8 5 0 Editorial correspondence The Journal of Pediatrics May 1995

Reply To the Editor:

Our article focused on the association between Helicobacterpy- lori and a diverse group of symptoms in neurologically impaired patients; we did not devote significant attention to the variable na-

ture of clinical presentations. One of our patients who had refusal

to feed had been thought to have predominantly a behavioral dis- order. Only after documentation of H. pylori infection and a

prompt increase in appetite with effective therapy did it become clear that this was not a behavioral disorder. It is our belief that the

usual symptoms of H. pylori infection such as nausea, vomiting, dyspeptic symptoms, or anorexia could potentially lead to a num-

ber of behavioral responses in the neurologically impaired patient. It will be interesting to observe, as this diagnosis is pursued more aggressively in this group of patients, the full spectrum of clinical

manifestations. At the same time, for some of our patients H. py- lori infection was coexistent with other gastrointestinal problems,

particularly gastroesophageal reflux. Thus attributing a specific

behavior or symptom to the presence of H. pylori infection in a specific patient requires demonstration of improvement of this

symptom with effective therapy for Helicobacter infection, and documentation of resolution of the infectious process.

Roy Proujansky, MD Stephen Shaffer, MD

Nancy Vinton, MD Steven Bachraeh, MD

AlJ?ed L duPont Institute Wilmington, DE 19899

9/35/63157

Promotion of healthy eating habits in children

To the Editor: I enjoyed the article by Whitaker et al., ~ but was disappointed

that the results were only modest. During the study intervention,

the selection of low-fat food items by students in the school cafe- terias increased by 4% compared with baseline. The intervention involved modifying elementary school lunch menus to emphasize the low-fat entrees. The parents of the students were mailed a

package that included a modified menu, an educational pamphlet on healthy diets, and a letter explaining the availability of low-fat

diets in the menu. No component of the intervention directly ed-

ucated the children on the significance of low-fat diets in disease prevention. This specific component is essential for promoting pos-

itive behavior change. Behavior change can result from the modification of three types

of factors that influence health behaviors--predisposing factors,

enabling factors, and reinforcing factorsfl Predisposing factors in- clude individuals' knowledge, attitudes, and beliefs surrounding a

particular health issue. Enabling factors provide access to resources or teach particular skills to assist in the modification of the behav- ior. Reinforcing factors either positively or negatively influence a particular behavior to encourage and maintain behavior change. In

this study, the predisposing factors were not specifically ad- dressed.

Encouraging changes in the dietary habits of children for health

promotion and disease prevention can be a challenging and diffi- cult task. Effective change can be achieved by multiple and inte-

grative strategies that target all three types of factors that influence the behavior.

Sherry R. Crump, AID Morehouse School of Medicine

Department of Community Health and Preventive Medicine

720 Westview Dr. S.W. Atlanta, GA 30310

9/35/63154

REFERENCES

1. Whitaker RC, Wright JA, Koepsell TD, Finch A J, Psaty BM. Randomized intervention to increase children's selection of low-fat foods in school lunches. J PEmATR 1994;125:535-40.

2. Green LW. Prevention and health education. In: Last JM, Wallace RB, eds. Public health and preventive medicine. 13th edt. Norwalk, Connecticut: Appleton & Lange, 1992:787-802.

Reply To the Editor:

We agree, in principle, with an approach to dietary interventions that integrates different strategies for behavior change, 1 but we

deliberately omitted a direct educational component targeting the students. In choosing among intervention strategies, we considered

their potential efficacy, cost, ease of implementation, and general-

izability. Failure to consider these factors may lead to designing interventions that cannot be maintained in the study setting after the formal research has ended, or cannot be transferred to other settings where resources are more modest. Our approach, therefore,

was to find a minimal, rather than maximal, intervention that would result in changing a specific observed dietary behavior--selection of low-fat foods in school lunches.

Unfortunately, there is little evidence that changes in nutrition knowledge, attitudes, or beliefs in children (predisposing factors)

are related to changes in observed (as distinct from reported) di- etary behavior. 2 The beneficial effects, if any, of classroom nutri-

tion education on eating behavior have been hard to detect. Nutri- tion education curricula are difficult to implement evenly across

units of intervention (schools, classes, or students). School food- service departments may not have adequate resources, and teach- ers may already be burdened by competing curriculum demands (e.g., drug use and violence prevention).

We also believe that the simultaneous application of different strategies (for example, classroom nutrition education and altered food choice availability) may leave the investigator unable to de- termine the relative efficacy of each strategy. Those who wish to go on and implement components of a studied, multifaceted interven- tion may be unable to assess which components of the intervention

were most potent. Given these considerations, we decided on two interventions (in-

The Journal of Pediatrics Editorial correspondence 8 5 1 Volume 126, Number 5, Part i

creased availability of low-fat foods and menu labeling), applied

them in succession, and determined the relatively greater impact of the former. Both interventions are still in place in this school dis-

trict 2 years after the end of data collection. Our findings do not deny the potential value of attempting to influence nutrition knowledge, attitudes, and beliefs. However, had either of our

interventions also concurrently attempted to change these predis- posing factors, we would have been unable to say "what worked."

