- Email: [email protected]
Dangers of suppressing menstruation
CORRESPONDENCE
mild disease will progress but it is difficult to accept the view that most patients should undergo a perhaps unnecessary operation to ensure that no patient has disease progression, especially since follow-up is rather straightforward. We certainly agree that epidemiological data indicate that patients with primary hyperparathyroidism have an increased incidence of cardiovascular disease. Although this applies to the entire population of patients with this disorder it is not known whether this is the case for the mild form of the disease. Furthermore, the evidence is indirect and it has never been shown in prospective randomised studies that the operation reduces cardiovascular morbidity and mortality. Toft also states that the operation improves bone mass but this is not a relevant argument because only patients with bone mass within the reference range (within SD of 2 z-scores) fulfills the National Institutes of Health Consensus criteria for follow-up. Patients with primary hyperparathyroidism who have a reduced bone mass in relation to age-matched and sex-matched controls should certainly undergo the operation, since a 5–10% improvement of bone mass may be expected postoperatively.2,3 If, as Toft suggests, nearly all patients with primary hyperparathyroidism should be advised to undergo parathyroidectomy, the logical consequence would be that a screening programme should be set up to identify all those in the population who have the disease. In a study by Lundgren and colleagues4 involving 5020 menopausal women (aged 55–75 years), who were participating in a mammography screening programme, the prevalence of primary hyperparathyroidism was 2·1%. Previously reported prevalence figures have been in the order of 0·1–0·2%. If the prevalence of the disease reported by Lundgren and colleagues is valid for the entire population of postmenopausal women, there are about 20 000–30 000 undetected cases of the disease (most probably with the mild form of the disease) in Sweden and perhaps more than 150 000 in UK. The medical and economical implications are substantial. An ongoing randomised controlled multi-centre study, The Scandinavian Investigation of Primary Hyperparathyroidism (SIPH), has been designed to compare the effect on blood chemistry, osteodensitometry, and morbidity and mortality of parathyroidectomy versus non-
THE LANCET • Vol 356 • August 5, 2000
operative management in patients with mild primary hyperparathyroidism. 10 Scandinavian centres participate in this study with the aim of recruiting 400–600 patients in 3 years. Hopefully, this study will answer the key question: does operation for mild primary hyperparathyroidism unravel symptoms unknown to the patients, and will it decrease mortality in this group of patients? At present there is not enough evidence that every patient with the disease would benefit from surgery. Precise recommendations how to manage patients with the mild form of the disease will have to await the results of prospective randomised studies. *Jörgen Nordenström, Jan Zedenius Endocrine Surgery Unit, Center for Metabolism and Endocrinology, Huddinge University Hospital, SE-141 86 Stockholm, Sweden (e-mail: jorgen.nordenströ[email protected]) 1
2
3
4
Toft AD. Surgery for primary hyperparathyroidism—sooner rather than later. Lancet 2000; 355: 1478–79. Abdelhadi M, Nordenström J. Bone mineral recovery after parathyroidectomy in patients with primary and renal hyperparathyroidism. J Clin Endocrinol Met 1998; 83: 3845–51. Silverberg SJ, Shane E, Jacobs TP, Siris E, Bilezikian JP. A 10-year prospective study of primary hyperparathyroidism with or without parathyroid surgery. N Engl J Med 1999; 341: 1249–55. Lundgren E, Ridefelt P, Åkerström G, Ljunghall S, Rastad J. Parathyroid tissue in normocalcemic and hypercalcemic primary hyperparathyroidism recruited by health screening. World J Surg 1996; 20: 727–35.
