- Email: [email protected]
Severe anaemia in west African children: malaria or malnutrition?
CORRESPONDENCE
disorder is important. “Myasthenia” typically denotes myasthenia gravis. However, this disorder was not identified in this patient—the authors noted that neither acetylcholine-receptor nor striated-muscle antibodies were detected, nor was thymoma. Because myasthenia gravis can be seronegative depending on the assay used, and the authors did not comment on diagnostic or therapeutic use of edrophonium or pyridostigmine, nor on repetitive stimulation of neuromuscular junctions, a diagnosis of this disorder remains unconfirmed. By quoting that statins are known to cause mitochondrial disturbances, including mitochondrial myopathy, and by proposing treatment of a potential recurrence in their patient with coenzyme Q10, they seem to suggest that this disorder caused her “strikingly fatiguable myogenic ptosis”. Yet their dire forecast that, untreated, respiratory muscle involvement may “prove lifethreatening” is more germane to myasthenia gravis than mitochondrial myopathy, as is their reference to penicillamine toxic effects. I discourage generic use of the term myasthenia for a non-myasthenia gravis or unidentified disorder. Instead, I recommend: (1) more diagnostic testing for myasthenia gravis and, in case the disorder is this one, interim therapy (while awaiting improvement after withdrawal of the iatrogenic-toxin) with pyridostigmine, or prednisone2 (now standard); (2) biopsy of a weak limbmuscle to seek the ragged-red fibres3 of mitochondrial myopathy (and lipid accumulation), and if present, biochemical testing for the toxic mechanism; and (3) avoidance of concomitant drugs—eg, fibrates, niacin, erythromycin, azole antifungals, and ciclosporin—that can augment statin myotoxicity.4,5 W K Engel Neuromuscular Center, Good Samaritan Hospital, USC Keck School of Medicine, 637 South Lucas Ave, Los Angeles, CA 900017-1912, USA 1 Parmar B, Francis PJ, Ragge NK. Statins, fibrates, and ocular myasthenia. Lancet 2002; 360: 717. 2 Warmolts JR, Engel WK, Whitaker JN. Alternate-day prednisone in a patient with myasthenia gravis. Lancet 1970; 2: 1198–99. 3 Engel WK. “Ragged-red fibers” in ophthalmoplegia syndromes and their differential diagnosis. Abstracts of the 2nd International Congress on Muscle Diseases; Perth, Australia, 1971. Excerpta Medica International Congress Series No 237. Amsterdam: Excerpta Medica, 1971: 28. 4 Bernini F, Poli A, Paoletti R. Safety of HMG-CoA reductase inhibitors: focus on atorvastatin. Cardiovasc Drugs Ther 2001; 15: 211–18. 5 Ucar M, Mjorndal T, Dahlqvist R. HMGCoA reductase inhibitors and myotoxicity. Drug Saf 2000; 22: 441–57.
86
The dangers of childhood Sir—In your excellent editorial (Sept 14, p 811),1 you point out the dangers children face close to home. We want to emphasise a silent epidemic that occurs close to homes in parts of the world where ponds, canals, and rivers are in abundance. As infectious childhood diseases are controlled, drowning has become the leading cause of death in children aged 1–4 years in Matlab, Bangladesh. It now accounts for more than half the deaths in this age-group. Globally, drowning has been reported as the 11th and 4th leading cause of death for 0–4-year-olds and 5–14-year-olds, respectively, for 1998.2 Drowning usually occurs close to homes and kills healthy children. Interventions to stop these tragic but preventable deaths have not been adequately explored or implemented in the developing world. This is another epidemic that does not make it to the global public headlines. *Andres de Francisco, Adnan A Hyder, Shams-El-Arifeen, Abdullah H Baqui *Global Forum for Health Research, c/o WHO, 1211 Geneva 27, Switzerland (AdF); Johns Hopkins University, MD, USA (AAH, AHB); and Centre for Health and Population Research, Bangladesh (SEA) (e-mail: [email protected]) 1 2
Editorial. The dangers of childhood. Lancet 2002; 360: 811. Krug E, ed. Injury: a leading cause of the global burden of disease. Geneva: WHO, 1999.
