149
for public policy8-eg, it would favour underinvestment in the long-term health for the poor, especially in developing countries which have higher rates of time preference.9 It almost certainly does not reflect the way people want governments to act on their behalf. 3,4 This debate has important policy implications, since reducing the discount rate from 6% to zero can have a dramatic effect on cost-effectiveness rankings and will favour treatments with delayed benefits. For example, the cost effectiveness of surgical treatment of teenage idiopathic scoliosis increases fourteen fold and the use of nicotine gum for male smokers five fold.3 Although technological change and the uncertain effects of long-term programmes need to be taken into account in health care decision-making, the discounting of health benefits should no longer be a thoughtless routine. A range of discount rates including zero should be shown in all economic
appraisals. 1. Drummond M, Stoddart G, Torrance G. Methods of economic evaluation of health care programmes. Oxford: Oxford University Press, 1987. 2. Johannesson M. On the discounting of gained life-years in costeffectiveness analysis. Int J Technol Assess Health Care 1992; 8: 369-64. 3. Parsonage M, Neuburger H. Discounting and health benefits. Health Economics 1992; 1: 71-76. 4. Sheldon TA. Discounting in health care decision making: time for a change? J Public Health Med (in press). 5. West RR. Valuation of life in long run health care programmes. BMJ
1985; 291: 1139-41 6. Cairns J. Discounting and health benefits: another perspective. Health Economics 1992; 1: 76-79. 7. Cohen DR, Henderson JB. Health, prevention and economics. Oxford: Oxford University Press, 1988: 155. 8. Robinson JC. The philosophical origins of the social rate of discount in cost-benefit analysis. Milbank Quart 1990; 68: 245-65. 9. Messing SD. Discounting health: the issue of subsistence and care in an underdeveloped country. Soc Sci Med 1973; 7: 911-16.
What
happened to growth monitoring?
"From birth to age three, children should be weighed every month. If there is no gain in weight for two months, something is wrong." This admonition to monitor child growth is the last of the ten Facts for Life promoted by UNICEF, WHO, and UNESCO to "dramatically improve the health of children in the developing world" by providing families with essential child health information.1 Growth monitoring is primarily an operational communication strategy for growth promotion based on screening of the under-fives, and often targeting those aged 4-36 months. The object is to detect growth falterers rather than those of poor nutritional status in whom growth promotion has already failed.2 "A healthy child gains weight each month" was the widely publicised slogan of Indonesia’s National
Nutrition Programme.33
A 1985 Lancet editorial on growth monitoring4 carried the subtitle "intermediate technology or expensive luxury?", and participants at an
colloquium held in Kenya in May, on for child development, agreed that promotion growth the question is still relevant in 1992.5Growth monitoring conducted at health centres has not yet international
been shown to be cost-effective. The separate contribution of growth monitoring to the effectiveness of child health programmes still needs to be documented in terms of coverage, maternal behaviour changes, child growth, morbidity, and mortality.6,7 The children most at risk are least likely to attend, while health workers seldom receive the level of training, management, or supervision required to deliver correct growth monitoring technology. Too often health workers neglect to involve mothers in the weighing and charting process, and do not explain the result, even if adverse. Moreover, they have neither the time nor the knowledge to individualise the subsequent advice, which is, after all, the raison d’etre of the whole exercise and which might justify the mother’s taking a day away from her subsistence agriculture or market to travel to the clinic, and her long wait for the weighing and again for the
consultation. The primary health care approach, of which growth monitoring should be an integral part, encourages devolvement of health knowledge and skills from health professionals to communities and individuals.