Dangers of suppressing menstruation Sir—Are the advocates of optional menstruation serious? P McGurgan and colleagues (May 13, p 1730)1 seem vaguely in agreement with the proposition of Sarah Thomas and Charlotte Ellerton2 but are concerned about the medical-legal risks for prescribers of oral contraceptive pills. Their suggestion that a progestagenreleasing intrauterine device (IUD) would be relatively free from complications is surprising in view of the well known complications of IUDs. Also, according to the manufacturer, 52 g levonorgestrel releases 20 g progestagen a day. This dose is powerful enough to induce amenorrhoea in some, but not all, women. Post-pill amenorrhoea is a side-effect of pill-taking and may be a symptom of a prolactinoma. Amenorrhoea is potentially a pathological condition. McGurgan and colleagues warn of
the vascular risks of combined pills, but seem unaware that either progestagens or oestrogens, given alone or in various combinations, increase both mood and vascular overreactivity. Depression is more likely with a progestagen than an oestrogen but either hormone can alter amine pathways and enzyme concentrations and increase the risk of mental illness.3 Their reference to a reduced risk of accidental death on oral contraceptives is not confirmed by the study by Beral and colleagues.4 Despite large participant losses, an increase in deaths from accidents and violence among users was recorded at the 25-year follow-up. In this study increased mortality from cerebrovascular disease, cervical, lung and liver cancers were also found, and significant increases in neurotic depression and attempted suicide, heart attacks, breast cancer, and fractures were reported. An increased risk of sixty conditions among pill takers or ex-takers was recorded in the first few years of the study. Pregnancy-related deaths from thrombosis mostly happen in the puerperium, a time when progestagens may be prescribed. The risk is greatest for women with the antiphospholipid syndrome, which has a sex ratio of nine women to one man. A common cause of this autoimmune disease, which carries a lifetime increase in risk of thrombosis, appears to be previous exposure to contraceptive hormones. The claim that contraceptive pills are safer than pregnancy is unlikely to stand up to close scrutiny. Many women have long-term endometrial or endocervical infections and a regular monthly bleed is a natural way of flushing out the endometrium. Progestagens shrivel the endometrium and usually reduce the amount of withdrawal bleeding, but they can also dilate and overdevelop endometrial blood vessels. This can cause menorrhagia or haemorrhage in some women. And to top it all, breast cancer has been found to be increased after very short-term use of oral contraceptives (mean 3 years).5 Surely the proponents of continuous hormone exposure must be joking? Ellen C G Grant 20 Coombe Ridings, Kingston-upon-Thames, KT2 7JU, UK 1
2
McGurgan P, O’Donovan P, Duffy S, Rogerson L. Should menstruation be optional for women? Lancet 2000; 355: 1730. Thomas SL, Ellerston C. Nuisance or natural and healthy: should monthly menstruation be optional for women? Lancet 2000; 355: 922–24.
513
For personal use only. Not to be reproduced without permission of The Lancet.
CORRESPONDENCE 3
4
5
Grant ECG. The Pill: hormone replacement therapy, vascular and mood over-reactivity, and mineral imbalance. J Nutr Environ Med 1998; 8: 105–16. Beral V, Hermon C, Kay C, Hannaford P, Darley S, Gillian R. Mortality associated with oral contraceptive use: 25 year followup of cohort of 46 000 women from Royal College of General Practitioners’ oral contraception study. BMJ 1999; 318: 96–100. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 epidemiological studies. Lancet 1996; 347: 1713–27.
Iraq’s children and responsibility Sir—Your May 27 editorial1 concerning the economic sanctions on Iraq is too complacent in its assessment of the international community’s responsibility. Whilst it may be comforting to believe that the primary responsibility for this disaster is Saddam’s, this does not square with the facts. In March, 1991, a United Nations (UN) mission to Iraq reported a situation of near-apocalyptic destruction in the wake of the Gulf War with “most means of modern life support . . . destroyed or rendered tenuous”. This devastation was deliberate—the result of a decision by the allies to attack, and in some cases destroy, objects indispensable to the survival of the civilian population (most notably the electricity system).2 And it was in these circumstances that the Security Council decided to keep economic sanctions in place, a deeply wicked act, the consequences of which were well understood at the time. By the time of the first oil-for-food resolution (UNSCR 706, Aug 15, 1991) there had already been an estimated 47 000 excess deaths among children under age 5 years.3 It was clear even then that oil-for-food had political, rather than humanitarian, motivation. As one US official rather candidly explained, (The Independent, July 24, 1991), oil-for-food was “a good way to maintain the bulk of sanctions and not be on the wrong side of a potentially emotive issue”. That the programme was “neither designed . . . or . . . sufficient to meet the basic needs of the Iraqi people” was of little importance. That oil-for-food was initially rejected by the Iraqi Government came as no surprise to the USA. Indeed, according to James Fine, an aid agency staff member involved in the
514
discussions in Baghdad, even by late July, 1991, “UN officials were convinced . . . that the US intention was to present Saddam Hussein with so unattractive a package that Iraq would reject it and thus take on the blame, at least in western eyes, for the continued civilian suffering”—which was exactly what happened.5 Your editorial says that “The courageous policy . . . is to suspend (not abandon) sanctions”. However, as the oil industry journal Middle East Economic Survey has noted: “very few oil companies [will be] prepared to invest billions of dollars and mobilize personnel and resources only to be told after four months that they can no longer operate in Iraq”. Iraq’s oil industry, upon whose exports the humanitarian programme depends, is in desperate need of just such investment. A policy of suspension would continue to treat the well being of ordinary
people in Iraq as a political football. In March the UN Humanitarian Coordinator for Iraq, Hans von Sponeck, resigned his post in protest over the sanctions. According to him, “the way out is to life the embargo, and delink the disarmament discussion from the humanitarian discussion”. This is not a question of courage—it is an urgent moral imperative. Andrea Needham, on behalf of Voices in the Wilderness UK Voices in the Wilderness UK, 16b Cherwell Street, Oxford OX4 1BG, UK (e-mail: [email protected]) 1 2 3
4
5
Editorial. Iraq’s children. Lancet 2000; 1837. Needless deaths in the Gulf War. Middle East Watch 1991: 160–93. Acherio A, Chase R, Cote T, et al. Effect of the Gulf War on infant and child mortality in Iraq. N Engl J Med 1992; 327: 931–36. UNICEF. Questions and answers for the Iraq child mortality surveys. Geneva: UNICEF, July, 1999. Fine J. The Iraq sanctions catastrophe. Middle East Report 1992; 174: 36–39.
