensitive methods for assessment of the hemostatic state are essential for providing adequate therapy to patients with β-thalassemia. The present study was designed to monitor the changes in the hemostatic state of a patient with β-thalassemia at the primary stage and under heparin treatment following splenectomy. The hemostatic state of the patient was assessed using conventional tests (activated partial thromboplastin time, prothrombin index, thrombin time), fibrinogen and D-dimer assays, thromboelastography (TEG), thrombin generation test, and a novel thrombodynamics clot growth assay. Thrombodynamics parameters indicated the hypercoagulation state on the primary evaluation which progressed after splenectomy: stationary clot growth velocity increased from 32 to 38 μm/min (normal range 20–30 μm/min). Hypercoagulation state was confirmed by Doppler echocardiography, which detected portal vein thrombosis on day 23 after surgery. The results of the other tests’ parameters were in the normal ranges before splenectomy. The TEG parameters were sensitive to low molecular weight heparin (LMWH) injections; but the values were close to the normal ranges before and after injections. The thrombodynamics assay demonstrated a high sensitivity to LMWH injections, and registered a decrease of the hypercoagulability in the course of therapy (P < 0.05). TGT was not performed during LMWH therapy. This clinical case demonstrates the potential of the thrombodynamics assay to serve as a sensitive method for coagulation system monitoring and prediction of prothrombotic tendencies in patients with hemolytic anemias.     

Heart failure and COPD: Partners in crime?

Chronic obstructive pulmonary disease (COPD) and heart failure (HF) are both common diseases with major impact and seem to coexist more frequently than expected from their separate population prevalences. However, estimates of combined prevalence must be interpreted carefully because of imperfections and difficulties in assessment of both diseases. This review aims to highlight HF prevalence in patients with COPD and vice versa, with a critical analysis of studies performed. First, definition, diagnosis, and prevalence of COPD and of HF will be discussed. Subsequently, an overview of important studies concerning combined prevalence with their limitations will be presented. Finally, pathogenic mechanisms and diagnostic considerations in clinical practice will be discussed.