Tuberculosis and its incidence, special nature, and relationship with chronic obstructive pulmonary disease

Figures & data

Table 1 Key comparisons between tuberculosis and COPD

	Tuberculosis	COPD
Epidemiology	Increasing incidence noted worldwide contributed by epidemic of HIV among other factors; in western world, incidence higher in immigrants originating from high prevalence areas (Dye et al 2006);	Worldwide prevalence in adults ≥40 years estimated at 9–10% (Halbert et al 2006); prevalence increasing due to rise in cigarette smoking (particularly in females) and an increasing elderly in population hence resulting greater susceptibility to loss of lung function
	Predominantly affects young adults	Predominantly affects older adults (usually over 40 years)
Burden: Current and future ranking in disability adjusted life years (DALYs	7th leading cause of DALYs in 1990 projected to remain 7th in 1990 (Murray et al 1997; Michaud et al 2001)	12th leading cause of DALYs in 1999; (Michaud et al 2001); estimated to the 5th leading cause in 2020 (Lopez et al 1998)
Burden: Current and future mortality	Currently 7th leading cause of death worldwide; will remain the 7th leading cause in 2020 (Murray et al 1997)	Currently 5th leading cause of death worldwide; Projected to become the 3rd leading cause of death by 2020 (Murray et al 1997)
Disease susceptibility and inheritance	Evidence of genetic susceptibility with a Mendelian pattern of inheritance (Casanova et al 2002;Alcais et al 2005; Baghdadi et al 2006)	Interaction between host, genetic and environmental factors (McCloskey et al 2001; Pauwels et al 2001)
	Complex interaction between genetic and environmental factors; some evidence that cigarette smoking may alter clinical presentation of TB (Shprykov et al 1994; Leung et al 2003) as well as increasing risk of developing active disease (Maurya et al 2002; Davies et al 2006)	Environmental factors central to disease development eg, cigarette smoke, biomass fuels in developing countries (Pauwels et al 2001)
		Genetic factors eg, alpha-1 anti-trypsin deficiency interact with environmental exposure; familial clustering reported (McCloskey et al 2001)
Pathogenesis	Involvement of matrix metalloproteinase (MMP) system among others resulting in characteristic parenchymal destruction (Hrabec et al 2002; Price et al 2003; Elkington et al 2005; Elkington et al 2006) Sequelae of tuberculosis include development of chronic airflow obstruction and bronchiectasis (Grancher 1878; Jones et al 1950; Bromberg et al 1963; Frame et al 1987; Nicotra et al 1995; Hnizdo et al 2000; Park et al 2001; Palwatwichai et al 2002; Lee et al 2003; Ramos et al 2006; 67–76)	Involvement of matrix metalloproteinase (MMP) system resulting in parenchymal destruction although many other factors involved at this and at the airway level (Braunhut et al 1994; Finlay et al 1997; Frankenberger et al 2001; Imai et al 2001; Mao et al 2003;Vernooy et al 2004; Higashimoto et al 2005)
Treatment	Curable in the majority of cases with appropriate anti-tuberculous chemotherapy; Potential for development of chronic airflow obstruction and bronchiectasis among sequelae	Not curable;To date, only smoking cessation and LTOT shown to influence mortality with LVRS in a selected sequelaesubgroup (Pauwels et al 2001)

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