Hodgkin’s lymphoma is characterized by an increase in circulation cytokines, which are known to be able to induce nitric oxide (NO) production. Exhaled nitric oxide (FENO) has been proposed as an inflammatory marker of the airways, and it has also been shown to be increased in lung cancer (1). So far no reports have used exhaled NO to follow the progress of cancer during treatment. The authors followed-up a patient with Hodgkin’s disease with extended NO analysis of the exhaled breath. The patient’s alveolar NO fraction was 9 ppb NO before diagnosis, which decreased to 7 ppb NO after four treatment periods, and after eight periods the fraction was 3 ppb NO. We conclude that extended NO analysis is a simple noninvasive tool to follow-up an inflammatory process in the human body, as well as following treatment during disease. Case report. A 27-year-old female with epilepsy and atopic dermatitis complained of coughing and shortness of breath. She had no history of airway atopy or asthma-like symptoms. She was referred to the lung clinic where the diagnosis of asthma was excluded. However, the exhaled NO levels were extremely high. Exhaled NO was measured with a chemiluminescence analyser (Sievers NOA 280, Sievers, Boulder, CO, USA) and a flow sensor, (D-lite TM , Datex-Ohmeda, Helsinki, Finland) was used to measure NO at different expiratory flow rates. Following the ATS guideline for NO measurement (2), it was seen that patient had more then tenfold increase in exhaled NO. Using an extended NO analysis (3) revealed high alveolar fraction (FANO), as well as an increase in airway wall fraction (FwNO) and airway wall diffusion rate of NO (DwNO), see Table 1. During a four-month period she developed fever, night sweats, and weight loss (BMI 24). Her symptoms became aggravated and she developed a vena cava superior compression with an oedema of upper thorax, head and neck. She had lymph node enlargement in the neck and axillae. Chest x-ray showed a large mediastinal mass. Laboratory analysis revealed elevated LDH, C-reactive protein and peripheral Blymphocytes. Fine-needle aspiration and lymph node biopsy showed a Hodgkin’s disease of mixed cellularity. The disease was classified as stage II by staging with CT-scan and bone marrow biopsy. She received treatment with eight courses of baseline BEACOPP, i.e. Bleomycin 10 mg/m 2 day 8, Etoposide 100 mg/m 2 day 1 � /3, Doxorubicin 25 mg/m 2 day 1, Cyclophosphamide 650 mg/ m 2 day 1, Vincristine 1.4 mg/m 2 (max 2 mg) day 8, Procarbazine 100 mg/m 2 day 1 � /7 and Prednisone 40 mg/m 2 day 1 � /14 (4). When she had finished four out of eight treatment periods the exhaled NO, CRP and B-lymphocytes had decreased. The CT scan showed shrinkage of the lymphoma mass. The patient developed severe haematological toxicity after every
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