A 36-year-old man was admitted to our department for bilateral symmetric polyarthralgia touching large and small joints for two months. He also complained of bone pain in the forearm and legs, shortness of breath, and dry cough without dyspnea. He was not a smoker or alcoholic. His medical history was without specialties, including lung and liver diseases.
On physical examination, vital signs, including body mass index, were normal. A musculoskeletal examination revealed a digital clubbing with Schamroth's sign (Figure 1), bilateral and symmetric swelling of the elbow, wrist, and ankles. Palpation of the bony reliefs of the forearms and legs is also painful. The rest of the somatic examinations were normal including the lungs, heart, liver, and skin.
Laboratory findings revealed elevated acute phase reactants with erythrocyte sedimentation rate (ESR) at 90 mm and C-reactive protein (CRP) at 98.1 mg/L. Immunological examinations were negative (antinuclear antibodies (ANAs), anticitrullinated protein antibodies (ACPAs), rheumatoid factors (RFs), antinuclear antibodies (ANAs), and anti-ds DNA antibodies). Serum thyroid-stimulating hormone (TSH) and free thyroid hormones (FT3 and FT4) were normal. Renal and hepatic functions were within the normal range. Acid-fast Bacillus(AFB) smear microscopy in sputum samples of 3 successive days was negative. A sputum culture was negative for Mycobacterium tuberculosis. Bronchoscopy was normal and cultures from bronchoalveolar lavage (BAL) samples were negative for Mycobacteria and Aspergillus. Hydatid and Aspergillus serologies were negative. The human immunodeficiency virus antibody test was negative.
A chest X-ray and computed tomography (CT) showed an apical pulmonary cavity in the right lung with bronchiolitis and hilar lymphadenopathy (Figure 2(a)). Plain X-ray revealed a monolayer periosteal reaction along the bones of the forearm and legs without acro-osteolysis. Bone scintigraphy showed longitudinally radiotracer uptake along all long bones of the upper and lower extremities confirm periostosis of the tubular bones (Figure 3(a)).
In front of digital clubbing, we discussed acromegaly, thyroid acropachy, and HOA. However, the absence of prognathism and the presence of periostosis quickly excluded acromegaly. Thyroid acropachy is a manifestation of Graves' disease, in our patient, eliminated by the absence of Graves' ophthalmopathy and pretibial myxedema with TSH normal. The negativity of immunological examinations excluded inflammatory arthritis. The diagnosis of HOA was made based on the association of digital clubbing, periostosis of the tubular bones, and seronegative arthritis. Given the negativity of the AFS smear microscopy and the presence of an apical pulmonary cavity in the right lung, in our epidemiological context of tuberculosis, the diagnosis of SNPT was presumed. Indeed, our patient was treated with broad-spectrum antibiotics for 15 days but without clinical improvement. The second series of 3 AFS smear microscopy in sputum samples was done but returned negative. Finally, the diagnosis retained was the association of HOA and SNPT.
He was treated with antitubercular therapy for six months according to the national program for the fight against tuberculosis (isoniazid, rifampin, ethambutol, and pyrazinamide for two months (intensive phase), followed by isoniazid and rifampin for four months (continuation phase)).
HOA symptoms had remitted after three months of treatment. Chest CT performed two months after stopping treatment showed regression of the lung cavity (Figure 2(b)). Bone scintigraphy performed six months later showed improvement in scintigraphic abnormalities (Figure 3(b)).
Furthermore, the patient did not present any adverse and unanticipated events during the treatment period.