DEPARTMENT OF ERROR Intrauterine growth retardation and adult cardiovascular risk factors—In this Research letter by R John Irving and colleagues (June 17, p 2135), the correct version of the table is shown below: Controls
Characteristics Males Females Females taking oral contraceptives Birthweight (kg) Gestational age at birth (weeks) Weight at 44 weeks after mother’s last menstrual period (kg) Age when studied (years) Adult height (m) Adult weight (kg)
11 16 4
13 21 4
Low birthweight appropriate for gestational age 9 10 2
Low birthweight with IUGR
4 11 2
3·13 (0·45) 1·68 (0·22)† 1·66 (0·22) 1·70 (0·22) 39·3 (1·90) 33·4 (2·3)† 31·9 (1·5) 35·2 (1·7)† 3·92 (0·42)
3·71 (0·52)
24·0 (0·7) 24·3 (0·5) 1·68 (0·10) 1·67 (0·09) 64·9 (11·1) 66·9 (12·7)
Blood pressure (mm Hg) Adult systolic 115 (9) Adult diastolic 73 (7) Fasting plasma Glucose (mmol/L) Insulin (mU/L) Triglyceride (mmol/L) Total cholesterol (mmol/L) High-density liproprotein cholesterol (mmol/L)
All low birthweight
122 (12)* 78 (7)*
3·97 (0·33)
3·36 (0·52)†
24·4 (0·4) 24·3 (0·6) 1·70 (0·08) 1·63 (0·09)* 71·7 (13·4) 60·8 (8·7)† 123 (9) 80 (7)
120 (14) 77 (6)
4·2 (0·4) 4·9 (2·8) 0·8 (0·3) 4·0 (0·9)
4·5 (0·4)* 5·1 (2·0) 0·9 (0·3) 4·3 (0·9)
4·4 (0·4) 5·6 (2·1) 0·9 (0·4) 4·5 (1·0)
4·6 (0·3) 4·3 (1·6) 0·8 (0·3) 4·0 (0·6)
1·4 (0·3)
1·4 (0·3)
1·3 (0·3)
1·5 (0·3)
Data are mean (SD). Comparisons were made between controls and all low-birthweight participants, and between the two groups of low birthweight participants (those with birthweight appropriate for gestational age and IUGR), by unpaired student t test. *p<0·02. †p<0·001.
Characteristics in infancy and adulthood Morbidity and mortality in patients randomised to double-blind treatment with long-acting calciumchannel blocker or diuretic in the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT)—In this Article by Morris J Brown and colleagues (July 29, p 366), in the Methods section of the Summary (p 366), co-amilozide should have contained hydrochlorothiazide 25 mg. On page 369, the fourth line of the left column should be, “of hypertension (38 and 38); loss to follow-up (66 and 83)”. In table 5, percentage signs should have appeared in all the parentheses in the nifedipine and co-amilozide columns; the asterisk in the first row of numbers should have appeared next to the word “Composite” in the first column; the footnote mark in the third row under Secondary outcomes should have been “All (first event)‡”; and the second footnote should have read “†Primary outcomes plus non-cardiovascular deaths, renal failure, angina, and transient ischaemic attacks.”.