Community-based growth monitoring, arising as a response to the community’s perception of its health problems and their relative importance, seems the best way to evoke community solutions to malnutrition and disease in children,especially if fathers and grandmothers also take part. However, growth monitoring has a long history of advocacy, exhortation, and rhetoric. Operational research is an essential component of any national strategy for community-based schemes, the aim being to identify and strengthen, via training and supervision, weak links in the chain. The starting point is sensitisation and mobilisation of communities for growth monitoring activities; the chain ends with effective interventions identified, explained, and understood by mothers (and communities). The mothers must find the strategy affordable and acceptable; if so, they will be able and willing to implement the proposals. Between these two ends of the chain there are four steps: issue and regular use of growth charts; correct weighing and plotting; distinction between normal growth and poor growth by mothers; and identification and explanation of reasons for poor
growth. 1. UNICEF. Facts of life: a communication challenge. Benson, Oxfordshire: P & LA, 1989. 2. Dixon RA. Monitoring the growth of the world’s children. Ann Trop Paediatr 1991; 11: 3-9. 3. Achadi E, Berman P. Growth monitoring in Indonesia: an assessment of coverage and regularity of attendance, Gedangan Village, Central Java, June 1978-November 1981. Food Nutr Bull, 1988; 1: 56-60. 4. Editorial. Growth monitoring: intermediate technology or expensive luxury? Lancet 1985; ii: 1337-38. 5. Anon. Growth promotion, not growth monitoring. Lancet 1992; 339: 1409.
150
6. Gerein N, Ross DA. Is growth monitoring worthwhile? An evaluation of its use m three child health programmes in Zaire. Soc Sci Med 1991; 32: 667-75. 7. Nabarro D, Chinnock P. Growth monitoring: inappropnate promotion of an appropriate technology. Soc Sci Med 1988; 26: 941-48.
Diagnosis of Sjögren’s syndrome Almost half a century ago Henrik Sjogren, a Swedish ophthalmologist, recorded the association of dry eyes (which he called "keratoconjunctivitis sicca") dry mouth, and rheumatoid arthritis and concluded that this was a specific disease. Gradually the term
Sjogren’s syndrome (SS)
was
adopted,2superseding
sicca syndrome3and Mikulicz syndrome,4which have been used for various expressions of the same condition. Multiorgan involvement, notably of the lungs, kidneys, and skin, emphasises the systemic nature of SS.5 Further refinement in classification came about with the recognition in the past two decades that SS can occur alone (primary SS) or in association with rheumatoid arthritis, systemic lupus erythematosus, and occasionally scleroderma
(secondary SS). Histological changes seen on light microscopy of the salivary glands of patients with primary SS are indistinguishable from those seen in the secondary condition.3 Despite these advances in definition of S S there are no universally accepted diagnostic criteria. This gap in our knowledge, together with the unknown frequency of largely or wholly symptomless SS, has led to difficulties in estimating the prevalence of the condition.9 There are at least four diagnostic "schools"lO-13 All four require the presence of objectively abnormal ocular tests (Schirmer or Rose Bengal staining) and lymphocyte infiltration around labial salivary glands in biopsy specimens. Three require the presence of subjective dryness of the mouth or eyes (commonly described as a gritty sensation) or the demonstration of objective evidence of salivary gland dysfunction (reduced salivary flow or abnormalities on sialography or salivary scintigraphy). However, only one schoopo requires the presence singly or multiply of IgM rheumatoid factor, antinuclear antibodies, anti SS-A [Ro], or anti SS-B [La]14 in the serum, despite the frequent occurrence of these autoantibodies in patients with SS.15,16 Anti-La [SS-B] and anti-Ro are the autoantibodies most specific to SS,1’ although anti-La and (especially) anti-Ro are also found in patients with systemic lupus erythematosus. None of the diagnostic schools adequately grades the symptoms of SS. At first glance it may seem difficult to understand why these broadly similar definitions of SS cannot easily be reconciled. Nevertheless, some of the required tests are invasive and may be refused or may fail,lg and there is variation between the diagnostic schools on scoring methods for the Schirmer test and labial salivary gland biopsy. Faced with the apparent complexity of the diagnostic criteria, the busy clinician may fall into the trap of diagnosing SS by symptoms
