Our study indicates that SLIT had a positive effect on the reduction of a multiple symptom-medication score, mainly by significantly reducing rescue medication use, but had no significant effect on symptoms alone in children with rhinoconjunctivitis to grass pollen compared with a placebo.

Background: Recent work indicates that subcutaneous specific immunotherapy induces specific T-cell anergy, a shift in the TH1/TH2 ratio, and antibody production in favor of IgG4. There are few data on sublingual immunotherapy (SLIT), especially in children. Methods: We assessed the proliferation of peripheral blood mononuclear cells (³H-thymidine incorporation) and secretion of interleukin (IL)-4, interferon (IFN)γ and IL-5 (ELISA) after in vitro stimulation with allergen or phytohemagglutinin (PHA) in 29 children with allergic rhinoconjunctivitis receiving SLIT with grass pollen before, and after 1 and 2 years of treatment in a multicenter placebo-controlled study on the efficacy of the treatment. Further, non-specific intracellular production of IL-4, IL-13, IFNγ, IL-2, IL-10 and IL-5 (FACS) and serum total and specific IgE and IgG4 (ELISA) were analyzed. Results: Proliferation and IL-4 and IL-5 secretion after stimulation with allergen or PHA did not differ between the groups. In addition, we observed no effect of SLIT on intracellular cytokine production. IFNγ secretion after allergen coculture was comparable between the groups. Following PHA stimulation, IFNγ secretion was significantly higher in the SLIT group after 1 year, and a trend was observable already before and after 2 years of treatment, probably due to the inhomogeneity in the groups despite randomization (for age and asthma). No significant changes were observed for sIgE/sIgG4 ratios over time either in or between the groups. Conclusion: During 2 years of SLIT in children with a positive effect on rescue medication use, we observed no significant effects on in vitro T-cell immune responses or immunoglobulins. So far, pediatric studies demonstrating stable effects of SLIT on such reactions are missing, probably due to limited effects of SLIT on systemic immunologic reactions.

To study the sensitivity and allergy to latex in children, we investigated sera of 306 atopic and 303 non-atopic children (median age 4.5 years) for specific IgE to latex. In patients with specific IgE to latex, a questionnaire was sent to families and provocation tests were carried out. 60/306 atopic children (20.8%) and 1/303 non-atopic children (0.3%) showed specific IgE to latex in serum. The proportion of atopic, latex-sensitized and provocation positive children was 12/48 (25%). Specific IgE to latex was significantly higher (p < 0.03) in symptomatic compared to non-symptomatic patients. Specificity of a positive history was 92%, sensitivity 50%. Atopic dermatitis tended to be more prevalent among the 12 provocation positive atopic children (75%) compared to 36 provocation negative children (58%). There was a tendency that children of the symptomatic group underwent surgical interventions more frequently compared to non-symptomatic children. In conclusion, latex sensitization and latex allergy seem to have occurred more often in atopic children than previously known. Risk factors for the development of a sensitization to latex are atopy and the clinical diagnosis of atopic dermatitis; risk factors for a clinically manifest allergy to latex are an elevated specific IgE to latex, a positive history upon contact to material containing latex and probably frequent operations. Provocation tests should be performed to plan avoidance measures in latex-allergic children especially before surgical interventions.

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Uremic hyperphosphatemia still represents a considerable challenge to physicians treating patients with advanced kidney insufficiency. Phosphatebinding agents containing aluminium were the therapy of choice for many years, although, as we now 45know, at the price of serious organ damage such as osteopathy, anemia and encephalopathy (1-3). Since dietetic intervention is practicable in only a few cases, therapeutic strategies not involving aluminium were sought intensively. The use of calcium carbonate, today a preferred treatment for uremic hyperphosphatemia, goes back to the investigations of Clarkson et al. (4), who reported as early as 1966 that high-dose calcium carbonate therapy (20 g of calcium carbonate per day) could succeed in lowering serum phosphate levels in nondialysis patients with kidney insufficiency. In carefully administered balance tests, the same authors demonstrated that calcium carbonate binds phosphate primarily in the intestine. It was, however, also shown that a considerable percentage of the administered calcium is simultaneously absorbed by the intestine. Recent studies by Ramirez et al. ( 5 ) confirmed these results and showed that, while the administration of calcium carbonate does result in considerable intestinal binding of phosphate, 28% of the calcium carbonate taken is absorbed. Sheikh et al. (6) recently published similar results on calcium absorption following administration of calcium carbonate. Their in vivo investigations showed that, of a dosage of 2.5 g of calcium carbonate (1 . O g of calcium), about 250 mg of calcium were absorbed. Since most published therapeutic studies involve dosages of approximately 8.1 st 4.9 g of this substance (7), the amount of calcium absorbed by the body could, at least theoretically, be over 800 mg per day, or just under 300 g per year.It is well known that the pathogenesis of uremic osteopathy is not solely a result of phosphate retention. Insufficient 1,25 dihydroxy-vitamin D3 (1,25 (OH)*D3) formation is, of course, a major pathogenetic mechanism and administering 1,25 (OH)2D3 to patients with advanced or dialytically treated kidney insufficiency is appropriate. Simultaneous administration of 1,25 (OH)zD3 with calcium carbon-