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Chronic beryllium disease — SCE Respiratory MCQ

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HardOccupational Lung DiseaseChronic beryllium diseaseSCE Respiratory

A 52-year-old aerospace machinist has progressive exertional dyspnoea and dry cough. For 18 years he has machined beryllium–copper components, including tasks generating fine dust. HRCT shows bilateral hilar lymphadenopathy, upper-zone perilymphatic nodules and early traction bronchiectasis. Bronchoalveolar lavage is lymphocytic, and transbronchial biopsies contain non-necrotising granulomas; mycobacterial and fungal investigations are negative. Serum angiotensin-converting enzyme is elevated. A peripheral-blood beryllium lymphocyte proliferation test (BeLPT) is abnormal on a single sample. He has not received systemic corticosteroids. Which investigation should be arranged next to most securely distinguish chronic beryllium disease from sarcoidosis?

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Correct answer: B — Repeat the peripheral-blood BeLPT on a separate sample

Explanation lettering: D = shown as A · E = shown as C · C = shown as D · A = shown as E

The exposure history, sarcoid-like radiology and non-necrotising granulomas should prompt evaluation for chronic beryllium disease (CBD), which is a close phenocopy of sarcoidosis. CBD requires evidence of beryllium-specific sensitisation in addition to compatible pulmonary disease. BeLPT is the key exposure-specific test, but false-positive and inter-laboratory variation occur; an isolated abnormal blood result should therefore be confirmed with a separate measurement before attributing the granulomatous disease to beryllium. Testing before systemic corticosteroids also avoids potential suppression of lymphocyte responsiveness. Repeating ACE (A) cannot discriminate CBD from sarcoidosis: ACE is neither sufficiently sensitive nor specific and may be elevated in either granulomatous process. Urinary beryllium (C) may document recent exposure but does not establish beryllium-specific immune sensitisation or causation. HLA-DPB1 Glu69 (D) is associated with susceptibility to sensitisation and CBD, but carriage is neither necessary nor sufficient for diagnosis. A repeat biopsy with polarised-light microscopy (E) is unnecessary because granulomatous pulmonary inflammation is already demonstrated; the decisive missing evidence is reproducible beryllium sensitisation, not visualisation of deposited metal. Once sensitisation is confirmed in this clinical context, CBD is substantially more defensible than sarcoidosis.

Reference: RR1221: Systematic review of the methods and frequency for undertaking workplace respiratory health surveillance (First published 2025) — https://www.hse.gov.uk/research/assets/docs/rr1221.pdf An official American Thoracic Society statement: diagnosis and management of beryllium sensitivity and chronic beryllium disease (2014) — https://pubmed.ncbi.nlm.nih.gov/25398119/ Diagnoses of chronic beryllium disease within cohorts of sarcoidosis patients (2006) — https://publications.ersnet.org/content/erj/27/6/1190