The aim of this study was to assess the diagnostic yield of the tumour markers carcinoembryonic antigen, carbohydrate antigen 15-3, carbohydrate antigen 19-9 and carbohydrate antigen 125, in serum and bronchoalveolar lavage fluid in a group of patients with bronchogenic carcinoma. Serum and bronchoalveolar lavage fluid samples were collected in a group of 90 patients with benign or malignant pulmonary diseases. After appropriate processing, tumour markers were determined by enzyme immunoassay. The diagnostic yields (sensitivity, specificity and predictive values) in each environment (serum and bronchoalveolar lavage fluid) were obtained by using ''Receivers operating characteristic'' curve. Determined individually, carcinoembryonic antigen, carbohydrate antigen 19-9 and carbohydrate antigen 125, showed the greatest diagnostic accuracy in bronchoalveolar lavage fluid. Carbohydrate antigen 15-3 did so in serum. Carcinoembryonic antigen was the most relevant marker in bronchoalveolar lavage fluid. For the factors evaluated in this study, determination of carcinoembryonic antigen, carbohydrate antigen 19-9 and carbohydrate antigen 125 in bronchoalveolar lavage fluid were clinically more useful markers in comparison with serum, although the latter may also be helpful in certain situations. Although there is no specific tumour marker for lung cancer, the combination of several can be used to diagnose most patients with lung cancer and also to rule out false positive and negative cases.
AimsTo investigate the relationship between HbA1c and glucose in people with co‐existing liver disease and diabetes awaiting transplant, and in those with diabetes but no liver disease.MethodsHbA1c and random plasma glucose data were collected for 125 people with diabetes without liver disease and for 29 people awaiting liver transplant with diabetes and cirrhosis. Cirrhosis was caused by non‐alcoholic fatty liver disease, hepatitis C, alcoholic liver disease, hereditary haemochromatosis, polycystic liver/kidneys, cryptogenic/non‐cirrhotic portal hypertension and α‐1‐antitrypsin‐related disease.ResultsThe median (interquartile range) age of the diabetes with cirrhosis group was 55 (49–63) years compared to 60 (50–71) years (P=0.13) in the group without cirrhosis. In the diabetes with cirrhosis group there were 21 men (72%) compared with 86 men (69%) in the group with diabetes and no cirrhosis (P=0.82). Of the group with diabetes and cirrhosis, 27 people (93%) were of white European ethnicity, two (7%) were South Asian and none was of Afro‐Caribbean/other ethnicity compared with 94 (75%), 16 (13%), 10 (8%)/5 (4%), respectively, in the group with diabetes and no cirrhosis (P=0.20). Median (interquartile range) HbA1c was 41 (32–56) mmol/mol [5.9 (5.1–7.3)%] vs 61 (52–70) mmol/mol [7.7 (6.9–8.6)%] (P<0.001), respectively, in the diabetes with cirrhosis group vs the diabetes without cirrhosis group. The glucose concentrations were 8.4 (7.0–11.2) mmol/l vs 7.3 (5.2–11.5) mmol/l (P=0.17). HbA1c was depressed by 20 mmol/mol (1.8%; P<0.001) in 28 participants with cirrhosis but elevated by 28 mmol/mol (2.6%) in the participant with α‐1‐antitrypsin disorder. Those with cirrhosis and depressed HbA1c had fewer larger erythrocytes, and higher red cell distribution width and reticulocyte count. This was reflected in the positive association of glucose with mean cell volume (r=0.39) and haemoglobin level (r=0.49) and the negative association for HbA1c (r=–0.28 and r=–0.26, respectively) in the diabetes group with cirrhosis.ConclusionHbA1c is not an appropriate test for blood glucose in people with cirrhosis and diabetes awaiting transplant as it reflects altered erythrocyte presentation.
BACKGROUND Chronic Obstructive Pulmonary Disease (COPD) is one of the leading causes of chronic morbidity and mortality. Apart from tobacco smoke, biomass fuel has been implicated as an important etiological factor for development of COPD. Oxidantantioxidant imbalance is known to play a key role in pathophysiology of COPD. The study was undertaken to evaluate the role of oxidative stress and antioxidant status among COPD cases due to tobacco smoking and biomass exposure. METHODS Serum MDA, and erythrocyte SOD and GSH levels, were estimated among 40 COPD cases due to tobacco smoking (Group 1), 20 COPD cases due to biomass exposure (Group 2). 40 age and sex matched healthy controls (Group 0) were also included. Serum MDA, SOD and GSH were measured calorimetrically by TBA method, Marklund & Marklund method and method by Beutler et al respectively. RESULTS IBM SPSS Ver. 20 was used for statistical analysis and preparation of tables. Significantly higher levels of MDA were seen among COPD cases due to tobacco smoke (58.08±52 vs 15.3705±6.6; p value <0.01) compared to controls. SOD levels were significantly lower in both case groups compared to controls (1123.3±301.2, 1147.01±200.5 vs 1315.23±209.1; p value<0.01). GSH levels were lower in tobacco smoking group when compared to biomass exposed group (7.98±2.7 vs 9.61±2.1; p value 0.01). Positive correlation was found between FEV1% and SOD in group 1 cases. CONCLUSIONS The results support the hypothesis of presence of increased oxidative stress and oxidant-antioxidant imbalance in pathogenesis of COPD. It plays an important role in disease severity which is higher among COPD in tobacco smokers compared to biomass exposed COPD.
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