Quadruple treatments for Helicobacter pylori Sir—In their discussion on the treatment of ulcers caused by Helicobacter pylori, Francis K L Chan and W K Leung (Sept 21, p 933)1 do not mention the short-term quadruple treatments2,3 that are available by combining all three antibiotics generally used for standard triple therapy with a proton-pump inhibitor or ranitidine, within 5 days. Although better indicated in selected patients,4 short-term quadruple treatments for eradication of Helicobacter pylori could offer advantages in terms of adherence, costs, and adverse effects, by contrast with standard triple therapy for 7–14 days. *Luca Mascitelli, Francesca Pezzetta Pronto Soccorso/Area d’Emergenza, Ospedale San Michele, Piazza Rodolone, 1 33013 Gemona del Friuli (FP); and *Casa di Cura “Città di Udine”, Viale Venezia, 410 33100 Udine, Italy (LM) (e-mail: [email protected])
1
2
3
4
Chan FKL, Leung WK. Peptic-ulcer disease. Lancet 2002; 360: 933–41. Treiber G, Ammon S, Schneider E, Klotz U. Amoxicillin/metronidazole/ omeprazole/clarithromycin: a new, short quadruple therapy for Helicobacter pylori eradication. Helicobacter 1998; 3: 54–58. Catalano F, Branciforte G, Catanzaro R, et al. Helicobacter pylori-positive duodenal ulcer: three-day antibiotic eradication regimen. Aliment Pharmacol Ther 2000; 14: 1329–34. Treiber G, Wittig J, Ammon S, et al. Clinical outcome and influencing factors of a new short-term quadruple therapy for Helicobacter pylori eradication. Arch Intern Med 2002; 162: 153–60.
Severe anaemia in west African children: malaria or malnutrition? Sir—H Verhoef and colleagues (Sept 21, p 908)1 show that intermittent administration of iron has a more pronounced effect on the haemoglobin status of Kenyan children than sulfadoxinepyrimethamine. We have done an analysis of risk factors for severe anaemia in a cohort of young children in rural Burkina Faso. The cohort consisted of 709 children aged 6–31 months, who were recruited for a randomised placebo-controlled trial on the effects of zinc supplementation on malaria morbidity.2 Village-based morbidity surveillance took place over the main malaria transmission period in 1999 (June to December), supplemented by two cross-sectional clinical surveys which included anthropometric measurements. Malaria is holoendemic but highly seasonal in the area. Anaemia status, defined by packed cell volume measurements (Compur Microspin, Bayer Diagnostics, Germany) during the December survey, was available for 544 (79%) of the 685 children successfully followed up. The mean packed cell volume was 29·2% (range 18–38), and 77 (14%) were defined as being severely anaemic (packed cell volume ⭐24%). The mean SD scores for height-for-age (HAZ), weight-for-age (WAZ), and weightfor-height (WHZ) were –1·6, –2·0, and –1·2, respectively, in June; and –1·5, –2·0, and –1·3, respectively, in December. We compared children with and without severe anaemia for the number of falciparum malaria episodes (fever plus ⭓5·000
THE LANCET • Vol 361 • January 4, 2003 • www.thelancet.com
For personal use. Only reproduce with permission from The Lancet Publishing Group.
