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Improvement of atopic dermatitis by reduced salt intake
breastfed or were born before the installation of copper tubings in their homes. 4 had clinically unapparent liver disease; they were siblings of other children with more severe forms. 5 children with manifest liver cirrhosis have survived, 1 after liver transplantation; 13 have died. Copper concentrations in the water used are reported to have ranged "between 0-4 and 15-5 mg/L". Scheinberg and Sternlieb make clear that high copper content of drinking water as a single factor cannot be the reason for childhood cirrhosis. However, our observations and Eife’s data suggest that we should continue to consider copper as a possible co-factor in the pathogenesis of infantile cirrhosis. -
The Dokumentations-und Informationsstelle fur Umweltfragen has fmancial support from the Deutsche Bundesstiftung Umwelt.
Karl Ernst
v
Muhlendahl, Heribert Lange
Dokumentations-und Informatlonsstelle fur Umweltfragen der Akademie fur Kmderheilkunde und Jugendmedizin, Kmderhospital, D 49082 Osnabruck, Germany
doubt be producing more interesting results over the next few years that will help to elaborate the importance of the neonatal immune responses in relation to the evolution of allergy and asthma. The observations that have come from large birth cohort studies are of immense importance. They will herald a new era in allergy research and offer the prospect for effective prediction of allergy and for prevention of disease.’ no
JO
University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK
1
2
3
Eife R, Reiter K, Sigmund B, Schramel P, Dieter HH, Müller-Höcker J. Die frühkindliche Leberzirrhose als Folge der chronischen Kuperintoxikation. Bundesgesundheitsbl 1991; 327-29.
1
Reduced interferon-&ggr; secretion in neonates and subsequent atopy SiR-Ghosh and colleagues (Oct 8, p 983) confirm our findings of reduced peripheral blood mononuclear cell (PBMC) interferon-y (IFN-y) secretion in neonates who subsequently developed eczema.’ They dismiss our work in a half sentence in their discussion. We showed not only reduced IFN-y production from antiCD3-stimulated PBMCs in neonates who subsequently developed eczema but also that impaired IFN-y production to p-lactoglobulin stimulation predicted milk-allergyassociated disease. We demonstrated that the defect was allergen specific because eczematous 1-year-olds without milk allergy did not have defective IFN-y production on plactoglobulin stimulation at birth. Ghosh and colleagues’ present no information on the proliferative responses to phytohaemagglutinin (PHA) that they used as their sole stimulant of PBMCs. PHA proliferative responses at birth are reduced in babies from atopic families and are lower in those who subsequently develop allergic problems.2,3 With reduced proliferation, it would not be surprising to observe also a reduced generation of cytokines such as IFN-y. Thus, on the basis of PHA stimulation alone, IFN-y production cannot be related to "a primary component of the atopic state". It could merely represent immunological immaturity in a potential atopic. It is for this reason that we did not report PHA or anti-CD3 stimulation alone. We showed that p-lactoglobulin proliferative responses were higher in those who developed milk-associated eczema and that despite this they still had reduced IFN-y production. This finding, we believe, does point to a more fundamental relation between the defect and
predisposition to specific allergies. Ghosh and colleagues associate their cord blood findings with atopic diseases in general rather than eczema alone, despite the fact that their seventeen individuals with socalled atopic disease age 1 year all had eczema but only three had apparent asthma. The diagnosis of asthma was based on three or more wheezing episodes, and at least half such infants will not develop atopic asthma.’ Furthermore, they did not do allergy skin tests on the whole cohort and some of the so-called atopic eczema patients had negative skin prick tests. We are sure that Ghosh and colleagues will be continuing their follow-up of the cohort of infants and will a
1516
Warner, J A Warner, E A Miles, A C Jones
Child Health,
4
5
Warner JA, Miles EA, Jones AC, Quint DJ, Colwell BM, Warner JO. Is deficiency of interferon gamma production by allergen triggered cord blood cells a predictor of atopic eczema? Clin Exp Allergy 1994; 24: 423-30. Miles EA, Warner JA, Lane AC, Jones AC, Colwell BM, Warner JO. T-lymphocyte activation at birth: implications for atopy. Pediatr Allergy Immunol (in press). Holt PG, Clough JB, Holt BJ, Baron-Hay MJ, Rose AH, Robinson BWS. Genetic risk for atopy is associated with delayed postnatal maturation of T-cell competence. Clin Exp Allergy 1992; 22: 1093-99. Van Asperen PP, Mukki A. Role of atopy in the natural history of wheeze and bronchial hyperresponsiveness in childhood. Pediatr Allergy Immunol 1994; 5: 178-83. Holt PG. A potential vaccine strategy for asthma and applied atopic disease. Lancet 1994; 344: 456-58.
