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Too little, too late: measles epidemic in South Africa
Correspondence
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Too little, too late: measles epidemic in South Africa
Submissions should be made via our electronic submission system at http://ees.elsevier.com/ thelancet/
160
Mid-April saw the beginning of a 2-week South African mass measles vaccination campaign in response to an ever-growing epidemic. In late 2009, a stepped increase in measles cases was noted in Gauteng Province and, despite a provincial vaccination campaign in October, 2009, the National Institute of Communicable Diseases reported 12 277 cases countrywide by April 28, 2010.1 In 2002, a hospital-based study in the provinces of Gauteng and the Western Cape noted a 96% decrease in admitted cases and a 100% decline in deaths after a catch-up measles vaccination campaign in 1996–97.2 Routine immunisation programmes do not seem to have sustained these levels subsequently. Last year’s Lancet Series on the status of South African health care after 15 years of democracy failed to stress the importance of routine immunisation programmes and coverage as surrogate markers of the health-care delivery system.3 The current measles rates should be a clear indicator to health-care workers that there is no room for complacency. The outbreak was not widely reported in the media. As we await the official evaluation report of the coverage achieved during the two rounds of the campaign (ie, April 12–23 and May 24–28, 2010), anecdotal reports suggest that there was poor uptake on the part of some schools and parents. Clearly there is a need for ongoing promotional campaigns not only in the public sector but also in the private sector, which serves 20% of the population—infectious diseases know no boundaries. Similarly a strategy to encourage regional cross-country cooperation is warranted given the high levels of immigration to the country.4 Supplementary campaigns are by definition a catch-up game and may be too little, too late. Instead, those
of us in the health-care sector need to engage in crucial discussions supported by current research evidence to identify the reasons behind this outbreak and to approach the problem from both ends. Although in recent months a stronger leadership has been seen with respect to HIV/ AIDS, we need to see this same approach address our concerns about measles and give South Africa a chance to achieve elimination status. We declare that we have no conflicts of interest.
*Nandi Siegfried, Charles S Wiysonge, David Pienaar [email protected] South African Cochrane Centre, Medical Research Council, PO Box 19070, Tygerberg 7505, South Africa (NS); University of Cape Town, Cape Town, South Africa (CSW); and Western Cape Department of Health, Cape Town, South Africa (DP) 1
2
3
4
National Institute of Communicable Diseases. Measles outbreak. http://www.nicd.ac.za (accessed April 28, 2010). Uzicanin A, Eggers R, Webb E, et al. Impact of the 1996-1997 supplementary measles vaccination campaigns in South Africa. Int J Epidemiol 2002; 31: 968–76. Chopra M, Lawn JE, Sanders D, et al, for The Lancet South Africa team. Achieving the health Millennium Development Goals for South Africa: challenges and priorities. Lancet 2009; 374: 1023–31. Wiysonge CS, Nomo E, Mawo JN, Ticha JM. Accelerated measles control in sub-Saharan Africa. Lancet 2006; 367: 394–95.
Vitamin deficiency and renal cortical necrosis Lesley Archer and colleagues (Feb 20, p 696)1 report the case of a 17-yearold girl with renal cortical thrombosis associated with severe hyperhomocysteinaemia. The patient was described as having eating disorders and not consuming fruit and vegetables. On the basis of serum vitamin concentrations, Archer and colleagues argue that hyperhomocysteinaemia was caused by vitamin B12 deficiency, and after 6 weeks’ vitamin supplementation they obtained a significant decrease in and final normalisation of homocysteinaemia. The Case Report is
very interesting and instructive; however, we would like to raise some points. On the basis of dietary habits, use of oestroprogestinic therapy, and serum vitamin concentrations (vitamin B12 723 nmol/L, folate 4·53 nmol/L), we suggest a folate rather than B12 deficiency, the reference values used in our and many other laboratories being 164–835 pmol/L and 7–28 nmol/L, respectively. We recommend obtaining measurements of holotrascobalamin (the active form of vitamin B12) and red-blood-cell folate (storage of the vitamin) concentrations for a complete assessment of vitamin status.2,3 The efficacy of vitamin supplementation was remarkable, but Archer and colleagues did not specify contents and doses of the supplementation. To our knowledge, this is the first paper reporting such a significant reduction in homocysteinaemia after only 6 weeks’ treatment.4 How much do Archer and colleagues think peritoneal dialysis contributed to the normalisation of homocysteine concentrations? We declare that we have no conflicts of interest.
*Cristina Novembrino, Rachele De Giuseppe, Federica de Liso, Paola Bonara, Fabrizia Bamonti [email protected] Dipartimento Scienze Mediche, Università degli Studi di Milano, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy (CN, RDG, FdL, FB); and Dipartimento di Medicina Interna, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy (PB) 1
2
3
4
Archer L, Kilburn-Toppin F, Sneddon K, et al. A “fussy eater” with renal failure. Lancet 2010; 375: 696. Green R. Indicators for assessing folate and vitamin B12 status and for monitoring the efficacy of intervention strategies. Food Nutr Bull 2008; 29: S52. De Vecchi AF, Bamonti-Catena F, Finazzi S, et al. Homocysteine, vitamin B12, serum and erythrocyte folate in peritoneal dialysis patients. Clin Nephrol 2001; 55: 313. Clarke R, Armitage J. Vitamin supplements and cardiovascular risk: review of the randomized trials of homocysteine-lowering vitamin supplements. Semin Thromb Hemost 2000; 26: 341.
