Sequelae of COVID-19 pneumonia: Is it correct to label everything as post-COVID lung fibrosis?

One of the common long-term consequences observed in survivors of COVID-19 pneumonia is the persistence of respiratory symptoms and/or radiological lung abnormalities. The exact prevalence of these post-COVID pulmonary changes is yet unclear. Few authors, based on their early observations, have labeled these persistent computed tomography (CT) abnormalities as post-COVID lung fibrosis, which appears to be an overstatement. Lately, it is being observed that many of the changes seen in post-COVID lungs are temporary and tend to show resolution on follow-up, with only a few developing into lung fibrosis. Thus, based on the presumptive diagnosis of lung fibrosis, these patients should not be blindly started on anti-fibrotic drugs. One must not forget that these drugs can do more harm than good, if used injudiciously. It is better to use the term "post-COVID interstitial lung changes", which covers a broader spectrum of pulmonary changes seen in patients who have recovered from COVID-19 pneumonia. At the same time, it is essential to identify the sub-set of COVID-19 survivors who are at an increased risk of developing lung fibrosis and to carefully chalk out management strategies so as to modify the course of the disease and prevent irreversible damage. Meticulous and systematic longitudinal follow-up studies consisting of clinical, laboratory, imaging, and pulmonary function tests are needed for the exact estimation of the burden of lung fibrosis, to understand the nature of residual pulmonary changes, and to predict the likelihood of development of lung fibrosis in COVID-19 survivors.

Amyloidosis secondary to chronic pulmonary aspergillosis: Case report and a systematic review of literature.

Secondary amyloidosis results from the deposition of abnormally folded proteins in body organs due to chronic inflammatory disorders. Kidneys are the most commonly affected organ and manifest as nephrotic syndrome with or without renal failure. Chronic pulmonary aspergillosis (CPA) is a chronic infection of lung parenchyma affecting those with an underlying structural lung disease. Herein, we present a case of CPA where the initial manifestation was that of nephrotic syndrome due to renal amyloidosis. We also perform a systematic review for studies describing secondary amyloidosis due to CPA.

Monitoring treatment response in chronic pulmonary aspergillosis: role of clinical, spirometric and immunological markers.

OBJECTIVES: The treatment response in chronic pulmonary aspergillosis (CPA) is usually assessed based on the improvement in clinical and imaging findings. Herein, we evaluate serum Aspergillus fumigatus-specific IgG, serum galactomannan, weight change, and lung function for assessing treatment response in subjects with CPA. METHODS: We categorized treatment response as favourable (improved or stable clinical response with radiologically improved or stable disease) or unfavourable (worsening of symptoms or radiological progression) after 6 months of treatment with antifungal azoles. We measured A. fumigatus-specific IgG, serum galactomannan, weight, and lung function at baseline, 3 months, and 6 months in those with favourable and unfavourable treatment response. RESULTS: One hundred and twenty-six consecutive treatment-naïve subjects (53.2% (67/126) males; mean ± SD age, 42.3 ± 14.7 years) with CPA were included. One hundred and six and 20 were classified as having favourable and unfavourable response, respectively. After 6 months of treatment, the decline in serum A. fumigatus-specific IgG (n = 119) was similar in those with favourable or unfavourable response (mean ± SD, -26.3 ± 45.5 mgA/L vs. -3.4 ± 65.6 mgA/L; p 0.20). There was no significant change in the serum galactomannan (favourable vs. unfavourable: mean ± SD, -0.11 ± 2.8 vs. -0.62 ± 2; p 0.92) or FEV1 (favourable vs. unfavourable: mean ± SD, 24 ± 250 mL vs. -62 ± 154 mL; p 0.19) after 6 months of treatment. There was significant loss of weight (mean ± SD, -2.5 ± 4.5 kg) in subjects with unfavourable response. CONCLUSION: Serum A. fumigatus-specific IgG and serum galactomannan inconsistently decrease following treatment and may not be useful indicators for monitoring treatment response in CPA. Similarly, there is little change in pulmonary function following treatment. A gain in body weight is seen in those with favourable response.

