How well do health programmes reach the poor?

How well do health programmes reach the poor?

COMMENTARY COMMENTARY How well do health programmes reach the poor? See page 561 Published online Feb 4, 2003 http://image.thelancet.com/extras/02cm...

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COMMENTARY

COMMENTARY

How well do health programmes reach the poor? See page 561 Published online Feb 4, 2003 http://image.thelancet.com/extras/02cmt344web.pdf

The study by Joanna Schellenberg and colleagues on inequities among Tanzania’s poor appearing in today’s Lancet is of interest not only in itself, but also as an illustration of a technique now available to examine socioeconomic disparities in health conditions and service delivery. Among other things, the technique makes it easier than before to determine how well health programmes are reaching the poor. The technique, known as programme-incidence or coverage-inequality analysis, is the equity analogue to the well-known cost-effectiveness analysis for measuring the efficiency of a health programme. That is, while costeffectiveness analysis examines the amount of programme output per unit of input, programme-incidence analysis is used to determine the distribution of programme outputs across socioeconomic groups within the population that the programmes serve. The principal elements of programme-incidence, coverage-inequality, and related techniques have been laid out elsewhere.1 The techniques usually rely on survey data about the household’s socioeconomic status and whether household members have been reached by a particular service programme (eg, have attended a programme clinic session, have taken a drug or received an injection offered by the programme). The households are divided into groups (typically quintiles) by socioeconomic status, the frequency of programme service use is tabulated for each group, and the intergroup differences are assessed by any of several statistical disparity measures. By substituting health status for use of a health programme, the same approach can be used to measure disparities in health conditions or disease prevalence. Whilst this procedure is conceptually straightforward, its application has until recently not been practical because of difficulties in measuring socioeconomic status. Reliable information about income or consumption, the most widely used socioeconomic indicators, has required far more time and specialised expertise than that available to organisers of field surveys dealing with complicated health issues that themselves often present significant challenges in measurement. But this situation has begun to change, because of a shift toward use of wealth rather than income or consumption to indicate socioeconomic status. The change has been made possible by several recent studies showing that a wealth index based on data about household assets, attributes, and possessions yields results similar to those produced with income or consumption information.2–5 The asset questions involved (eg, source of 540

water, type of roofing, possession of bicycles, radios, and cooking utensils) typically require no more than 4–5 min to administer and generally produce credible responses. While many important issues remain to be resolved (eg, which items should be included in an index, and how they should be weighted in the index’s construction), use of wealth to measure socioeconomic status is becoming increasingly accepted; and it is what makes possible studies like today’s Lancet piece. What Schellenberg and colleagues did was to include a few common sense household-asset questions in their survey instrument, use the responses to these and other questions to construct a socioeconomic index, and then tabulate the findings on health status and service use by socioeconomic quintile. This straightforward technique produced findings that are far from intuitive: that there are significant socioeconomic differences in an apparently homogeneously poor rural area, for example, and that the main difference between the more and less poor in health is not in the likelihood of being ill but in the access to adequate treatment once ill. Such findings constitute significant additions to a small but rapidly growing body of knowledge produced by other wealth-based studies yielding similar results. For example, a recent wealth-based investigation of fever in 22 malarious African countries also shows an only modestly higher rate of illness among the more poor than the less poor, but a much smaller likelihood of obtaining suitable treatment.6 A study of over 40 countries reports that even those interventions generally thought to be especially “pro-poor”, such as oral rehydration therapy and immunisation, tend to attain better coverage among better-off groups than among disadvantaged ones.7 Data from the same study show even larger coverage inequalities for other services, such as attended deliveries, that are particularly important for the poor.8 These and other findings make it clear that efforts to serve disadvantaged population groups are not reaching their intended beneficiaries nearly so well as their sponsors often believe. This lack is a result of obvious importance for initiatives aspiring to serve the poor, like the Global Fund for AIDS, Tuberculosis and Malaria and the drive to achieve Millennium Development Goals for health. The lack also suggests that without more serious efforts to reach the poor than have marked past efforts, most benefits from such initiatives could well accrue to better-off groups. The developments described above also make it practical for epidemiological and health-service researchers to consider adding a distributional dimension to their investigations. Many investigators will find that their previously collected datasets already contain adequate information on assets and are sufficiently large THE LANCET • Vol 361 • February 15, 2003 • www.thelancet.com

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COMMENTARY

to support an analysis like that of Schellenberg and colleagues. If not, researchers will often be able to collect rather easily the necessary asset information and undertake such analyses in future investigations. When such is the case, they will be in a position to contribute significantly toward a determination of what health problems are of greatest importance for the poor, and which programmes are most effective in reaching the poor. DRG is expressing personal views not those of his employers.