Robert C. Whitaker, MD, MPH Jeffrey A. Wright, MD

Department of Pediatrics University of Washington School of Medicine

Seattle, WA 98195

Thomas D. Koepsell, MD, MPH Bruce M. Psaty, MD, PhD

Department of Epidemiology University of Washington School of Public Health and

Community Medicine Seattle, WA 98195

Anita J. Finch, MS, RD Bellevue Public Schools, District No. 405

Bellevue, WA 98009 9/35/63155

R E F E R E N C E S

t. Green LW. Prevention and health education. In: Last JM, Wallace RB, eds. Maxcy-Rosenau-Last public health and preventive medicine. 13th ed. Norwalk, Connecticut: Appleton & Lange, 1992:787-802.

2. Contento IR, Manning AD, Shannon B. Research perspective on school-based nutrition education. J Nutr Educ 1992;24:247- 60.

Congenital nephrotic syndrome in neonatal lupus syndrome To the Editor:

Massengil et al.i reported the occurrence of nephrotic syndrome

in one 6-week-old and one 3-month-old child with infantile systemic lupus erythematosus (SLE), simulating a congenital nephrotic

syndrome. Both children were born to mothers without clinical or serologic evidence of SLE or other connective tissue disease. The authors stressed the importance of distinguishing infantile SLE from the neonatal lupus syndrome (NLS), a condition occurring in children born to mothers with SLE or some other connective tissue disease 2, 3 Most children with NLS have congenital heart block or

cutaneous SLE caused by transplacental transport of antibodies to

the fetus. Deposition of immunoglobulins and complement in car- diac tissue has been reported and implicated in the pathogenesis of congenital heart block. 4, 5 However, to the best of our knowledge,

nephrotic syndrome or nephritis has not been reported in NLS. An explanation could be that there is no antibody deposition in the fe-

ta! kidney, perhaps because the renal antigens involved are not yet

present. We studied renal tissue from an 18-week-old fetus born to a 28-

year-old woman with SLE Test results for anti-double-stranded

DNA, anticardiolipin, anti-IgG, and anti-ribonucleoprotein anti- bodies were positive, and the patient had low levels of the third and

fourth components of complement. The woman had a good response to prednisone therapy and never had clinical signs of re- nal disease. A renal biopsy was never performed. Eight months be-

fore, her first pregnancy ended in a stillbirth at 15 weeks. In the

eighteenth week of her second pregnancy, she had HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets),

and labor was induced. At that time she was still receiving a high dose of prednisone and had no clinical signs of active disease. Au-

topsy of the fetus did not show macroscopic or microscopic abnor-

malities. Renal histologic findings were in accordance with fetal age, and no pathologic changes were observed. Immunofluores-

cence microscopy demonstrated focal deposition of IgG, the third

component of complement and fibrin along capillary loops and in the mesangium of maturing deep cortical glomeruli, without dep-

osits of IgM, IgA, or the Clq subunit of the first component of complement. No deposits were found in primitive superficial cor- tical glomeruli. Studies with antibodies against IgA, IgG, IgM, the third component of complement, the c lq subunit of the first com-

ponent of complement, and fibrin showed no glomerular staining in

another t8-week and a 19-week-old fetus. These data suggest that gtomerular immunodeposits are proba-

bly present in at least some neonates born to mothers with SLE.

Their presence is apparently not sufficient to cause clinical symp- toms, because nephritis has never been reported in NLS. Alterna-

tively, lupus nephritis may occur in NLS but be unnoticed.

P. J. Westenend, MD Department of Pathology

University Hospital Nijmegen PO Box 9101

6500 HB Nijmegen, The Netherlands 9/35/62986

R E F E R E N C E S

1. Massengil SF, Richard GA, Donnelly WH. Infantile systemic lupus erythematosus with onset simulating congenital ne- phrotic syndrome. J PEDIATR 1994;124:27-31.

2. Kitridou RC, Mintz G. The neonatal lupus syndrome. In: Wallace D J, Hahn BH, Quismorio JP Jr, Klinenberg JR, eds. Dubois' lupus erythematosus. 4th ed. Philadelphia: Lea & Fe- biger, 1993:516-22.

3. Buyon JL. Neonatal lupus syndromes. Am J Reprod Immunol 1992;28:259-63.

4. Litsey SE, Noonan JA, O'Connor WN, Cottrill CM, Mitchell B. Maternal connective tissue disease and congenital heart block. Demonstration of immunoglobulin in cardiac tissue. N Engl J Med 1985;312:98-100.

5. Taylor PV, Scott JS, Gerlis LM, Esscher E, Scott O. Mater- nal antibodies against fetal cardiac antigens in congenital complete heart block. N Engl J Med 1986;315:667-72.