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Ann Saudi MedAnn Saudi MedAnnals of Saudi Medicine0256-49470975-4466King Faisal Specialist Hospital and Research Centre 1859639810.5144/0256-4947.2008.303asm-4-303What's Your Diagnosis?A 32-year-old male with progressive pulmonary symptoms and disseminated small radio-opacities throughout both lung fields Rajabi Mohammad A. From the Department of Surgery, Isfahan University of Medical Science, Isfahan, IranCorrespondence and reprints: Mohammad Ali Rajabi, MD, Associate Professor of Surgery, Isfahan University of Medical Science Sofe St. Al Zahra Hospital, PO Box 901 Isfahan, Iran, T: +983-11-668-7611, F: +983-11-668 7611, rajabi@med.mui.ac.irJul-Aug 2008 28 4 303 304 01 1 2008 Copyright © 2008, Annals of Saudi Medicine2008This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
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A 32-year-old man who suffered from repeated periods of fever, dizziness and increasing respiratory symptoms was admitted to Shariati General Hospital of Isfahan in December 1993. He had a history of recurrent febrile lower respiratory infection. He also had a history of exposure to mustard gas in 1988, during the Iraq-Iran war. There were no hereditary respiratory diseases in his family. His entire medical record, including chest x-rays and laboratory tests before 1988 were normal.

After exposure to mustard gas, the patient had dermatitis and conjunctivitis, cheilitis and pneuomonitis, which healed after about 2 months but the patient had progressive respiratory complications including productive cough, dyspnea and repeated periods of pneumonia. Asthmatic-like symptoms and signs continued but were relatively controlled through corticosteroid therapy. The patient needed to be hospitalized 2 to 3 times a year. In the first 3 to 4 years of the disease course the patient had no cyanosis or clubbing of the fingers, but later he manifested cyanosis and clubbing and in the last 4 months of his life he experienced orthopnea. In the fifth year following mustard gas exposure the patient’s chest x-ray revealed remarkably uniform opacification of both lungs produced by disseminated, very fine sand-like, discrete radio-opaque micro-nodules of almost equal sizes throughout both lungs; thus the lungs appeared to be sprinkled with sand, predominantly in the lower zones. Apical bullae were present on both sides (Figure 1). Routine lab tests including complete blood count, erythrocyte sedimentation rate, blood urea nitrogen, blood sugar and urinalysis exhibited normal values; however, a certain tendency to polycythemia in the hemogram was detected. Respirometry showed a severe restrictive pattern consistent with an end-stage pulmonary condition: forced vital capacity (FVC) was 49% (2.23 L), forced expiratory volume in one second (FEV1) was 53% (2.08 L) and FEV1/FVC was 93.1%. On rigid bronchoscopy, there was no tumor, mass or signs of tuberculosis, but there was mucosal atrophy and areas of edema without any specific findings in bronchial biopsy and in lavage fluid examination. The patient was treated with diphosphonates, bronchodilators, glucocorticoids and bronchoalveolar lavage, but his condition deteriorated over the next several months and he died in November 2001 due to cardiopulmonary failure.

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Figure 1 Chest x-ray showing dense micronodular pattern.