CF, a 26-years-old man of North African origin, was hospitalized for persistent cough on July 2003. Chest x-ray showed at this moment bilateral hilar adenopathy and tenuous infiltration of the upper right lobe. HRTC showed multiple irregular parenchymal opacities of alveolar interstitial type at the upper lobes and bilateral hilar enlargement.
Diagnosis of pulmonary TB was made after bronchoscopy on July 2003, for positivity of M. tuberculosis DNA and RNA in bronchoalveolar lavage fluid. Culture of sputum and BAL fluid were negative. Tuberculin skin test was negative. Anti TB therapy was started on July and continued for six months until January 2004.
HIV infection had been diagnosed just one month before this hospitalization, on June 2003, with a CD4+ count of 371/mmc (19.6%), HIVRNA 139,000 cp/ml (wild type) and HCV coinfection (HCV type 1a). Antiretroviral therapy with (azt + 3tc) + nvp was also started on June 2003. During the first year he attained a good viro-immunological response, but later he became less compliant, and on November 2004 he was lost to follow up.
On April 2006 he was readmitted at day service during a period of jail detention: CD4+ were 374/mmc (26%), HIV viremia was 3055 cp/ml and HCV RNA titre was 3,097,802 cp/ml. ART therapy was switched to tdf + 3tc + lpv/r. Chest x-ray showed pulmonary apical bilateral infiltrates without pleural effusion, but the patient was lost to follow up for a second time before doing further investigations.
After two years, on March 2008, he was conducted to the service for consultation: he was in good conditions, but since 2007 he was developing chronic cutaneous maculopapular lesions at the right arm. Adherence to ART therapy was suboptimal and he was highly viremic, with 166,469 cp/ml of HIVRNA on July 2008. Therapy was modified to (tdf + ftc) + lpv/r. During the following year he developed multiple symmetric lymphadenopathies (neck, axillae and groin). Chest x-ray showed: bilateral fibronodular apical-subclavian lesions with hilar enlargement and prominence of the left second cardiac arch. CT-scan revealed mediastinal and intra-abdominal periaortic severe adenopathy (4 cm diameter).
Biopsy of the forearm cutaneous lesions showed granulomatous infiltration of sarcoid type without caseous necrosis. BAAR or fungi were not detected by specific stains of the tissue.
He was hospitalized in another institution for dyspeptic symptoms on October 2009. Total body CT-scan showed enlarged intra-abdominal lymph nodes (max 2.5 cm in diameter), hilar bilateral adenopathy (3 cm in diam.) and apical pulmonary fibrosis with reticulonodular infiltrates of lymphatic origin (galaxy sign). Biopsy of an axillary lymph node showed foci of chronic granulomatous epithelioid inflammation with giant multinucleated cells. No mycobacteria spp, fungi or other parasites were demonstrated by molecular or histological techniques. Bronchoscopy was also performed with BAL and the research of malignant cells and mycobacteria spp was negative (MTB and atypical mycobacteria) by PCR and culture. He was dismissed on November 2009 with the diagnosis of: "Chronic granulomatous lymphadenitis, Chronic Active Hepatitis HCV-related, Duodenitis in patient with HIV infection C3, Opioid addiction undergoing pharmacological therapy".
Afterwards he continued ART therapy with better adherence, but after few months he presented general malaise, weight loss, persistent nausea and anorexia with emesis, increasing groin adenopathy and was newly hospitalized for the clinical suspect of lymphoma. Node biopsy showed: "Chronic granulomatous non necrotising epithelioid gigantocellular lymphadenitis with confluent foci as observed in sarcoidosis". PCR for M. tuberculosis DNA and for atypical mycobacteria from node sections was negative. Culture for M tuberculosis and other mycobacteria was also negative. IGRA test (Quantiferon-TB test) was negative. Functional respiratory tests were also performed: Walking test was normal, Spirometry showed moderate-severe obstructive disease, with reduction of CO diffusion. Salivary glands echography showed parenchymal disomogeneity with ectasic ducta. Eye examination was normal.
Steroid therapy was started on July 2010 with prednisone at the dose of 1 mg/kg/die: after one month lymph nodes were considerably reduced; the patient was gaining weight; he had neither fever nor constitutional symptoms. He continued ART therapy with (azt + 3tc) + lpv/r.
Corticosteroid therapy was continued for 6 months (including one month of voluntary auto-suspension), but on March 2011 AST/ALT values were increased (446/315 mU/ml). Liver biopsy was decided, but the patient was definitely lost to follow up for personal reasons.