CORRESPONDENCE
Height-for-age Weight-for-age Weight-for-height Number of falciparum malaria episodes in previous 6 months Falciparum malaria ⭐10 days before haemoglobin measurement (yes/no)
Children with severe anaemia (n=77)
Children without severe anaemia (n=467)
Odds ratio (95% CI)
–1·99 (1·40) –2·44 (1·13) –1·62 (0·79) 1·29 (1·04)
–1·39 (1·36) –1·76 (1·12) –1·21 (0·89) 1·31 (0·97)
0·72* (0·60–0·86) 0·58* (0·46–0·73) 0·58* (0·43–0·78) 0·92† (0·71–1·18)
32/435
0·32† (0·07–1·39)
2/75
Data are mean (SD) unless otherwise stated. *For continuous anthropometric score, odds ratio refers to increase of 1, adjusted for sex and age. †Adjusted for sex, age, and weight-for-age.
Association between severe anaemia, falciparum malaria, and malnutrition in young west African children
Plasmodium falciparum per L) over the 6-month observation period, for the prevalence of falciparum malaria within 10 days before the December survey, and for their mean HAZ/WAZ/WHZ SD scores. In logistic regression analyses (adjusted for age and sex), anaemia was not associated with the frequency of malaria episodes, nor with malaria prevalence. However, it was significantly associated with malnutrition, defined as HAZ, WAZ, and WHZ of –2 or less (table). These data contribute to the growing evidence for the importance of malnutrition in the development of anaemia in young children living in malaria-endemic areas.3 Given the well known grave implications of malnutrition on morbidity and mortality, programmes with the aim of improving the health of young children in developing countries need to put much more emphasis on improving the overall nutritional situation of young children.4,5 Finally, these findings also have implications for use of anaemia as an outcome in malaria control trials. *Olaf Müller, Corneille Traoré, Albrecht Jahn, Heiko Becher *Department of Tropical Hygiene and Public Health, Ruprecht-Karls-University, INF 324, 69124 Heidelberg, Germany (OM, AJ, HB); and Centre de Recherche en Santé de Nouna, Burkina Faso (CT) (e-mail: [email protected]) 1
2
3
Verhoef H, West CE, Nzyuko SM, et al. Intermittent administration of iron and sulfadoxine-pyrimethamine to control anaemia in Kenyan children: a randomised controlled trial. Lancet 2002; 360: 908–14. Müller O, Becher H, Baltussen van Zweeden A, et al. Effect of zinc supplementation on malaria and other morbidity in west African children: randomised double blind placebo controlled trial. BMJ 2001; 322: 1567–72. Nussenblatt V, Semba RD. Micronutrient malnutrition and the pathogenesis of malarial anaemia. Acta Tropica 2002; 82: 321–37.
4
5
Rice AL, Sacco L, Hyder A, Black RE. Malnutrition as an underlying cause of childhood deaths associated with infectious diseases in developing countries. Bull World Health Organ 2000; 78: 1207–21. Müller O, Jahn A, von Braun J. Micronutrient supplementation for malaria control—hype or hope? Trop Med Int Health 2002; 7: 1–3.