alone; this approach inevitably leads to misdiagnosis. Rheumatologists will be familiar with the patient deemed to have SS who, on more thorough assessment, proves to have sarcoidosis, age-associated ocular drying, or drug-induced dry mouth.5.18 In an attempt to lower the diagnostic hurdles, researchers continue to devise easier and more informative tests for busy clinicians. Speight et al 18 found that whole unstimulated salivary flows in patients with SS were lower than in controls; flows of 0-1 ml/min or less were highly specific for dry mouth (xerostomia). Unfortunately, as these researchers point out, this test identifies only xerostomia and not its causes. It is also not for the squeamish; subjects had to "drool or spit" into a beaker for 15 min to provide saliva for measurement. Coll et al,19 using a stepwise approach to the diagnosis of SS, conclude that combined Rose Bengal conjunctival staining and salivary gland scintigraphy will identify most patients with SS; labial salivary gland biopsy can be reserved for dubious cases. Positive results to both Rose Bengal staining and salivary scintigraphy in their study were invariably associated with a positive (grade 3 or 4)20 labial biopsy, Coll’s group acknowledge that labial salivary gland biopsy remains the benchmark diagnostic standard but now reserve this test for Rose-Bengal-positive patients with negative scintigraphy. The diagnostic path in SS therefore remains a matter of personal choice for the physician. When a patient presents with symptoms suggestive of dry eyes (including grittiness) or dry mouth, details should be sought about current drugs known to cause dryness and past illnesses including sarcoidosis. In the ill patient with night sweats, weight loss, and lymphadenopathy the possibility of lymphoma should be considered. The first-line investigation should be a Schirmer test or Rose Bengal staining of the corneas. If dryness is confirmed, blood should be taken for SS-associated autoantibodies. What one does next depends on the quality and availability of local diagnostic services. Both labial biopsy and salivary gland scintigraphy have a low morbidity but the wide availability, precision (at least at excluding other conditions21), and easy validation of labial biopsy are likely in most centres to remain powerful points in its favour compared with salivary gland scintigraphy. The exact choice of diagnostic path matters less than the recognition that failure to investigate dryness of eyes and mouth arising de novo may represent a lost opportunity to withdraw a harmful drug or to treat a disease such as sarcoidosis.21 1. Wollheim FA. Henrik Sjögren and Sjögren’s syndrome. Scand J Rheumatol 1986; 61 (suppl): 11-16. 2. Kelly CA, Griffiths ID. Sjögren’s syndrome: an often missed rheumatic disease. Rheumatol Now 1990; 4: 12-15. 3. Strand V, Talal N. Advances in the diagnosis and concept of Sjögren’s syndrome (autoimmune exocrinopathy). Bull Rheum Dis 1980; 30: 1046-52. 4. Morgan WS, Castleman B. A clinicopathologic study of "Mikulicz’s disease". Am J Pathol 1953; 29: 471-503.
for public policy8-eg, it would favour underinvestment in the long-term health for the poor, especially in developing countries which have higher rates of time preference.9 It almost certainly does not reflect the way people want governments to act on their behalf. 3,4 This debate has important policy implications, since reducing the discount rate from 6% to zero can have a dramatic effect on cost-effectiveness rankings and will favour treatments with delayed benefits. For example, the cost effectiveness of surgical treatment of teenage idiopathic scoliosis increases fourteen fold and the use of nicotine gum for male smokers five fold.3 Although technological change and the uncertain effects of long-term programmes need to be taken into account in health care decision-making, the discounting of health benefits should no longer be a thoughtless routine. A range of discount rates including zero should be shown in all economic
appraisals. 1. Drummond M, Stoddart G, Torrance G. Methods of economic evaluation of health care programmes. Oxford: Oxford University Press, 1987. 2. Johannesson M. On the discounting of gained life-years in costeffectiveness analysis. Int J Technol Assess Health Care 1992; 8: 369-64. 3. Parsonage M, Neuburger H. Discounting and health benefits. Health Economics 1992; 1: 71-76. 4. Sheldon TA. Discounting in health care decision making: time for a change? J Public Health Med (in press). 5. West RR. Valuation of life in long run health care programmes. BMJ
1985; 291: 1139-41 6. Cairns J. Discounting and health benefits: another perspective. Health Economics 1992; 1: 76-79. 7. Cohen DR, Henderson JB. Health, prevention and economics. Oxford: Oxford University Press, 1988: 155. 8. Robinson JC. The philosophical origins of the social rate of discount in cost-benefit analysis. Milbank Quart 1990; 68: 245-65. 9. Messing SD. Discounting health: the issue of subsistence and care in an underdeveloped country. Soc Sci Med 1973; 7: 911-16.
What
happened to growth monitoring?