THE LANCET • Vol 356 • August 5, 2000
For personal use only. Not to be reproduced without permission of The Lancet.
mild disease will progress but it is difficult to accept the view that most patients should undergo a perhaps unnecessary operation to ensure that no patient has disease progression, especially since follow-up is rather straightforward. We certainly agree that epidemiological data indicate that patients with primary hyperparathyroidism have an increased incidence of cardiovascular disease. Although this applies to the entire population of patients with this disorder it is not known whether this is the case for the mild form of the disease. Furthermore, the evidence is indirect and it has never been shown in prospective randomised studies that the operation reduces cardiovascular morbidity and mortality. Toft also states that the operation improves bone mass but this is not a relevant argument because only patients with bone mass within the reference range (within SD of 2 z-scores) fulfills the National Institutes of Health Consensus criteria for follow-up. Patients with primary hyperparathyroidism who have a reduced bone mass in relation to age-matched and sex-matched controls should certainly undergo the operation, since a 5–10% improvement of bone mass may be expected postoperatively.2,3 If, as Toft suggests, nearly all patients with primary hyperparathyroidism should be advised to undergo parathyroidectomy, the logical consequence would be that a screening programme should be set up to identify all those in the population who have the disease. In a study by Lundgren and colleagues4 involving 5020 menopausal women (aged 55–75 years), who were participating in a mammography screening programme, the prevalence of primary hyperparathyroidism was 2·1%. Previously reported prevalence figures have been in the order of 0·1–0·2%. If the prevalence of the disease reported by Lundgren and colleagues is valid for the entire population of postmenopausal women, there are about 20 000–30 000 undetected cases of the disease (most probably with the mild form of the disease) in Sweden and perhaps more than 150 000 in UK. The medical and economical implications are substantial. An ongoing randomised controlled multi-centre study, The Scandinavian Investigation of Primary Hyperparathyroidism (SIPH), has been designed to compare the effect on blood chemistry, osteodensitometry, and morbidity and mortality of parathyroidectomy versus non-
THE LANCET • Vol 356 • August 5, 2000
operative management in patients with mild primary hyperparathyroidism. 10 Scandinavian centres participate in this study with the aim of recruiting 400–600 patients in 3 years. Hopefully, this study will answer the key question: does operation for mild primary hyperparathyroidism unravel symptoms unknown to the patients, and will it decrease mortality in this group of patients? At present there is not enough evidence that every patient with the disease would benefit from surgery. Precise recommendations how to manage patients with the mild form of the disease will have to await the results of prospective randomised studies. *Jörgen Nordenström, Jan Zedenius Endocrine Surgery Unit, Center for Metabolism and Endocrinology, Huddinge University Hospital, SE-141 86 Stockholm, Sweden (e-mail: jorgen.nordenströ[email protected]) 1
2
3
4
Toft AD. Surgery for primary hyperparathyroidism—sooner rather than later. Lancet 2000; 355: 1478–79. Abdelhadi M, Nordenström J. Bone mineral recovery after parathyroidectomy in patients with primary and renal hyperparathyroidism. J Clin Endocrinol Met 1998; 83: 3845–51. Silverberg SJ, Shane E, Jacobs TP, Siris E, Bilezikian JP. A 10-year prospective study of primary hyperparathyroidism with or without parathyroid surgery. N Engl J Med 1999; 341: 1249–55. Lundgren E, Ridefelt P, Åkerström G, Ljunghall S, Rastad J. Parathyroid tissue in normocalcemic and hypercalcemic primary hyperparathyroidism recruited by health screening. World J Surg 1996; 20: 727–35.