Tianeptine, plasma serotonin, and pulmonary hypertension Sir—After reading the Commentary by Raed A Dweik (Sept 21, p 886),1 we felt obliged to add some information. Free serotonin in the plasma is known to trigger bronchial and pulmonary vascular constriction.2 Blood serotonin arises from enterochromaffin cells, and the concentration of serotonin in the lung is closely correlated with that of platelets in the blood.3 Normally, total blood serotonin comprises 95–97% platelet serotonin and 3–5% free serotonin. The ratio of free serotonin to platelet serotonin increases as a result of platelet aggregation and interference with serotonin uptake by platelets.4 Platelet aggregation is seen during stressful situations (secondary to an increase in plasma epinephrine concentration), whereas platelet serotonin uptake is affected by circulating acetylcholine or dopamine concentrations, increases in which are seen during parasympathetic hyperactivity and other pathophysiological phenomena.5 The above information is consistent with the successful treatment of patients with bronchial asthma and pulmonary hypertension seen with low doses of tianeptine—a drug inadequately labelled as an antidepressant.2–5 In summary, all pathophysiological or clinical investigations dealing with bronchial or pulmonary vascular constriction should not ignore the role of plasma serotonin, which, in our
THE LANCET • Vol 361 • January 4, 2003 • www.thelancet.com
experience, is one of the most important aetiopathogenic factors of both disorders. *Fuad Lechin, Alex E Lechin, Bertha van der Dijs Instituto de Medicina Experimental, Universidad Central de Venezuela (BvdD), Apartado 80.983, Caracas 1080-A, Venezuela (FL); and Department of Clinical Science, University of Houston, Houston, TX, USA (AEL) (e-mail: [email protected]) 1
2
3
4
5
Dweik RA. Pulmonary hypertension and the search for the selective pulmonary vasodilator. Lancet 2002; 360: 886–87. Lechin F, van der Dijs B. Serotonin and pulmonary vasoconstriction. J Appl Physiol 2002; 92: 1363–64. Lechin F, van der Dijs B, Lechin AE. Severe asthma and plasma serotonin. Allergy 2002; 57: 258–59. Lechin F, van der Dijs B, Lechin AE. Plasma serotonin, pulmonary hipertensión and bronchial asthma. Clin Sci 2002; 103: 345–46. Lechin F, van der Dijs B, Lechin ME. Neurocircuitry and neuroautonomic disorders. Reviews and therapeutic strategies, chapter 12. Basel: Karger AG, 2002.
Physical activity and prevention of type 2 diabetes Sir—Two landmark prospective studies1,2 have shown that incidence of type 2 diabetes can be decreased by 58% in individuals with impaired glucose tolerance (IGT) through diet and exercise. However, these studies did not address whether the accompanying 4–6 kg weight loss itself was responsible for the striking decreases in incidence rates, or whether exercise had an independent effect. Nor did these studies address whether the beneficial effects of the intervention would be sustained beyond the relatively short duration of the studies. Insights into these questions can be gleaned from the Old Order Amish. These 30 000 or so individuals, whose
87
For personal use. Only reproduce with permission from The Lancet Publishing Group.
disorder is important. “Myasthenia” typically denotes myasthenia gravis. However, this disorder was not identified in this patient—the authors noted that neither acetylcholine-receptor nor striated-muscle antibodies were detected, nor was thymoma. Because myasthenia gravis can be seronegative depending on the assay used, and the authors did not comment on diagnostic or therapeutic use of edrophonium or pyridostigmine, nor on repetitive stimulation of neuromuscular junctions, a diagnosis of this disorder remains unconfirmed. By quoting that statins are known to cause mitochondrial disturbances, including mitochondrial myopathy, and by proposing treatment of a potential recurrence in their patient with coenzyme Q10, they seem to suggest that this disorder caused her “strikingly fatiguable myogenic ptosis”. Yet their dire forecast that, untreated, respiratory muscle involvement may “prove lifethreatening” is more germane to myasthenia gravis than mitochondrial myopathy, as is their reference to penicillamine toxic effects. I discourage generic use of the term myasthenia for a non-myasthenia gravis or unidentified disorder. Instead, I recommend: (1) more diagnostic testing for myasthenia gravis and, in case the disorder is this one, interim therapy (while awaiting improvement after withdrawal of the iatrogenic-toxin) with pyridostigmine, or prednisone2 (now standard); (2) biopsy of a weak limbmuscle to seek the ragged-red fibres3 of mitochondrial myopathy (and lipid accumulation), and if present, biochemical testing for the toxic mechanism; and (3) avoidance of concomitant drugs—eg, fibrates, niacin, erythromycin, azole antifungals, and ciclosporin—that can augment statin myotoxicity.4,5 W K Engel Neuromuscular Center, Good Samaritan Hospital, USC Keck School of Medicine, 637 South Lucas Ave, Los Angeles, CA 900017-1912, USA 1 Parmar B, Francis PJ, Ragge NK. Statins, fibrates, and ocular myasthenia. Lancet 2002; 360: 717. 2 Warmolts JR, Engel WK, Whitaker JN. Alternate-day prednisone in a patient with myasthenia gravis. Lancet 1970; 2: 1198–99. 3 Engel WK. “Ragged-red fibers” in ophthalmoplegia syndromes and their differential diagnosis. Abstracts of the 2nd International Congress on Muscle Diseases; Perth, Australia, 1971. Excerpta Medica International Congress Series No 237. Amsterdam: Excerpta Medica, 1971: 28. 4 Bernini F, Poli A, Paoletti R. Safety of HMG-CoA reductase inhibitors: focus on atorvastatin. Cardiovasc Drugs Ther 2001; 15: 211–18. 5 Ucar M, Mjorndal T, Dahlqvist R. HMGCoA reductase inhibitors and myotoxicity. Drug Saf 2000; 22: 441–57.