"From birth to age three, children should be weighed every month. If there is no gain in weight for two months, something is wrong." This admonition to monitor child growth is the last of the ten Facts for Life promoted by UNICEF, WHO, and UNESCO to "dramatically improve the health of children in the developing world" by providing families with essential child health information.1 Growth monitoring is primarily an operational communication strategy for growth promotion based on screening of the under-fives, and often targeting those aged 4-36 months. The object is to detect growth falterers rather than those of poor nutritional status in whom growth promotion has already failed.2 "A healthy child gains weight each month" was the widely publicised slogan of Indonesia’s National
Nutrition Programme.33
A 1985 Lancet editorial on growth monitoring4 carried the subtitle "intermediate technology or expensive luxury?", and participants at an
colloquium held in Kenya in May, on for child development, agreed that promotion growth the question is still relevant in 1992.5Growth monitoring conducted at health centres has not yet international
been shown to be cost-effective. The separate contribution of growth monitoring to the effectiveness of child health programmes still needs to be documented in terms of coverage, maternal behaviour changes, child growth, morbidity, and mortality.6,7 The children most at risk are least likely to attend, while health workers seldom receive the level of training, management, or supervision required to deliver correct growth monitoring technology. Too often health workers neglect to involve mothers in the weighing and charting process, and do not explain the result, even if adverse. Moreover, they have neither the time nor the knowledge to individualise the subsequent advice, which is, after all, the raison d’etre of the whole exercise and which might justify the mother’s taking a day away from her subsistence agriculture or market to travel to the clinic, and her long wait for the weighing and again for the
consultation. The primary health care approach, of which growth monitoring should be an integral part, encourages devolvement of health knowledge and skills from health professionals to communities and individuals.
Community-based growth monitoring, arising as a response to the community’s perception of its health problems and their relative importance, seems the best way to evoke community solutions to malnutrition and disease in children,especially if fathers and grandmothers also take part. However, growth monitoring has a long history of advocacy, exhortation, and rhetoric. Operational research is an essential component of any national strategy for community-based schemes, the aim being to identify and strengthen, via training and supervision, weak links in the chain. The starting point is sensitisation and mobilisation of communities for growth monitoring activities; the chain ends with effective interventions identified, explained, and understood by mothers (and communities). The mothers must find the strategy affordable and acceptable; if so, they will be able and willing to implement the proposals. Between these two ends of the chain there are four steps: issue and regular use of growth charts; correct weighing and plotting; distinction between normal growth and poor growth by mothers; and identification and explanation of reasons for poor
growth. 1. UNICEF. Facts of life: a communication challenge. Benson, Oxfordshire: P & LA, 1989. 2. Dixon RA. Monitoring the growth of the world’s children. Ann Trop Paediatr 1991; 11: 3-9. 3. Achadi E, Berman P. Growth monitoring in Indonesia: an assessment of coverage and regularity of attendance, Gedangan Village, Central Java, June 1978-November 1981. Food Nutr Bull, 1988; 1: 56-60. 4. Editorial. Growth monitoring: intermediate technology or expensive luxury? Lancet 1985; ii: 1337-38. 5. Anon. Growth promotion, not growth monitoring. Lancet 1992; 339: 1409.
150
6. Gerein N, Ross DA. Is growth monitoring worthwhile? An evaluation of its use m three child health programmes in Zaire. Soc Sci Med 1991; 32: 667-75. 7. Nabarro D, Chinnock P. Growth monitoring: inappropnate promotion of an appropriate technology. Soc Sci Med 1988; 26: 941-48.
