Cardiac autonomic dysfunction is an independent determinant of adverse outcomes in many diseases. The available literature on the relative changes in sympathetic and parasympathetic components in chronic obstructive pulmonary disease (COPD) is equivocal, the clinical and physiological correlates are poorly defined and association with markers of systemic inflammation has not been explored. As both autonomic dysfunction and systemic inflammation may contribute to cardiovascular morbidity in COPD, we hypothesized that these may be associated. Sixty three stable patients of COPD and 36 controls underwent spirometry, estimation of diffusion capacity, six-minute walk test and measurements of serum interleukin-6 (IL-6) and high-sensitivity C-Reactive protein. Cardiac autonomic activity was evaluated by standard five-minute heart rate variability (HRV) recordings to obtain time- and frequency-domain indices and the averaged heart rate. We observed that HRV indices of overall autonomic modulation, the standard deviation of time intervals between consecutive normal beats (SDNN) and total power, were greater in patients with higher levels of indices of both parasympathetic and sympathetic activity. The heart rate was significantly higher in patients indicating an overall sympathetic dominance and was inversely correlated with diffusion capacity. Serum IL-6 was inversely correlated with pNN50, an index of parasympathetic activity, and positively with LF/HF ratio, a measure of sympathetic: parasympathetic balance. None of the HRV indices was significantly correlated with physiological measures of severity. It was concluded that patients with COPD have increased cardiac autonomic modulation with sympathetic dominance. This is associated with decreased lung diffusion capacity and systemic inflammation.

Introduction: Chest X-ray (CXR) has been used since long as an aid in the diagnosis of pulmonary tuberculosis (PTB) and also to determine the extent of the disease. The present study was conducted to evaluate the correlation of disease extent on CXR based on the Timika CXR score with clinical and microbiological parameters at baseline, in sputum positive cases of pulmonary tuberculosis. Material and methods: The study was conducted at a tertiary referral centre for chest diseases in Bangalore, Karnataka from January 2017 to January 2018. This is a prospective study of new sputum smear positive pulmonary tuberculosis cases diagnosed in the Department of Pulmonary Medicine. At baseline, patients' symptoms and signs on chest auscultation were recorded. The clinical scoring was done by the Karnofsky performance score (KPS) and TB score I (Bandim TB score) and II. Baseline CXR postero-anterior (PA) view of each patient was assessed independently by two chest physicians and evaluated by the Timika CXR scoring method. Routine blood investigations and sputum smear for acid fast bacilli were done. The correlation between the CXR score and other disease severity parameters was analysed. Results: Clinical scores such as the KPS and TB score I and II, did not correlate with the presence of cavitary disease on CXR (p > 0.05). 48.6% of patients with cavitary disease had higher baseline AFB density in sputum (i.e. sputum smear microscopy grade 3+) as compared to 40% of patients with non cavitary disease, which was not statistically significant. CXR score > 71 was significantly associated with longer duration of symptoms, higher clinical scores (KPS and TB score I, II) and lower Body Mass Index (BMI) at diagnosis of PTB (p < 0.05). 65.2% of the patients with CXR score > 71 had significantly higher baseline AFB density as compared to only 32.4% with CXR score ≤ 71 (p < 0.04). CXR score > 71 also had significant association with higher ESR. Conclusion: Cavitary disease on CXR is associated with a higher mycobacterial load at baseline. The Timika CXR score is a simple, standard scoring system which can be used by a chest physician in a clinical setting. The CXR score significantly correlates with a broad range of clinical and microbiological measures of disease severity in PTB patients. Thus, it has a role in risk stratification, especially in patients not producing sputum or sputum negative PTB at diagnosis.

Introduction: Tubercular pleural effusion is the second most common extrapulmonary form of tuberculosis in India. Developing nations like India face several health challenges and with limited resources, appropriate planning and channelization of the same is the need of the hour. Material and methods: The objective of the study was to determine the role of cartridge-based nucleic acid amplification test (CBNAAT) in the diagnosis of tubercular pleural effusion (TPE) and also to study if any association exists between CBNAAT and pleural fluid adenosine deaminase (ADA) and lymphocyte counts. Clinically suspected TPE, lymphocyte predominant (≥ 70%) exudates (according to the Lights criteria) with ADA ≥ 40 U/L and microbiologically confirmed pulmonary tuberculosis patients with a co-existent pleural effusion were included. Pleural fluid CBNAAT was performed on all the samples. Results: Out of a total of 75 patients, 57 were males and 18 were females. A lymphocyte predominance of ≥ 70% was seen in 73 subjects (97%). Mean ADA was 61.7 U/L ± 16.2 (SD). Pleural fluid CBNAAT was positive for Mycobacterium tuberculosis (MTB) in 24 patients (32%). Out of these patients, rifampicin resistance was detected in 2 individuals (8.3%). Sputum smear for acid fast bacilli (AFB) was positive in 3 (4%) patients, whereas in sputum CBNAAT MTB was detected in 8 (10.6%) persons. Association between pleural fluid ADA, lymphocyte count and CBNAAT positivity was evaluated by Student T-test. There was a significant association between higher ADA levels and CBNAAT (p value = 0.001). Conclusions: Pleural fluid CBNAAT, owing to its low sensitivity, should not be included in the diagnostic protocol of TPE in high prevalence areas. A high ADA ≥ 40 U/L in combination with Light's criteria to define exudates, with lymphocyte predominance is sufficient evidence to diagnose TPE and initiate anti-tubercular therapy, thereby deferring the need to perform an invasive pleural biopsy.

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