Improvement of atopic dermatitis by reduced salt intake SiR-Barthel and Stuhlmuller (Oct 15, p 1089) report an improvement in atopic dermatitis when salt intake was restricted. They claim their report to be the first describing this effect. I draw these workers’ attention to the textbook of diseases in infancy’ by Heinrich Finkelstein, edited in 1912 in the same city (Berlin) in which these authors reside. Finkelstein clearly states on pages 559-61 the advantageous effect on eczema of what he termed "eczema soup", which basically consisted of a "desalted milk" and of salt-restricted food in general. He emphasised that a clinical amelioration, including an improvement in itching, can be expected within 3-4 days after salt restriction. A major improvement could be expected after about 3 weeks. Finkelstein also emphasised that only certain cases, mainly those with a major secretory component, respond to a reduced salt intake. However, he underscores the fact that this event is only a minor factor in the pathogenesis of this disease.
Hansjosef Böhles Department of Paediatrics, Johann Wolfgang Goethe-University, 60590 Frankfurt/Main, Germany
1
H Finkelstein. Lehrbuch der Säuglingskrankheiten: Fischer’s medicin. Berlin: Buchhandlung H Kornfeld, 1912.
CORRECTIONS timing of withdrawal bleeding a guide to endometrial safety during sequential oestrogen-progestagen replacement therapy?-The penultimate sentence of the summary of this article by Sturdee and colleagues (Oct 8, p 979) should have read "The prevalence of hyperplasia was 2-4% with 10 days of progestagen per cycle and 2.8% with 12 days". The caption of the figure should have read "First bleeding day after progestagen in relation to endometrial histology in 244 women with 3 days or less of variation between cycles". Is the
acid and peanut oil-In this letter by Truswell and Choudhury (Oct 8, p 1030) the phrase "Peterson and co-workers turned off the gas chromatograph..." should have begun with the word "Perhaps". We apologise for this omission.
Arachidonic
The Dokumentations-und Informationsstelle fur Umweltfragen has fmancial support from the Deutsche Bundesstiftung Umwelt.
Karl Ernst
v
Muhlendahl, Heribert Lange
Dokumentations-und Informatlonsstelle fur Umweltfragen der Akademie fur Kmderheilkunde und Jugendmedizin, Kmderhospital, D 49082 Osnabruck, Germany
doubt be producing more interesting results over the next few years that will help to elaborate the importance of the neonatal immune responses in relation to the evolution of allergy and asthma. The observations that have come from large birth cohort studies are of immense importance. They will herald a new era in allergy research and offer the prospect for effective prediction of allergy and for prevention of disease.’ no
JO
University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK
1
2
3
Eife R, Reiter K, Sigmund B, Schramel P, Dieter HH, Müller-Höcker J. Die frühkindliche Leberzirrhose als Folge der chronischen Kuperintoxikation. Bundesgesundheitsbl 1991; 327-29.