Diagnosis of Sjögren’s syndrome Almost half a century ago Henrik Sjogren, a Swedish ophthalmologist, recorded the association of dry eyes (which he called "keratoconjunctivitis sicca") dry mouth, and rheumatoid arthritis and concluded that this was a specific disease. Gradually the term
Sjogren’s syndrome (SS)
was
adopted,2superseding
sicca syndrome3and Mikulicz syndrome,4which have been used for various expressions of the same condition. Multiorgan involvement, notably of the lungs, kidneys, and skin, emphasises the systemic nature of SS.5 Further refinement in classification came about with the recognition in the past two decades that SS can occur alone (primary SS) or in association with rheumatoid arthritis, systemic lupus erythematosus, and occasionally scleroderma
(secondary SS). Histological changes seen on light microscopy of the salivary glands of patients with primary SS are indistinguishable from those seen in the secondary condition.3 Despite these advances in definition of S S there are no universally accepted diagnostic criteria. This gap in our knowledge, together with the unknown frequency of largely or wholly symptomless SS, has led to difficulties in estimating the prevalence of the condition.9 There are at least four diagnostic "schools"lO-13 All four require the presence of objectively abnormal ocular tests (Schirmer or Rose Bengal staining) and lymphocyte infiltration around labial salivary glands in biopsy specimens. Three require the presence of subjective dryness of the mouth or eyes (commonly described as a gritty sensation) or the demonstration of objective evidence of salivary gland dysfunction (reduced salivary flow or abnormalities on sialography or salivary scintigraphy). However, only one schoopo requires the presence singly or multiply of IgM rheumatoid factor, antinuclear antibodies, anti SS-A [Ro], or anti SS-B [La]14 in the serum, despite the frequent occurrence of these autoantibodies in patients with SS.15,16 Anti-La [SS-B] and anti-Ro are the autoantibodies most specific to SS,1’ although anti-La and (especially) anti-Ro are also found in patients with systemic lupus erythematosus. None of the diagnostic schools adequately grades the symptoms of SS. At first glance it may seem difficult to understand why these broadly similar definitions of SS cannot easily be reconciled. Nevertheless, some of the required tests are invasive and may be refused or may fail,lg and there is variation between the diagnostic schools on scoring methods for the Schirmer test and labial salivary gland biopsy. Faced with the apparent complexity of the diagnostic criteria, the busy clinician may fall into the trap of diagnosing SS by symptoms
alone; this approach inevitably leads to misdiagnosis. Rheumatologists will be familiar with the patient deemed to have SS who, on more thorough assessment, proves to have sarcoidosis, age-associated ocular drying, or drug-induced dry mouth.5.18 In an attempt to lower the diagnostic hurdles, researchers continue to devise easier and more informative tests for busy clinicians. Speight et al 18 found that whole unstimulated salivary flows in patients with SS were lower than in controls; flows of 0-1 ml/min or less were highly specific for dry mouth (xerostomia). Unfortunately, as these researchers point out, this test identifies only xerostomia and not its causes. It is also not for the squeamish; subjects had to "drool or spit" into a beaker for 15 min to provide saliva for measurement. Coll et al,19 using a stepwise approach to the diagnosis of SS, conclude that combined Rose Bengal conjunctival staining and salivary gland scintigraphy will identify most patients with SS; labial salivary gland biopsy can be reserved for dubious cases. Positive results to both Rose Bengal staining and salivary scintigraphy in their study were invariably associated with a positive (grade 3 or 4)20 labial biopsy, Coll’s group acknowledge that labial salivary gland biopsy remains the benchmark diagnostic standard but now reserve this test for Rose-Bengal-positive patients with negative scintigraphy. The diagnostic path in SS therefore remains a matter of personal choice for the physician. When a patient presents with symptoms suggestive of dry eyes (including grittiness) or dry mouth, details should be sought about current drugs known to cause dryness and past illnesses including sarcoidosis. In the ill patient with night sweats, weight loss, and lymphadenopathy the possibility of lymphoma should be considered. The first-line investigation should be a Schirmer test or Rose Bengal staining of the corneas. If dryness is confirmed, blood should be taken for SS-associated autoantibodies. What one does next depends on the quality and availability of local diagnostic services. Both labial biopsy and salivary gland scintigraphy have a low morbidity but the wide availability, precision (at least at excluding other conditions21), and easy validation of labial biopsy are likely in most centres to remain powerful points in its favour compared with salivary gland scintigraphy. The exact choice of diagnostic path matters less than the recognition that failure to investigate dryness of eyes and mouth arising de novo may represent a lost opportunity to withdraw a harmful drug or to treat a disease such as sarcoidosis.21 1. Wollheim FA. Henrik Sjögren and Sjögren’s syndrome. Scand J Rheumatol 1986; 61 (suppl): 11-16. 2. Kelly CA, Griffiths ID. Sjögren’s syndrome: an often missed rheumatic disease. Rheumatol Now 1990; 4: 12-15. 3. Strand V, Talal N. Advances in the diagnosis and concept of Sjögren’s syndrome (autoimmune exocrinopathy). Bull Rheum Dis 1980; 30: 1046-52. 4. Morgan WS, Castleman B. A clinicopathologic study of "Mikulicz’s disease". Am J Pathol 1953; 29: 471-503.