Davidson R Gwatkin World Bank, Washington, DC 20433, USA (e-mail: [email protected]) 1

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Reading list for incidence analysis. Determining who benefits from health, nutrition, population programs and policies: an introduction to the professional literature on program incidence analysis and related techniques. http://www.worldbank.org/poverty/health/library/ incidence.htm (accessed Dec 19, 2002). Filmer D, Pritchett LH. Estimating wealth effects without expenditure data—or tears; an application to educational enrollments in states of India. Demography 2001; 38: 115–32. Morris SS, Carketti C, Hoddinott J, Christiaensen LJM. Validity of rapid estimates of household wealth and income for health surveys in rural Africa. J Epidemiol Community Health 2000; 54: 381–87. Rutstein S. Wealth vs expenditure: comparison between DHS wealth index and household expenditures in four departments of Guatemala. Paper presented at meeting on Health inequities: challenges for the future. The new research and policy agenda, Puyuhuapi, Chile, October, 1999. Sahn DE, Stifel D. Exploring alternative measures of welfare in the absence of expenditure data. Cornell Food and Nutrition Policy working paper no 97, October, 2001: http://www.people.cornell.edu/ pages/des16/sahn/wp97.pdf (accessed Dec 19, 2002). Filmer D. Fever and its treatment among the more and less poor in Sub-Saharan Africa. World Bank Development Economics Research Group working paper 2789, March, 2002: http://econ.worldbank.org /view.php?type=5&id=13157 (accessed Dec 19, 2002). Gwatkin DR. The need for equity-oriented health reforms. Int J Epidemiol 2001; 30: 720–23. Gwatkin DR. The poor come last: socio-economic inequalities in the use of maternal and child health services in developing countries. Paper presented at meeting of Fogarty International Center, National Institutes of Health, Bethesda, MD, July, 2002.

Treatment options for genetically determined immunodeficiency See page 553 Soon after the discovery of HLA in 1967, life-saving treatment in the form of allogeneic bone-marrow transplantation became available for patients with fatal primary immunodeficiency syndromes.1,2 However, the applicability of this treatment was severely limited by whether or not there was an HLA-matched normal sibling donor.3 Without such, these transplantations most often resulted in fatal graft-versus-host disease (GVHD). If death did not occur, event-free survival was adversely affected by several factors, including: older age of the recipient at transplantation, pre-existing or nosocomially acquired infections, pretransplant chemotherapy, immunosuppressive drugs used to prevent GVHD, chronic GVHD, and the underlying genetic defect. In this issue of The Lancet, Corinne Antoine and colleagues review the experience of members of the European Group for Blood and Marrow Transplantation and the European Society for Immunodeficiency with allogeneic haemopoietic stem-cell transplantation during 1968–99. This analysis shows steady improvement in survival that correlates with the time period in which the transplantation was done. The improvement in survival over time is attributed to more effective prevention and THE LANCET • Vol 361 • February 15, 2003 • www.thelancet.com

treatment of infections and GVHD. Unquestionably, the most important discovery occurred in the early 1980s when findings from rodent studies in the late 1970s, that removal of post-thymic T cells from the donor marrow would prevent GVHD, were successfully applied to human infants with severe combined immunodeficiency syndrome (SCID).4 This success allowed use of a parent as a donor and virtually assured that every infant with SCID would have a related stem-cell donor. For non-SCID primary immunodeficiencies, experience to date has proved that stem-cell transplantation can also provide a cure for many of these defects, but only after those with such an immunodeficiency undergo chemoablation. The data of Antoine and colleagues suggest that, in these types of patients, HLA grafts that are carefully matched from unrelated donors are almost as beneficial as those from genetically HLA-identical relatives. Since infants with SCID cannot reject a graft because they do not have T cells, it is not necessary to give pretransplant chemoablation for the bone-marrow transplant to be accepted. Nevertheless, because B-cell function does not develop in more than half these infants, some centres have chosen to use chemoablation before transplantation in an effort to engraft donor B cells. However, this approach does not guarantee that B cells will be reconstituted,5 and survival rates have been as low as 46% when chemoablation is used.6,7 The highest survival rate (97%) was in infants transplanted soon after birth with T-cell-depleted haploidentical (half-matched) parental marrow without pretransplant chemoablation or posttransplant GVHD prophylaxis.8,9 There are over 1200 patients if we combine those with primary immunodeficiency diseases given allogeneic haemopoietic stem-cell transplantation in Antoine’s series with the number in a 1996 survey of US centres of immunodeficiency patients who had received such transplants.10 Whilst allogeneic haemopoietic stem-cell transplantation has been life-saving, it is not perfect. Many of these patients have residual GVHD as well as immune defects, including impaired or absent antibody production and impaired function of natural killer cells in some molecular types of SCID. More worrisome is the fact that, in some of these patients, T-cell function diminishes with time despite early evidence of good immune reconstitution—the reason is unknown. As new information emerged about the molecular causes of many of these syndromes, optimism arose that gene therapy would eventually replace bone-marrow transplantation as a more effective and safer form of therapy. Within the past 3 years, the group at Hôpital Necker in Paris headed by Alain Fischer has treated 11 patients with SCIDX1 with gene-corrected autologous bone-marrow cells, and all 11 survive.11,12 Nine infants developed normal T-cell and B-cell function after the treatments; two did not and were given allogeneic bone-marrow transplants. The nine who did develop normal immune function did not require intravenous immunoglobulin infusions and were at home off all medications. Thus the effectiveness of gene therapy in conferring immune function in those infants with SCID-X1 seemed to be far superior to that of allogeneic haematopoietic stem-cell transplantation. Tragically, however, serious adverse events have occurred in the fourth and fifth patients treated by the French group. Both children developed leukaemia-like processes, with expanded clonal populations of T cells. The clones carry the inserted ␥c cDNA, and the leukaemias are considered to have been induced by the retroviral gene therapy by a process called insertional mutagenesis. The positions of insertion in both children are in or near a gene on chromosome 11 called 541

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