ObjectivesTo examine trends in asthma hospitalisation and mortality rates from 2000 to 2014 in Kuwait according to sex, age and nationality.MethodsFor this nationwide, retrospective observational study, data from hospital discharge records and death certificates listing asthma as the primary reason for hospitalisation or mortality were obtained from the National Center for Health Information database using International Classification of Diseases, Tenth Revision codes J45 and J46. Trends in sex-adjusted, age-adjusted and nationality-adjusted hospitalisation and mortality rates were examined. Poisson regression models were applied to test for linear trends overtime and estimate adjusted rate ratios and 95% CI.ResultsDuring the 15-year study period, a total of 43 652 hospitalisations and 484 deaths due to asthma exacerbations were identified. The average annual adjusted rates of asthma hospitalisation and mortality were estimated to be 134.9 (95% CI 131.8 to 138.1) and 2.1 (95% CI 1.8 to 2.4) per 100 000 population, respectively. Hospitalisation rates decreased by 49.5% in the total population (from 180.8 to 91.3 admissions per 100 000 population between 2000 and 2014, ptrend <0.001) and by 57.9% in the age group of 5–44 years (from 77.3 to 32.5 admissions per 100 000 population, ptrend <0.001). Mortality rates decreased from 4.1 to 0.9 deaths per 100 000 population between 2000 and 2014 in the total population (77.6% decrease, ptrend <0.001) and from 0.6 to 0.2 deaths per 100 000 population among those aged 5–44 years (61.9% reduction, ptrend=0.005). Kuwaiti compared with non-Kuwaiti subjects had higher risk of asthma hospitalisation and mortality. Among children aged ≤19 years, the risk of hospitalisation was higher in boys compared with girls; however, among adults, women experienced more hospitalisations than men.ConclusionsAsthma hospitalisation and mortality rates have substantially decreased between 2000 and 2014 in Kuwait, with persisting differences between genders, age groups and citizens versus non-citizens. The observed decreasing trends in Kuwait are in agreement with global trends.
In recent years, several defined antigens of Mycobacterium tuberculosis have become available either by purifying the natural antigens using biochemical procedures, or by producing large quantities of recombinant antigens, using recombinant DNA technology. In this study, we evaluated these defined antigens of M. tuberculosis, along with the complex antigens, for humoral immune responses in an IgG-specific enzyme-linked immunosorbent assay (ELISA). We hoped to develop a tuberculosis-specific ELISA of diagnostic potential. Our results show that IgG antibodies to the complex antigens (i.e. culture filtrate, cell wall and sonicate) and to some of the defined antigens (i.e. 38-kD antigen and lipoarabinomannan) of M. tuberculosis were significantly elevated in the sera of tuberculous patients, as compared to healthy contacts of tuberculous patients and patients suffering from nonmycobacterial infections. Among the IgG subclasses, IgG2 antibody reactive with culture filtrate, cell wall, and lipoarabinomannan antigens was elevated in the sera of most tuberculous patients. Since the complex antigens are difficult to standardize, and batch-to-batch variations may occur with respect to the amount of active components in different batches, the use of defined antigens of M. tuberculosis in ELISA may be a better alternative in the early and specific diagnosis of tuberculosis.
Two cases of primary pulmonary tuberculosis presenting as mass densities and simulating neoplasms in children are reported. This manifestation has not been previously reported in children. It probably represents an unusual immunological response to the mycobacterium.
The relationship between zinc treatment and interleukin-1 alpha (IL-1 alpha) production by cultured alveolar macrophages (AM) in patients with pulmonary tuberculosis and bacterial pneumonia was investigated. AM (1 x 10(6) cells/ml) from 6 patients with pulmonary tuberculosis, 7 patients with bacterial pneumonia and 4 healthy volunteers were cultured with either two different concentrations of zinc chloride (Znl = 1 microgram/ml and Zn2 = 5 micrograms/ml) or cell culture media alone (control) for an initial period of 6 hours and then stimulated with 3 different immunomodulator agents and reincubated for a further 24 h. IL-1 alpha in culture supernatants was measured by enzyme-linked immunosorbent assay (ELISA). In the absence of Znl or Zn2 Polyinosinic:Polycytidylic acid (Poly I:C 1 microgram/ml), Lipopolysaccharide (LPS 100 ng/ml) and Tumour necrosis factor-alpha (TNF-alpha 10 ng/ml) significantly increased the production of IL-1 alpha from AM in both patients and healthy subjects (p < 0.001) compared to control (media only). Zn1 and Zn2 significantly increased the production of IL-1 alpha (p < 0.001) in culture supernatants in the absence of either Poly I:C, LPS or TNF-alpha in patients but not in healthy group. In contrast, the presence of LPS or TNF-alpha significantly reduced Zn1 or Zn2-stimulated release of IL-1 alpha from AM in patients and healthy subjects (p < 0.01). However, Poly I:C decreased only Zn1-stimulated release of IL-1 alpha. These results suggest that zinc can regulate the production of IL-1 alpha from AM in patients with pulmonary tuberculosis or bacterial pneumonia.
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