Background and AimUlcerative colitis (UC) patients have several extraintestinal and systemic manifestations. As studies on the frequency and predictors of pulmonary involvement in patients with UC are inconsistent, we undertook this prospective study.MethodsEighty‐seven patients with UC (in remission 49, 56.3%, active disease 38, 43.6%, median age: 40 years, range: 16–66, 55, 62.2% males) and 50 healthy controls (median age: 38 years, range: 14–69, 34, 68% males) underwent pulmonary function tests (PFTs) including forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), Tiffeneau value (FEV1/FVC), mid‐expiratory flow rate, and diffusion lung capacity for carbon monoxide with spirometer.ResultsSubjects with UC and control were comparable in age and gender. PFT was abnormal in 24 (27.5%) patients (active disease 15/38, 39.4%, remission 9/49, 18.4%) and 1 (2%) control (P < 0.005). Of the 24 patients with abnormal PFT, small airway, restrictive, and obstructive defects were detected in 12 (50%), 11 (45.8%), and 1 (4.2%) patients, respectively. Patients with abnormal PFT more often had active disease (15/24, 62.5% vs 23/63, 36.5%; P = 0.03). No relation of PFT abnormalities was found with age, sex, duration of disease, body mass index, serum albumin, and hemoglobin levels, and other extraintestinal manifestation (arthritis/arthralgia) and drugs used to treat UC.ConclusionUC patients with active disease have abnormal pulmonary functions with predominant involvement of small airways. Active UC was more often associated with abnormal PFT than the disease in remission.

Aim: Cirrhosis with portal hypertension (PHT) may be associated with increased small intestinal permeability (SIP), predisposing to malnutrition and bacterial translocation causing septicaemia, endotoxaemia and spontaneous bacterial peritonitis. However, data on SIP in extrahepatic portal venous obstruction (EHPVO), in which PHT occurs without hepatic dysfunction, are scanty. Such studies would help to know the effect of PHT on SIP independent of hepatic dysfunction; hence, we undertook this study.Methods: A total of 96 patients with PHT (cirrhosis 71, EHPVO 25) underwent evaluation of SIP using urinary lactulose/mannitol excretion ratio over 6 hours after oral administration of 15 mL (10 g) lactulose and 5 g mannitol using 1H-NMR spectroscopy by a method described by us previously.Results: Gender of patients with EHPVO and cirrhosis was comparable but patients with EHPVO were younger in age. The causes of cirrhosis were cryptogenic (n=22), alcohol (n=20), post-viral (n=21) and others (n=8). Twenty-seven (38%) patients with cirrhosis had ascites. Abnormal SIP was detected in 47 (49%) patients (40/71, 56% with cirrhosis vs. 7/25, 28% with EHPVO, p=0.01). Patients with cirrhosis had a higher urinary lactulose/mannitol excretion ratio than those with EHPVO (0.09, range 0-0.87 mmol vs. 0.05, 0-0.19 mmol; p=0.008). Patients with abnormal SIP had a higher Child score, and more often had cirrhosis than EHPVO, ascites and deranged liver function. On multivariate analysis, presence of cirrhosis, ascites, high serum bilirubin level and prothrombin time were associated with abnormal SIP. Conclusions: Cirrhosis was associated with abnormal SIP, which was related to liver dysfunction. However, SIP was normal in patients with EHPVO.

Aim: Cirrhosis with portal hypertension (PHT) may be associated with increased small intestinal permeability (SIP), predisposing to malnutrition and bacterial translocation causing septicaemia, endotoxaemia and spontaneous bacterial peritonitis. However, data on SIP in extrahepatic portal venous obstruction (EHPVO), in which PHT occurs without hepatic dysfunction, are scanty. Such studies would help to know the effect of PHT on SIP independent of hepatic dysfunction; hence, we undertook this study. Methods: A total of 96 patients with PHT (cirrhosis 71, EHPVO 25) underwent evaluation of SIP using urinary lactulose/mannitol excretion ratio over 6 hours after oral administration of 15 mL (10 g) lactulose and 5 g mannitol using 1H-NMR spectroscopy by a method described by us previously. Results: Gender of patients with EHPVO and cirrhosis was comparable but patients with EHPVO were younger in age. The causes of cirrhosis were cryptogenic (n=22), alcohol (n=20), post-viral (n=21) and others (n=8). Twenty-seven (38%) patients with cirrhosis had ascites. Abnormal SIP was detected in 47 (49%) patients (40/71, 56% with cirrhosis vs. 7/25, 28% with EHPVO, p=0.01). Patients with cirrhosis had a higher urinary lactulose/mannitol excretion ratio than those with EHPVO (0.09, range 0-0.87 mmol vs. 0.05, 0-0.19 mmol; p=0.008). Patients with abnormal SIP had a higher Child score, and more often had cirrhosis than EHPVO, ascites and deranged liver function. On multivariate analysis, presence of cirrhosis, ascites, high serum bilirubin level and prothrombin time were associated with abnormal SIP. Conclusions: Cirrhosis was associated with abnormal SIP, which was related to liver dysfunction. However, SIP was normal in patients with EHPVO.

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