86
The dangers of childhood Sir—In your excellent editorial (Sept 14, p 811),1 you point out the dangers children face close to home. We want to emphasise a silent epidemic that occurs close to homes in parts of the world where ponds, canals, and rivers are in abundance. As infectious childhood diseases are controlled, drowning has become the leading cause of death in children aged 1–4 years in Matlab, Bangladesh. It now accounts for more than half the deaths in this age-group. Globally, drowning has been reported as the 11th and 4th leading cause of death for 0–4-year-olds and 5–14-year-olds, respectively, for 1998.2 Drowning usually occurs close to homes and kills healthy children. Interventions to stop these tragic but preventable deaths have not been adequately explored or implemented in the developing world. This is another epidemic that does not make it to the global public headlines. *Andres de Francisco, Adnan A Hyder, Shams-El-Arifeen, Abdullah H Baqui *Global Forum for Health Research, c/o WHO, 1211 Geneva 27, Switzerland (AdF); Johns Hopkins University, MD, USA (AAH, AHB); and Centre for Health and Population Research, Bangladesh (SEA) (e-mail: [email protected]) 1 2
Editorial. The dangers of childhood. Lancet 2002; 360: 811. Krug E, ed. Injury: a leading cause of the global burden of disease. Geneva: WHO, 1999.
Quadruple treatments for Helicobacter pylori Sir—In their discussion on the treatment of ulcers caused by Helicobacter pylori, Francis K L Chan and W K Leung (Sept 21, p 933)1 do not mention the short-term quadruple treatments2,3 that are available by combining all three antibiotics generally used for standard triple therapy with a proton-pump inhibitor or ranitidine, within 5 days. Although better indicated in selected patients,4 short-term quadruple treatments for eradication of Helicobacter pylori could offer advantages in terms of adherence, costs, and adverse effects, by contrast with standard triple therapy for 7–14 days. *Luca Mascitelli, Francesca Pezzetta Pronto Soccorso/Area d’Emergenza, Ospedale San Michele, Piazza Rodolone, 1 33013 Gemona del Friuli (FP); and *Casa di Cura “Città di Udine”, Viale Venezia, 410 33100 Udine, Italy (LM) (e-mail: [email protected])
1
2
3
4
Chan FKL, Leung WK. Peptic-ulcer disease. Lancet 2002; 360: 933–41. Treiber G, Ammon S, Schneider E, Klotz U. Amoxicillin/metronidazole/ omeprazole/clarithromycin: a new, short quadruple therapy for Helicobacter pylori eradication. Helicobacter 1998; 3: 54–58. Catalano F, Branciforte G, Catanzaro R, et al. Helicobacter pylori-positive duodenal ulcer: three-day antibiotic eradication regimen. Aliment Pharmacol Ther 2000; 14: 1329–34. Treiber G, Wittig J, Ammon S, et al. Clinical outcome and influencing factors of a new short-term quadruple therapy for Helicobacter pylori eradication. Arch Intern Med 2002; 162: 153–60.
