Srirama Chandra Bhanja Medical College and Hospital

Silicosis is a preventable occupational lung disease caused by inhalation of crystalline silica and remains a significant cause of morbidity among young working populations in developing countries. It is characterised by progressive pulmonary fibrosis and irreversible respiratory impairment. While parenchymal lung involvement is well recognised, pleural manifestations are distinctly uncommon, and pleural effusion is rarely reported. The current case describes a 30-year-old male with a history of sandblasting exposure who presented with progressive dyspnoea and acute hypoxaemic respiratory failure. High-resolution computed tomography of the thorax demonstrated reticulonodular opacities with progressive massive fibrosis and bilateral pleural effusion, consistent with advanced silicosis. Diagnostic thoracentesis revealed a haemorrhagic exudative pleural effusion with low adenosine deaminase levels, normal glucose, and absence of malignant cells or granulomas. Microbiological studies were negative, and cardiac, hepatic, renal, and systemic causes of pleural effusion were excluded. Owing to severe respiratory failure, invasive procedures such as thoracoscopy or bronchoscopy could not be performed. The patient was treated with oxygen therapy, broad-spectrum antibiotics, systemic corticosteroids, and bronchodilators. Despite clinical stabilisation, persistent hypoxaemia necessitated Long-Term Oxygen Therapy (LTOT) and consideration for lung transplantation. After exclusion of common aetiologies, the pleural effusion was attributed to silica-induced pleural inflammation. This case highlights an unusual and under-recognised pleural manifestation of silicosis. In patients with relevant occupational exposure and unexplained exudative pleural effusion, silica-related pleural disease should be considered after excluding tuberculosis and malignancy. Early recognition is essential for appropriate management and prognostic assessment.

Background Discoid lupus erythematosus (DLE) on the scalp can be confused with various scarring alopecias. There is no large-scale trichoscopic study on scalp DLE, and the trichoscopic features in skin of colour are underreported. Objective This study aimed to analyse the clinical and trichoscopic features of DLE on the scalp in skin of colour. Methods This retrospective cross-sectional study analysed the clinical and trichoscopic images of all the biopsy and direct immunofluorescence-proven cases of scalp DLE. Results The prevalent trichoscopic features encompassed follicular, perifollicular, and interfollicular findings. Follicular features included follicular plugs (87%) and yellow dots (53%). Perifollicular findings comprised white scales (92%), white (94%) and brown structureless areas (87%), shiny white structures (SWSs; 75%), and erythema (74%). Interfollicular features included white to pinkish-white structureless areas (90%), white scales (88%), brown structureless areas (81%), shiny white structures (75%), and erythema (72%). Vascular patterns observed were linear irregular, linear, arborising, and polymorphous vessels. Limitations The study's limitations were small sample size, and a retrospective design. Conclusion Scalp DLE presents as two distinct clinical morphologies in skin of colour, and the trichoscopic features can vary depending on the clinical morphology.

Myths and misconceptions surrounding sickle cell disease (SCD) can shape stigma and influence the treatment and interaction with healthcare services. In India, where SCD disproportionately affects tribal populations, limited evidence exists on myths and misconceptions across endemic regions. This study explored culturally embedded myths and misconceptions related to SCD among tribal communities in India and examined their implications for stigma and healthcare-seeking behaviour. A qualitative descriptive study was conducted across nine SCD-endemic tribal districts in India. Data, collected through in-depth interviews with key informants and focus group discussions with community members, were analysed using thematic content analysis. Themes were organised around domains of causation, transmission, heredity, prognosis and treatment. The study identified diverse SCD-related beliefs, myths and misconceptions across the study sites. These were organised around domains and grouped into four broad categories: locally rooted explanatory beliefs, including supernatural, spiritual, dietary and lifestyle-related explanations; misconceptions arising from incomplete biomedical understanding, particularly regarding contagion, heredity and consanguineous marriage; distorted interpretations of medical or programme-related messages, especially around marriage, reproduction and long-term treatment; and social consequences related to stigma, fatalism, perceived productivity and economic burden. These categories overlapped across sites, with some beliefs being locally specific and others commonly reported across tribal settings. SCD-related myths and misconceptions in tribal India are socially embedded and extend beyond simple informational gaps. Culturally responsive communication and counselling approaches that acknowledge local explanatory frameworks, while strengthening accurate understanding of inheritance, treatment and long-term care, are needed within SCD care programmes in endemic regions.

Background: Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is a major driver of hospitalization, ventilatory support, intensive care use, and early mortality. Simple biochemical markers capable of identifying high-risk patients at admission are particularly valuable in resource-constrained settings. Serum uric acid (SUA), the end product of purine metabolism, rises in tissue hypoxia, oxidative stress, and systemic inflammation and may therefore reflect the biological burden of severe exacerbation. Aim: To evaluate whether admission serum uric acid is an independent prognostic marker of adverse in-hospital outcome in patients hospitalized with AECOPD. Materials and Methods: This prospective observational study included 85 consecutive adults admitted with AECOPD. Clinical history, comorbidity profile, oxygen saturation, arterial blood gas indices, inflammatory markers, renal function, and admission SUA were recorded before major therapeutic escalation. The primary endpoint was a composite adverse in-hospital outcome. Secondary outcomes included need for non-invasive ventilation (NIV), intensive care unit (ICU) admission, in-hospital mortality, and length of stay. Comparative statistics, receiver operating characteristic (ROC) analysis, and multivariable logistic regression were performed. Results: The mean age of the cohort was 65.11 ± 8.74 years, and 66 patients (77.6%) were male. Thirty-one patients (36.5%) experienced an adverse in-hospital outcome, 22 (25.9%) required NIV, 14 (16.5%) required ICU admission, and 12 (14.1%) died during hospitalization. Admission SUA was significantly higher in patients with adverse outcome than in those without adverse outcome (7.83 ± 1.05 vs 6.62 ± 1.00 mg/dL, p<0.001). ROC analysis showed good discriminatory performance of SUA for adverse in-hospital outcome (AUC 0.799, 95% CI 0.690-0.895), with an optimal cutoff of 7.5 mg/dL. On multivariable analysis, high SUA (≥7.5 mg/dL) remained an independent predictor of adverse outcome (adjusted OR 7.29, 95% CI 2.52-21.04; p<0.001). Conclusion: Admission serum uric acid is a clinically useful and independent prognostic marker in hospitalized AECOPD. Because it is inexpensive, widely available, and strongly associated with escalation of care and mortality, SUA may be incorporated into early bedside risk stratification together with arterial blood gas and renal function parameters.