www.thelancet.com Vol 376 July 17, 2010
AFP/Getty Images
Too little, too late: measles epidemic in South Africa
Submissions should be made via our electronic submission system at http://ees.elsevier.com/ thelancet/
160
Mid-April saw the beginning of a 2-week South African mass measles vaccination campaign in response to an ever-growing epidemic. In late 2009, a stepped increase in measles cases was noted in Gauteng Province and, despite a provincial vaccination campaign in October, 2009, the National Institute of Communicable Diseases reported 12 277 cases countrywide by April 28, 2010.1 In 2002, a hospital-based study in the provinces of Gauteng and the Western Cape noted a 96% decrease in admitted cases and a 100% decline in deaths after a catch-up measles vaccination campaign in 1996–97.2 Routine immunisation programmes do not seem to have sustained these levels subsequently. Last year’s Lancet Series on the status of South African health care after 15 years of democracy failed to stress the importance of routine immunisation programmes and coverage as surrogate markers of the health-care delivery system.3 The current measles rates should be a clear indicator to health-care workers that there is no room for complacency. The outbreak was not widely reported in the media. As we await the official evaluation report of the coverage achieved during the two rounds of the campaign (ie, April 12–23 and May 24–28, 2010), anecdotal reports suggest that there was poor uptake on the part of some schools and parents. Clearly there is a need for ongoing promotional campaigns not only in the public sector but also in the private sector, which serves 20% of the population—infectious diseases know no boundaries. Similarly a strategy to encourage regional cross-country cooperation is warranted given the high levels of immigration to the country.4 Supplementary campaigns are by definition a catch-up game and may be too little, too late. Instead, those
of us in the health-care sector need to engage in crucial discussions supported by current research evidence to identify the reasons behind this outbreak and to approach the problem from both ends. Although in recent months a stronger leadership has been seen with respect to HIV/ AIDS, we need to see this same approach address our concerns about measles and give South Africa a chance to achieve elimination status. We declare that we have no conflicts of interest.
*Nandi Siegfried, Charles S Wiysonge, David Pienaar [email protected] South African Cochrane Centre, Medical Research Council, PO Box 19070, Tygerberg 7505, South Africa (NS); University of Cape Town, Cape Town, South Africa (CSW); and Western Cape Department of Health, Cape Town, South Africa (DP) 1
2
3
4
National Institute of Communicable Diseases. Measles outbreak. http://www.nicd.ac.za (accessed April 28, 2010). Uzicanin A, Eggers R, Webb E, et al. Impact of the 1996-1997 supplementary measles vaccination campaigns in South Africa. Int J Epidemiol 2002; 31: 968–76. Chopra M, Lawn JE, Sanders D, et al, for The Lancet South Africa team. Achieving the health Millennium Development Goals for South Africa: challenges and priorities. Lancet 2009; 374: 1023–31. Wiysonge CS, Nomo E, Mawo JN, Ticha JM. Accelerated measles control in sub-Saharan Africa. Lancet 2006; 367: 394–95.
Vitamin deficiency and renal cortical necrosis Lesley Archer and colleagues (Feb 20, p 696)1 report the case of a 17-yearold girl with renal cortical thrombosis associated with severe hyperhomocysteinaemia. The patient was described as having eating disorders and not consuming fruit and vegetables. On the basis of serum vitamin concentrations, Archer and colleagues argue that hyperhomocysteinaemia was caused by vitamin B12 deficiency, and after 6 weeks’ vitamin supplementation they obtained a significant decrease in and final normalisation of homocysteinaemia. The Case Report is
very interesting and instructive; however, we would like to raise some points. On the basis of dietary habits, use of oestroprogestinic therapy, and serum vitamin concentrations (vitamin B12 723 nmol/L, folate 4·53 nmol/L), we suggest a folate rather than B12 deficiency, the reference values used in our and many other laboratories being 164–835 pmol/L and 7–28 nmol/L, respectively. We recommend obtaining measurements of holotrascobalamin (the active form of vitamin B12) and red-blood-cell folate (storage of the vitamin) concentrations for a complete assessment of vitamin status.2,3 The efficacy of vitamin supplementation was remarkable, but Archer and colleagues did not specify contents and doses of the supplementation. To our knowledge, this is the first paper reporting such a significant reduction in homocysteinaemia after only 6 weeks’ treatment.4 How much do Archer and colleagues think peritoneal dialysis contributed to the normalisation of homocysteine concentrations? We declare that we have no conflicts of interest.
*Cristina Novembrino, Rachele De Giuseppe, Federica de Liso, Paola Bonara, Fabrizia Bamonti [email protected] Dipartimento Scienze Mediche, Università degli Studi di Milano, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy (CN, RDG, FdL, FB); and Dipartimento di Medicina Interna, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy (PB) 1
2
3
4
Archer L, Kilburn-Toppin F, Sneddon K, et al. A “fussy eater” with renal failure. Lancet 2010; 375: 696. Green R. Indicators for assessing folate and vitamin B12 status and for monitoring the efficacy of intervention strategies. Food Nutr Bull 2008; 29: S52. De Vecchi AF, Bamonti-Catena F, Finazzi S, et al. Homocysteine, vitamin B12, serum and erythrocyte folate in peritoneal dialysis patients. Clin Nephrol 2001; 55: 313. Clarke R, Armitage J. Vitamin supplements and cardiovascular risk: review of the randomized trials of homocysteine-lowering vitamin supplements. Semin Thromb Hemost 2000; 26: 341.
www.thelancet.com Vol 376 July 17, 2010