1
Reduced interferon-&ggr; secretion in neonates and subsequent atopy SiR-Ghosh and colleagues (Oct 8, p 983) confirm our findings of reduced peripheral blood mononuclear cell (PBMC) interferon-y (IFN-y) secretion in neonates who subsequently developed eczema.’ They dismiss our work in a half sentence in their discussion. We showed not only reduced IFN-y production from antiCD3-stimulated PBMCs in neonates who subsequently developed eczema but also that impaired IFN-y production to p-lactoglobulin stimulation predicted milk-allergyassociated disease. We demonstrated that the defect was allergen specific because eczematous 1-year-olds without milk allergy did not have defective IFN-y production on plactoglobulin stimulation at birth. Ghosh and colleagues’ present no information on the proliferative responses to phytohaemagglutinin (PHA) that they used as their sole stimulant of PBMCs. PHA proliferative responses at birth are reduced in babies from atopic families and are lower in those who subsequently develop allergic problems.2,3 With reduced proliferation, it would not be surprising to observe also a reduced generation of cytokines such as IFN-y. Thus, on the basis of PHA stimulation alone, IFN-y production cannot be related to "a primary component of the atopic state". It could merely represent immunological immaturity in a potential atopic. It is for this reason that we did not report PHA or anti-CD3 stimulation alone. We showed that p-lactoglobulin proliferative responses were higher in those who developed milk-associated eczema and that despite this they still had reduced IFN-y production. This finding, we believe, does point to a more fundamental relation between the defect and
predisposition to specific allergies. Ghosh and colleagues associate their cord blood findings with atopic diseases in general rather than eczema alone, despite the fact that their seventeen individuals with socalled atopic disease age 1 year all had eczema but only three had apparent asthma. The diagnosis of asthma was based on three or more wheezing episodes, and at least half such infants will not develop atopic asthma.’ Furthermore, they did not do allergy skin tests on the whole cohort and some of the so-called atopic eczema patients had negative skin prick tests. We are sure that Ghosh and colleagues will be continuing their follow-up of the cohort of infants and will a
1516
Warner, J A Warner, E A Miles, A C Jones
Child Health,
4
5
Warner JA, Miles EA, Jones AC, Quint DJ, Colwell BM, Warner JO. Is deficiency of interferon gamma production by allergen triggered cord blood cells a predictor of atopic eczema? Clin Exp Allergy 1994; 24: 423-30. Miles EA, Warner JA, Lane AC, Jones AC, Colwell BM, Warner JO. T-lymphocyte activation at birth: implications for atopy. Pediatr Allergy Immunol (in press). Holt PG, Clough JB, Holt BJ, Baron-Hay MJ, Rose AH, Robinson BWS. Genetic risk for atopy is associated with delayed postnatal maturation of T-cell competence. Clin Exp Allergy 1992; 22: 1093-99. Van Asperen PP, Mukki A. Role of atopy in the natural history of wheeze and bronchial hyperresponsiveness in childhood. Pediatr Allergy Immunol 1994; 5: 178-83. Holt PG. A potential vaccine strategy for asthma and applied atopic disease. Lancet 1994; 344: 456-58.
Improvement of atopic dermatitis by reduced salt intake SiR-Barthel and Stuhlmuller (Oct 15, p 1089) report an improvement in atopic dermatitis when salt intake was restricted. They claim their report to be the first describing this effect. I draw these workers’ attention to the textbook of diseases in infancy’ by Heinrich Finkelstein, edited in 1912 in the same city (Berlin) in which these authors reside. Finkelstein clearly states on pages 559-61 the advantageous effect on eczema of what he termed "eczema soup", which basically consisted of a "desalted milk" and of salt-restricted food in general. He emphasised that a clinical amelioration, including an improvement in itching, can be expected within 3-4 days after salt restriction. A major improvement could be expected after about 3 weeks. Finkelstein also emphasised that only certain cases, mainly those with a major secretory component, respond to a reduced salt intake. However, he underscores the fact that this event is only a minor factor in the pathogenesis of this disease.
Hansjosef Böhles Department of Paediatrics, Johann Wolfgang Goethe-University, 60590 Frankfurt/Main, Germany
1
H Finkelstein. Lehrbuch der Säuglingskrankheiten: Fischer’s medicin. Berlin: Buchhandlung H Kornfeld, 1912.
CORRECTIONS timing of withdrawal bleeding a guide to endometrial safety during sequential oestrogen-progestagen replacement therapy?-The penultimate sentence of the summary of this article by Sturdee and colleagues (Oct 8, p 979) should have read "The prevalence of hyperplasia was 2-4% with 10 days of progestagen per cycle and 2.8% with 12 days". The caption of the figure should have read "First bleeding day after progestagen in relation to endometrial histology in 244 women with 3 days or less of variation between cycles". Is the
acid and peanut oil-In this letter by Truswell and Choudhury (Oct 8, p 1030) the phrase "Peterson and co-workers turned off the gas chromatograph..." should have begun with the word "Perhaps". We apologise for this omission.
Arachidonic