Severe anaemia in west African children: malaria or malnutrition? Sir—H Verhoef and colleagues (Sept 21, p 908)1 show that intermittent administration of iron has a more pronounced effect on the haemoglobin status of Kenyan children than sulfadoxinepyrimethamine. We have done an analysis of risk factors for severe anaemia in a cohort of young children in rural Burkina Faso. The cohort consisted of 709 children aged 6–31 months, who were recruited for a randomised placebo-controlled trial on the effects of zinc supplementation on malaria morbidity.2 Village-based morbidity surveillance took place over the main malaria transmission period in 1999 (June to December), supplemented by two cross-sectional clinical surveys which included anthropometric measurements. Malaria is holoendemic but highly seasonal in the area. Anaemia status, defined by packed cell volume measurements (Compur Microspin, Bayer Diagnostics, Germany) during the December survey, was available for 544 (79%) of the 685 children successfully followed up. The mean packed cell volume was 29·2% (range 18–38), and 77 (14%) were defined as being severely anaemic (packed cell volume ⭐24%). The mean SD scores for height-for-age (HAZ), weight-for-age (WAZ), and weightfor-height (WHZ) were –1·6, –2·0, and –1·2, respectively, in June; and –1·5, –2·0, and –1·3, respectively, in December. We compared children with and without severe anaemia for the number of falciparum malaria episodes (fever plus ⭓5·000
THE LANCET • Vol 361 • January 4, 2003 • www.thelancet.com
For personal use. Only reproduce with permission from The Lancet Publishing Group.
CORRESPONDENCE
Height-for-age Weight-for-age Weight-for-height Number of falciparum malaria episodes in previous 6 months Falciparum malaria ⭐10 days before haemoglobin measurement (yes/no)
Children with severe anaemia (n=77)
Children without severe anaemia (n=467)
Odds ratio (95% CI)
–1·99 (1·40) –2·44 (1·13) –1·62 (0·79) 1·29 (1·04)
–1·39 (1·36) –1·76 (1·12) –1·21 (0·89) 1·31 (0·97)
0·72* (0·60–0·86) 0·58* (0·46–0·73) 0·58* (0·43–0·78) 0·92† (0·71–1·18)
32/435
0·32† (0·07–1·39)
2/75
Data are mean (SD) unless otherwise stated. *For continuous anthropometric score, odds ratio refers to increase of 1, adjusted for sex and age. †Adjusted for sex, age, and weight-for-age.
Association between severe anaemia, falciparum malaria, and malnutrition in young west African children
Plasmodium falciparum per L) over the 6-month observation period, for the prevalence of falciparum malaria within 10 days before the December survey, and for their mean HAZ/WAZ/WHZ SD scores. In logistic regression analyses (adjusted for age and sex), anaemia was not associated with the frequency of malaria episodes, nor with malaria prevalence. However, it was significantly associated with malnutrition, defined as HAZ, WAZ, and WHZ of –2 or less (table). These data contribute to the growing evidence for the importance of malnutrition in the development of anaemia in young children living in malaria-endemic areas.3 Given the well known grave implications of malnutrition on morbidity and mortality, programmes with the aim of improving the health of young children in developing countries need to put much more emphasis on improving the overall nutritional situation of young children.4,5 Finally, these findings also have implications for use of anaemia as an outcome in malaria control trials. *Olaf Müller, Corneille Traoré, Albrecht Jahn, Heiko Becher *Department of Tropical Hygiene and Public Health, Ruprecht-Karls-University, INF 324, 69124 Heidelberg, Germany (OM, AJ, HB); and Centre de Recherche en Santé de Nouna, Burkina Faso (CT) (e-mail: [email protected]) 1
2
3
Verhoef H, West CE, Nzyuko SM, et al. Intermittent administration of iron and sulfadoxine-pyrimethamine to control anaemia in Kenyan children: a randomised controlled trial. Lancet 2002; 360: 908–14. Müller O, Becher H, Baltussen van Zweeden A, et al. Effect of zinc supplementation on malaria and other morbidity in west African children: randomised double blind placebo controlled trial. BMJ 2001; 322: 1567–72. Nussenblatt V, Semba RD. Micronutrient malnutrition and the pathogenesis of malarial anaemia. Acta Tropica 2002; 82: 321–37.
