No association between serum adenosine deaminase activity and disease activity in Crohn's disease.

BACKGROUND: Adenosine deaminase activity is proposed as a marker of inflammation in some inflammatory conditions. AIMS: To investigate the association of serum adenosine deaminase activity and disease activity in Crohn's disease patients. METHODS: In a cross-sectional study, 30 consecutive known cases of Crohn's disease (15 with active disease and 15 in remission) referring to a university hospital in Tehran (Iran) and 15 age- and gender-matched healthy controls were studied. Disease activity was assessed using the Crohn's disease activity index (cutoff >150). Total serum adenosine deaminase activity, C-reactive protein, erythrocyte sedimentation rate, and fecal calprotectin were evaluated in patients. Serum adenosine deaminase activity was measured in controls. RESULTS: Mean age of the patients was 36.8 ± 12.6 years, and 56.7 % were male. Serum adenosine deaminase activity in patients with active disease, patients in remission, and controls was 12.3 ± 5.9, 14.6 ± 6.2, and 11.9 ± 6.4 U/L, respectively (P = 0.458). Compared with patients in remission, those with active disease had higher erythrocyte sedimentation rate (40.4 ± 30.6 vs. 16.9 ± 16.0 mm/h, P = 0.014) and higher frequency of positive C-reactive protein (66.6 vs. 13.3 %, P = 0.004) and positive fecal calprotectin tests (86.6 vs. 33.3 %, P = 0.004). Serum adenosine deaminase activity was not correlated with erythrocyte sedimentation rate (r = 0.05, P = 0.761) and was not different between patients with positive and negative C-reactive protein (12.2 ± 5.4 vs. 14.2 ± 6.5 U/L, P = 0.393) and fecal calprotectin tests (11.7 ± 5.3 vs. 16.0 ± 6.5 U/L, P = 0.063). CONCLUSIONS: In patients with Crohn's disease, serum adenosine deaminase activity is not associated with clinical disease activity or with other inflammation markers and cannot be suggested as an inflammation marker.

Primary chest wall lymphoma with no history of tuberculous pyothorax: diagnosis and treatment.

OBJECTIVE: Primary chest wall neoplasm represents only 5% of chest wall neoplasm and among them primary chest wall lymphoma is uncommon. METHODS: A 28-year-old man had no history of tuberculous pyothorax or artificial pneumothorax therapy but did have a 4-month history of dyspnea, fever, chills, and night sweats. On physical examination, a mass about 10 x 10 cm was noted on the anterior chest wall on the right side, and computed tomographic scan demonstrated that it originated from the pleural wall. A 42-year-old man was admitted with intermittent left hemithoracic pain from about 6 months before his visit. A 5 x 5-cm tender mass in the posterior wall of the left hemithorax was palpated. Computed tomography showed mild plural effusion and erosion in the posterior segment of the left ninth rib. Surgery was performed for histologic diagnosis. RESULTS: With the diagnosis of large B cell lymphoma, chemotherapy was prescribed for the first patient, and the patient has been in complete remission for more than 5 months. For the second patient, the left ninth rib along with the originated mass was completely resected and chemotherapy was prescribed. The patient has been in complete remission for more than 8 months. CONCLUSION: Treatment of primary chest wall lymphoma was not clear and various treatment strategies were considered. Remission of considerable duration in our patients leads us to suggest that surgery followed by adjuvant chemotherapy can provide a reasonable outcome in patients in whom the chest wall lymphoma is the only site of disease.