Dangers of suppressing menstruation Sir—Are the advocates of optional menstruation serious? P McGurgan and colleagues (May 13, p 1730)1 seem vaguely in agreement with the proposition of Sarah Thomas and Charlotte Ellerton2 but are concerned about the medical-legal risks for prescribers of oral contraceptive pills. Their suggestion that a progestagenreleasing intrauterine device (IUD) would be relatively free from complications is surprising in view of the well known complications of IUDs. Also, according to the manufacturer, 52 g levonorgestrel releases 20 g progestagen a day. This dose is powerful enough to induce amenorrhoea in some, but not all, women. Post-pill amenorrhoea is a side-effect of pill-taking and may be a symptom of a prolactinoma. Amenorrhoea is potentially a pathological condition. McGurgan and colleagues warn of
the vascular risks of combined pills, but seem unaware that either progestagens or oestrogens, given alone or in various combinations, increase both mood and vascular overreactivity. Depression is more likely with a progestagen than an oestrogen but either hormone can alter amine pathways and enzyme concentrations and increase the risk of mental illness.3 Their reference to a reduced risk of accidental death on oral contraceptives is not confirmed by the study by Beral and colleagues.4 Despite large participant losses, an increase in deaths from accidents and violence among users was recorded at the 25-year follow-up. In this study increased mortality from cerebrovascular disease, cervical, lung and liver cancers were also found, and significant increases in neurotic depression and attempted suicide, heart attacks, breast cancer, and fractures were reported. An increased risk of sixty conditions among pill takers or ex-takers was recorded in the first few years of the study. Pregnancy-related deaths from thrombosis mostly happen in the puerperium, a time when progestagens may be prescribed. The risk is greatest for women with the antiphospholipid syndrome, which has a sex ratio of nine women to one man. A common cause of this autoimmune disease, which carries a lifetime increase in risk of thrombosis, appears to be previous exposure to contraceptive hormones. The claim that contraceptive pills are safer than pregnancy is unlikely to stand up to close scrutiny. Many women have long-term endometrial or endocervical infections and a regular monthly bleed is a natural way of flushing out the endometrium. Progestagens shrivel the endometrium and usually reduce the amount of withdrawal bleeding, but they can also dilate and overdevelop endometrial blood vessels. This can cause menorrhagia or haemorrhage in some women. And to top it all, breast cancer has been found to be increased after very short-term use of oral contraceptives (mean 3 years).5 Surely the proponents of continuous hormone exposure must be joking? Ellen C G Grant 20 Coombe Ridings, Kingston-upon-Thames, KT2 7JU, UK 1
2
McGurgan P, O’Donovan P, Duffy S, Rogerson L. Should menstruation be optional for women? Lancet 2000; 355: 1730. Thomas SL, Ellerston C. Nuisance or natural and healthy: should monthly menstruation be optional for women? Lancet 2000; 355: 922–24.
513
For personal use only. Not to be reproduced without permission of The Lancet.
CORRESPONDENCE 3
4
5
Grant ECG. The Pill: hormone replacement therapy, vascular and mood over-reactivity, and mineral imbalance. J Nutr Environ Med 1998; 8: 105–16. Beral V, Hermon C, Kay C, Hannaford P, Darley S, Gillian R. Mortality associated with oral contraceptive use: 25 year followup of cohort of 46 000 women from Royal College of General Practitioners’ oral contraception study. BMJ 1999; 318: 96–100. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 epidemiological studies. Lancet 1996; 347: 1713–27.
Iraq’s children and responsibility Sir—Your May 27 editorial1 concerning the economic sanctions on Iraq is too complacent in its assessment of the international community’s responsibility. Whilst it may be comforting to believe that the primary responsibility for this disaster is Saddam’s, this does not square with the facts. In March, 1991, a United Nations (UN) mission to Iraq reported a situation of near-apocalyptic destruction in the wake of the Gulf War with “most means of modern life support . . . destroyed or rendered tenuous”. This devastation was deliberate—the result of a decision by the allies to attack, and in some cases destroy, objects indispensable to the survival of the civilian population (most notably the electricity system).2 And it was in these circumstances that the Security Council decided to keep economic sanctions in place, a deeply wicked act, the consequences of which were well understood at the time. By the time of the first oil-for-food resolution (UNSCR 706, Aug 15, 1991) there had already been an estimated 47 000 excess deaths among children under age 5 years.3 It was clear even then that oil-for-food had political, rather than humanitarian, motivation. As one US official rather candidly explained, (The Independent, July 24, 1991), oil-for-food was “a good way to maintain the bulk of sanctions and not be on the wrong side of a potentially emotive issue”. That the programme was “neither designed . . . or . . . sufficient to meet the basic needs of the Iraqi people” was of little importance. That oil-for-food was initially rejected by the Iraqi Government came as no surprise to the USA. Indeed, according to James Fine, an aid agency staff member involved in the
514
discussions in Baghdad, even by late July, 1991, “UN officials were convinced . . . that the US intention was to present Saddam Hussein with so unattractive a package that Iraq would reject it and thus take on the blame, at least in western eyes, for the continued civilian suffering”—which was exactly what happened.5 Your editorial says that “The courageous policy . . . is to suspend (not abandon) sanctions”. However, as the oil industry journal Middle East Economic Survey has noted: “very few oil companies [will be] prepared to invest billions of dollars and mobilize personnel and resources only to be told after four months that they can no longer operate in Iraq”. Iraq’s oil industry, upon whose exports the humanitarian programme depends, is in desperate need of just such investment. A policy of suspension would continue to treat the well being of ordinary
people in Iraq as a political football. In March the UN Humanitarian Coordinator for Iraq, Hans von Sponeck, resigned his post in protest over the sanctions. According to him, “the way out is to life the embargo, and delink the disarmament discussion from the humanitarian discussion”. This is not a question of courage—it is an urgent moral imperative. Andrea Needham, on behalf of Voices in the Wilderness UK Voices in the Wilderness UK, 16b Cherwell Street, Oxford OX4 1BG, UK (e-mail: [email protected]) 1 2 3
4
5
Editorial. Iraq’s children. Lancet 2000; 1837. Needless deaths in the Gulf War. Middle East Watch 1991: 160–93. Acherio A, Chase R, Cote T, et al. Effect of the Gulf War on infant and child mortality in Iraq. N Engl J Med 1992; 327: 931–36. UNICEF. Questions and answers for the Iraq child mortality surveys. Geneva: UNICEF, July, 1999. Fine J. The Iraq sanctions catastrophe. Middle East Report 1992; 174: 36–39.