Meta-analysis of Indian studies evaluating adenosine deaminase for diagnosing tuberculous pleural effusion.

OBJECTIVE: To determine the diagnostic accuracy of pleural fluid adenosine deaminase (ADA) in diagnosing tuberculous pleural effusion (TPE) among Indian patients using systematic review and meta-analysis. DESIGN: The PubMed, Embase, IndMED and Cochrane databases and other relevant publications were searched to identify Indian studies evaluating the sensitivity and specificity of ADA in diagnosing TPE. Pooled diagnostic accuracy measures and 95% confidence intervals (95%CI) were generated using a bivariate random-effects model, and examined using forest plots and hierarchical summary receiver operating characteristic (HSROC) curves. RESULTS: Forty publications with 3524 patients were studied. Pooled sensitivity, specificity and diagnostic odds ratio estimates were high (0.94, 95%CI 0.89-0.96; 0.89, 95%CI 0.83-0.93; and 119.85, 95%CI 48.35-297.08, respectively). The area under the HSROC curve was 0.966. The most common ADA threshold was 40 international units (IU)/l in 18 studies. Pooled positive and negative likelihood ratios for thresholds between 38 and 42 IU/l were respectively 6.80 (95%CI 4.18-11.07) and 0.06 (95%CI 0.03-0.11). There was no clear change in diagnostic performance with increasing ADA thresholds. Multivariate meta-regression did not reveal any factor that significantly influenced the substantial heterogeneity between studies. CONCLUSION: Pleural fluid ADA has good diagnostic accuracy for TPE in Indian patients, and appears more useful at excluding TPE at a threshold value of around 40 IU/l.

Allergic bronchopulmonary aspergillosis complicating Swyer-James-Macleod's syndrome: case report and review of literature.

Allergic bronchopulmonary aspergillosis (ABPA) is a pulmonary disorder that results from immune responses mounted against antigens of Aspergillus fumigatus, resulting in non-specific respiratory symptoms and structural lung damage. Classically defined in individuals suffering from bronchial asthma and cystic fibrosis, ABPA has recently been described in other lung diseases including COPD, pulmonary tuberculosis, idiopathic bronchiectasis and others. Herein, we report the first case of ABPA complicating Swyer-James-Macleod's syndrome that was successfully treated with oral antifungal therapy.

Prevalence of Aspergillus sensitisation in pulmonary tuberculosis-related fibrocavitary disease.

SETTING: Aspergillus complicates the course of healed pulmonary tuberculosis (PTB), causing aspergilloma and chronic pulmonary aspergillosis. Whether Aspergillus also causes allergic sensitisation in PTB-related fibrocavitary disease and bronchiectasis remains unknown. OBJECTIVE: To investigate the prevalence of Aspergillus sensitisation in healed fibrocavitary PTB. DESIGN: In a case-control design, consecutive symptomatic new referrals with PTB-related fibrocavitary disease underwent spirometry, Aspergillus skin test and computed tomography of the chest, determination of serum IgE levels (total and Aspergillus fumigatus-specific), serum precipitins against A. fumigatus and eosinophil count. Aspergillus sensitisation was defined as either a positive Aspergillus skin test or A. fumigatus IgE >0.35 kUA/l. RESULTS: A total of 100 subjects (50 PTB-related fibrocavitary disease, 50 controls) with a mean age of 40.8 years (standard deviation [SD] 12.2) were enrolled. Aspergillus sensitisation was present in 16 (32%) cases and two (4%) controls. Fourteen cases (one control) had IgE values >1000 IU/ml, while two cases manifested eosinophilia. Aspergillus precipitins were positive in 13 cases (two controls); of these, 8 did not have Aspergillus sensitisation. The presence of airflow obstruction on spirometry was significantly associated with Aspergillus sensitisation on univariate analysis (OR 4.96, 95%CI 1.36-18.03). CONCLUSIONS: There is a high prevalence of Aspergillus sensitisation in PTB-related fibrocavitary disease. The clinical relevance and therapeutic implications of this finding require further investigation.