MATER IALS AND METHODScourse of diarrh ea. Maln utrition has been report ed to increase the absorption of potentially harmful antigens (2) and to impai r imm une responses (3). A poor nutrition al state may thu s increase the risk of protracted diarrh ea as well as enhance susceptibility to other infectio ns and to gastroi ntestinal allergy. The nutritio nal state of even well-no urished infants deteriorat es rapidly during diarrhea, either because of loss of appetite, deliberate withholding of oral feeds, or partial malabsorption caused by viral invasio n ofenterocytes (4).Rapid reintrodu ction of oral feedings after rehydration has been advocated to coun terac t the pote nti al hazards related to fasting during diarrhea (5). We have previously shown that rapid refeeding results in earlier cessatio n of diarrhea in well-nourished children; also, cow milk produ cts are tolerated (6). A furt her shortening of diarrhea resulted from administratio n of hu man Lactobacillus stra in (Lactobacillus GG, Gefilac, Valio Finni sh Co-operative Dairies' Associatio n, Helsinki, Finland ) together with the rapid refeeding schedule (7). The mechanisms behind such a favorable outc ome remain poorly understood. Th e effect of nutritional therapy may be immunologically med iated and may prove important in eradicating enteric infections in the imm unocompromised host.The objective of the present study was to evaluate the effect of L actobacillus GG on the intestinal immune response triggered by rotavirus infection in well-nourished children. For th is pu rpose, we used the ELISPOT assay, which measures ISC and sASC amo ng circulating lymphocytes. T hese cells are arrested du ring their maturation cycle in peripheral blood, giving indirect evidence of gut local im m une respo nse (8-10).Patients. Forty-four well-no urished children (33.4% female), between 7 and 37 mo of age, were enro lled in the present study. Th ey were admitted for acute gastroen teritis of less than 7 d du ration at the Departm ent of Pediatrics, Ta mpere U niversity Hospital, during a rotavirus epidemic .Informed consent was obtaine d from the patients' pare nts, and the protocol was approved by the hospital's Committee on Ethical Practice.Ma nagement and samples. U pon ad mission, the children were weighed and clinically examin ed. The severity of dehydration (%) was estimated. Th e children were treated according to sta ndard practice: oral rehyd ration was accom plished in 6 h with a , solution containing Na" 60 mmo l/ L and glucose 144 mm ol/L (Osmosal Novum, Leiras, Turku , Finland) given at twice the estimated fluid loss with a minimum of 30 mL/kg body weight. Th e patients were weighed daily. Th e attending nurs es followed the quality (characterized as watery, loose, or solid) and number of stools and vomitus. The du ration of diarrh ea was counted 14 1

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Key Clinical MessageOne should always consider iron deficiency (without anemia) as the cause of persisting, unexplained unspecific, often severe, symptoms, regardless of the primary underlying disease. The symptoms of iron deficiency may arise from the metabolic systems where many proteins are iron containing. Long‐standing iron deficiency may be challenging to treat.

Objective: To study the effects of GH treatment for up to 42 months on bone mineral density (BMD) and bone turnover. Design and methods: BMD with dual energy X-ray absorptiometry, serum type I procollagen carboxyterminal propeptide (PICP), serum type I collagen carboxy-terminal telopeptide (ICTP) and serum IGF-I were assessed in 71 adults with GH deficiency. There were 44 men and 27 women, aged 20 to 59 (median 43) years. Thirty-two patients completed 36 months and 20 patients 42 months of treatment. Results:The BMD increased for up to 30-36 months and plateaued thereafter. In the whole study group, the maximum increase of BMD was 5.0% in the lumbar spine (P < 0.001), 5.9% (P < 0.01) in the femoral neck, 4.9% (NS, P > 0.05) in the Ward's triangle and 8.2% (P < 0.001) in the trochanter area. The serum concentrations of PICP (202.6 Ϯ 11.5 vs 116.3 Ϯ 5.4 mg/l; mean -Ϯ S.E.M.) and ICTP (10.5 Ϯ 0.6 vs 4.4 Ϯ 0.3 mg/l) doubled (P < 0.001) during the first 6 months of GH treatment but returned to baseline by the end of the study (130.0 Ϯ 10.4 and 5.6 Ϯ 0.7 mg/l respectively), despite constantly elevated serum IGF-I levels (39.6 Ϯ 4.1 nmol/l at 42 months vs 11.9 Ϯ 0.9 nmol/l at baseline; P < 0.001). The responses to GH treatment of serum IGF-I, PICP, ICTP (P < 0.001 for all; ANOVA) and of the BMD in the lumbar spine (P < 0.05), in the femoral neck and the trochanter (P < 0.001 for both) were more marked in men than in women. At the end of the study the BMD had increased at the four measurement sites by 5.7-10.6% (P < 0.01-0.001) in patients with at least osteopenia at baseline and by 0.1-5.3% (NS P < 0.05) in those with normal bone status (P < 0.001 for differences between groups; ANOVA). Among patients who completed 36-42 months of treatment, the number of those with at least osteopenia was reduced to more than a half. The response of BMD to GH treatment was more marked in young than in old patients at three measurement sites (P < 0.05-<0.001; ANOVA). In the multiple regression analysis the gender and the pretreatment bone mass appeared to be independent predictors of three measurement sites, whereas the age independently determined only the vertebral BMD. Conclusions: GH treatment in GH-deficient adults increased BMD for up to 30-36 months, with a plateau thereafter. Concurrently with the plateau in BMD the bone turnover rate normalized. From the skeletal point of view GH-deficient patients exhibiting osteopenia or osteoporosis should be considered as candidates for GH supplementation of at least 3-4 years.

Mannan-binding protein (MBP) is an acute phase reactant, and its deficiency is associated with the common opsonic defect and suspectibility to infections and atopic constitution. The aim of this study was to investigate the changes occurring in the serum level of MBP in infancy and during later childhood. We studied the serum concentration of MBP in 611 Finnish children of different ages and 110 adults by using an enzyme immunoassay. In an analysis of successive serum samples from infants at the day of birth and at the ages of 1 and 5 months, and at 1 and 2 years, the serum concentration of MBP increased significantly after birth, and was at its highest (the mean and median were 8.13 and 8.49 mgl-1, respectively) at the age of 1 month. After that, it declined to the initial level until the age of 5 months. The MBP concentration continued to decrease during childhood, and after the age of 12 years the MBP values reached the adult level. In Finnish adults the mean and median concentrations of MBP were 4.48 and 4.02 mgl-1, respectively, which seem to be higher than those reported previously in other populations. The high concentration of MBP in infants may best be explained by exposure to novel environmental antigens in early childhood, which suggests a protective role for MBP during the period of immaturity of the immunosystem. In older children the high level of MBP can probably be explained by childhood infections and the ensuing need of MBP.