DEPARTMENT OF ERROR Intrauterine growth retardation and adult cardiovascular risk factors—In this Research letter by R John Irving and colleagues (June 17, p 2135), the correct version of the table is shown below: Controls
Characteristics Males Females Females taking oral contraceptives Birthweight (kg) Gestational age at birth (weeks) Weight at 44 weeks after mother’s last menstrual period (kg) Age when studied (years) Adult height (m) Adult weight (kg)
11 16 4
13 21 4
Low birthweight appropriate for gestational age 9 10 2
Low birthweight with IUGR
4 11 2
3·13 (0·45) 1·68 (0·22)† 1·66 (0·22) 1·70 (0·22) 39·3 (1·90) 33·4 (2·3)† 31·9 (1·5) 35·2 (1·7)† 3·92 (0·42)
3·71 (0·52)
24·0 (0·7) 24·3 (0·5) 1·68 (0·10) 1·67 (0·09) 64·9 (11·1) 66·9 (12·7)
Blood pressure (mm Hg) Adult systolic 115 (9) Adult diastolic 73 (7) Fasting plasma Glucose (mmol/L) Insulin (mU/L) Triglyceride (mmol/L) Total cholesterol (mmol/L) High-density liproprotein cholesterol (mmol/L)
All low birthweight
122 (12)* 78 (7)*
3·97 (0·33)
3·36 (0·52)†
24·4 (0·4) 24·3 (0·6) 1·70 (0·08) 1·63 (0·09)* 71·7 (13·4) 60·8 (8·7)† 123 (9) 80 (7)
120 (14) 77 (6)
4·2 (0·4) 4·9 (2·8) 0·8 (0·3) 4·0 (0·9)
4·5 (0·4)* 5·1 (2·0) 0·9 (0·3) 4·3 (0·9)
4·4 (0·4) 5·6 (2·1) 0·9 (0·4) 4·5 (1·0)
4·6 (0·3) 4·3 (1·6) 0·8 (0·3) 4·0 (0·6)
1·4 (0·3)
1·4 (0·3)
1·3 (0·3)
1·5 (0·3)
Data are mean (SD). Comparisons were made between controls and all low-birthweight participants, and between the two groups of low birthweight participants (those with birthweight appropriate for gestational age and IUGR), by unpaired student t test. *p<0·02. †p<0·001.
Characteristics in infancy and adulthood Morbidity and mortality in patients randomised to double-blind treatment with long-acting calciumchannel blocker or diuretic in the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT)—In this Article by Morris J Brown and colleagues (July 29, p 366), in the Methods section of the Summary (p 366), co-amilozide should have contained hydrochlorothiazide 25 mg. On page 369, the fourth line of the left column should be, “of hypertension (38 and 38); loss to follow-up (66 and 83)”. In table 5, percentage signs should have appeared in all the parentheses in the nifedipine and co-amilozide columns; the asterisk in the first row of numbers should have appeared next to the word “Composite” in the first column; the footnote mark in the third row under Secondary outcomes should have been “All (first event)‡”; and the second footnote should have read “†Primary outcomes plus non-cardiovascular deaths, renal failure, angina, and transient ischaemic attacks.”.
THE LANCET • Vol 356 • August 5, 2000
For personal use only. Not to be reproduced without permission of The Lancet.