4
5
Rice AL, Sacco L, Hyder A, Black RE. Malnutrition as an underlying cause of childhood deaths associated with infectious diseases in developing countries. Bull World Health Organ 2000; 78: 1207–21. Müller O, Jahn A, von Braun J. Micronutrient supplementation for malaria control—hype or hope? Trop Med Int Health 2002; 7: 1–3.
Tianeptine, plasma serotonin, and pulmonary hypertension Sir—After reading the Commentary by Raed A Dweik (Sept 21, p 886),1 we felt obliged to add some information. Free serotonin in the plasma is known to trigger bronchial and pulmonary vascular constriction.2 Blood serotonin arises from enterochromaffin cells, and the concentration of serotonin in the lung is closely correlated with that of platelets in the blood.3 Normally, total blood serotonin comprises 95–97% platelet serotonin and 3–5% free serotonin. The ratio of free serotonin to platelet serotonin increases as a result of platelet aggregation and interference with serotonin uptake by platelets.4 Platelet aggregation is seen during stressful situations (secondary to an increase in plasma epinephrine concentration), whereas platelet serotonin uptake is affected by circulating acetylcholine or dopamine concentrations, increases in which are seen during parasympathetic hyperactivity and other pathophysiological phenomena.5 The above information is consistent with the successful treatment of patients with bronchial asthma and pulmonary hypertension seen with low doses of tianeptine—a drug inadequately labelled as an antidepressant.2–5 In summary, all pathophysiological or clinical investigations dealing with bronchial or pulmonary vascular constriction should not ignore the role of plasma serotonin, which, in our
THE LANCET • Vol 361 • January 4, 2003 • www.thelancet.com
experience, is one of the most important aetiopathogenic factors of both disorders. *Fuad Lechin, Alex E Lechin, Bertha van der Dijs Instituto de Medicina Experimental, Universidad Central de Venezuela (BvdD), Apartado 80.983, Caracas 1080-A, Venezuela (FL); and Department of Clinical Science, University of Houston, Houston, TX, USA (AEL) (e-mail: [email protected]) 1
2
3
4
5
Dweik RA. Pulmonary hypertension and the search for the selective pulmonary vasodilator. Lancet 2002; 360: 886–87. Lechin F, van der Dijs B. Serotonin and pulmonary vasoconstriction. J Appl Physiol 2002; 92: 1363–64. Lechin F, van der Dijs B, Lechin AE. Severe asthma and plasma serotonin. Allergy 2002; 57: 258–59. Lechin F, van der Dijs B, Lechin AE. Plasma serotonin, pulmonary hipertensión and bronchial asthma. Clin Sci 2002; 103: 345–46. Lechin F, van der Dijs B, Lechin ME. Neurocircuitry and neuroautonomic disorders. Reviews and therapeutic strategies, chapter 12. Basel: Karger AG, 2002.
Physical activity and prevention of type 2 diabetes Sir—Two landmark prospective studies1,2 have shown that incidence of type 2 diabetes can be decreased by 58% in individuals with impaired glucose tolerance (IGT) through diet and exercise. However, these studies did not address whether the accompanying 4–6 kg weight loss itself was responsible for the striking decreases in incidence rates, or whether exercise had an independent effect. Nor did these studies address whether the beneficial effects of the intervention would be sustained beyond the relatively short duration of the studies. Insights into these questions can be gleaned from the Old Order Amish. These 30 000 or so individuals, whose
87
For personal use. Only reproduce with permission from The Lancet Publishing Group.