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Asbestos-related benign and malignant pleural diseases are endemic in some rural parts of central Turkey because of environmental exposure to asbestos fibres. We report here epidemiological data on 113 patients with diffuse malignant pleural mesothelioma (DMPM) diagnosed in our clinic in Eskişehir, located in central Turkey. Of the 113 patients, 59 were men and 54 women (male:female ratio = 1). Ninety-seven patients (86%) had non-occupational asbestos exposure; all were living in villages. Their mean age was 56 years. As the patients had been exposed to asbestos from birth, the latency period was equivalent to the age of the patients. Twenty-eight patients (29%) had lived in villages their entire lives. The other 69 (71%) had been born in a village but migrated to the city or had given up white-soil usage for various reasons. The mean exposure time was 55 years for those with a long exposure period and 25 years for those with a short exposure period, but there was no significant difference between the age of the disease appearance for both groups (55 and 56 years, respectively). Thus, the latency time of mesothelioma due to environmental exposure to asbestos was longer than that due to occupational exposure, but independent of the length of exposure. Soil samples from 67 villages were analysed, comprising a population of 10,120 villagers. Tremolite and some other types of asbestos were found. In conclusion, DMPM in our region is due to mainly to environmental exposure to asbestos. The risk is substantial as a large proportion of the villagers are exposed. After smoking, asbestos exposure is one of the most serious health hazards in our rural population.

Drugs which antagonize tumor necrosis factor alpha (TNF-alpha) are known to increase the risk of tuberculosis. We aimed to evaluate the risk of tuberculosis in patients treated with anti-TNF-alpha, in Turkey. Two hundred and forty patients receiving anti-TNF-alpha, from December 2005 to December 2007, were included in the study. All participants provided a history and underwent a physical examination, a chest X-ray, and a tuberculin skin test. Isoniazid treatment was initiated in those patients with a latent infection, and they were followed up at 2-month intervals. A Bacillus Calmette-Guerin (BCG) scar was present in 184 patients (77.6%). The mean tuberculin skin test induration of patients on admission was 10.7+/-7.0 mm. Male gender and the presence of a BCG scar were predictors of a higher tuberculin skin test result (P<0.05), while there was no significant effect of age on the tuberculin skin test (P>0.05). Of the 240 subjects, 229 (95.4%) received methotrexate or corticosteroid treatment prior to anti-TNF-alpha therapy. Isoniazid treatment preceded anti-TNF-alpha administration in 185 (77.1%) of the 240 patients. Two patients developed tuberculosis (incidence 833/100,000). There was no correlation between initial and 12-month tuberculin skin test results (P>0.05). Tuberculin skin test conversion was detected in five subjects during the 12-month follow-up; however, none developed active tuberculosis. One patient developed a drug reaction secondary to etanercept, and another demonstrated hepatotoxicity due to isoniazid. This study shows that anti-TNF-alpha therapy increases the risk of tuberculosis, despite treatment of latent infection.

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Although Legionnaires' disease (LD) is frequently accompanied by pleural effusion, the characteristics of pleural effusions in LD have not been well studied. Levels of adenosine deaminase (ADA) activity in pleural fluid >40 IU/L have a high sensitivity (81-100%) and specificity (83-100%) for tuberculosis. ADA activity in pleural effusions due to LD has not been previously reported. The case of a patient with LD complicated by a pleural effusion with high ADA activity is reported. In countries where the prevalence of tuberculosis is high and pleural fluid ADA activities are frequently measured, LD should be included in the differential diagnosis of an exudative pleural effusion with high ADA activity.