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106. Wood trimmer's disease—an allergic reaction to molds in Swedish saw mills
VOLUME 61 NUMBER 3
calories, fat, pmtein,
sugar, vitamin,
and mineral
intake
lenged acutely develop alveolitis, whereas chronic, repeated
revealed no si@icant differences from the recommended
challenge isassociated withwaninof thelesiims+ SIurpur-
daily allowance @DA) values in either population regard-
pose in the present study was to determine if systemic
less of the severity of asthma, nor were there significant differences between the two populations. Evaluation of growth parameters, in&ding the height, weight, skin fold, and arm circumference percentiles appropriate for sex and age, revealed no significant differences between the asthmatic and normal control subjects. The mean and SEM for the asthmatic patients’ height and weight percentiles were 50% & 6% and 56% * 7%, respectively, while those for the control population were 44% 2 6% and 47% ? 6%. These data show that mild to moderately severe asthma in the 4- to Wyr-old, nonsteroid-dependent asthmatic child is not associated with significant growth retardation or nutritional deficiencies.
and/or local antibodies account for development or waning of disease. Class-specific IgG and IgA antiovalbumin (GA) antibodies were measured in serum and alveolar washes by an amplified enzyme-linked immunosorbent assay (ELISA). Four groups were included in both acute and chronic experiments: (1) immunized-challenged; (2) immunized-not challenged; (3) unimmunized-challenged; (4) normal rabbits. Higher levels of serum IgG anti-OA and alveolar IgG and IgA anti-OA were found in chronically than in acutely challenged animals. Chronically challenged animals not preimmunized developed serum IgG anti-O.4 levels comparable with immunized animals and developed more alveolar IgG anti-OA than immunized unchallenged controls. Alveolar IgA antibody levels were highest in immunized chronically challenged animals. Thus, neither IgG nor IgA anti-OA in serum or alveolar fluid correlate with disease; local IgA anti-OA may be protective but further studies are needed.
1w.
rowth
of chronic
asthmatic
children.
Kuo C. Chang, M.D., Donald Miklich, Ph.D., Gale Barwise, B.S., and Hyman Chai, M.D., Denver, Cola. The effects of asthma per se and various steroid treatment schedules on linear growth of 231 chronic asthmatic children, 6 to 16 yr of age, were evaluated with the use of subject’s matched healthy sibling parent-pair and norm as controls. The asthmatic children who had never received steroids had significant growth retardation, averaging l.QO standard deviation (SD) below normative mean (p < 0.001). Children who had received occasional steroids also manifested comparable growth retardation (0.92 SD below normative mean, p < 0.0001). Those who were Freated with alternate-day or daily steroids for 2 yr or longer had growth retardation averaging 1.91 and 1.95 SD below the normative mean, respectively (p < 0.0001). Growth stunting intermediate in severity was found in those who were treated with frequent intermittent steroids (1.26 SD below normative mean, p < 0.0001). Regardless of which control system was used, results were similar. The subjects’ matched siblings and parents had heights comparable with those of the normal population. These data suggest that genetic and socioeconomic factors played no role in the growth retardation in our asthmatic patients” Growth retardation found in chronic asthmatic children appears due to the disease itself and is accelerated by steroid therapy.
ocal and systemic IgG and IgA antibodies in experimental hypersensitivity eumonitis. J. E. Butler, Ph.D., P. Swanson, S., H. Ratajczak, Ph.D., and H. B. Richerson, D., Iowa City, Iowa. A rabbit model of hypersensitivity pneumonitis was used to study humoral immunologic responses following inhalation of aerosolized antigen. Animals immunized and chal-
104. Circulating hypersensitivity
immune cQm~lexes pneumonitis. (3.
W. H. Yang, M.D., R. l-i. Khan, Ph.D., C. K. Osterland, M.D., and Jo H. Toqood, Montreal, Quebec, and London, Ontario,
in
Canada.
In an attempt to better understand the immunopathogenesis of hypersensitivity pneumonitis (HP), circulating immune complexes (IC) were measured in sera from 10 patients with ascertained bird fancier’s disease (BF) vs 10 individuals with exposure to avian droppings and serologically detectable relevant precipitins but without clinical, radiologic or pulmonary function abnormalities (ABF). Eleven documented farmer’s lung (FL) were also studied. Heat-decomplemented sera were reacted with Fc receptor-bearing cells (“modified” Raji cells and, in parallel, L-1210 murine tumor cells, selected for a high density of surface Fc receptor); after washing, the absorbed IgG IC were quantitated by fixation of radiolabelled protein A. Controls included human aggregated IgG (HAGG), preformed complexes, and sera from normal: a-gammaglobulinemia and vasculitis individuals. 30th assays (Raji and L-1210) gave identical results which are herein expressed as equivalent units HAGG @g/ml). No significant difference in the frequency of IC was observed between BF and ABF (2 positives in each group); the positive BF had, however, much higher values (143 and 274 vs 34 and 67 for ABF). Only I FL had barely detectable IC (20; upper limits of normal for the tests - 20). From these results, it is concluded that the presence of circulating IgG IC is not a hallmark of HP; local pulmonary immune responses may be more relevant to me pathogenesis.
calories, fat, pmtein,
sugar, vitamin,
and mineral
intake
lenged acutely develop alveolitis, whereas chronic, repeated
revealed no si@icant differences from the recommended
challenge isassociated withwaninof thelesiims+ SIurpur-
daily allowance @DA) values in either population regard-
pose in the present study was to determine if systemic
less of the severity of asthma, nor were there significant differences between the two populations. Evaluation of growth parameters, in&ding the height, weight, skin fold, and arm circumference percentiles appropriate for sex and age, revealed no significant differences between the asthmatic and normal control subjects. The mean and SEM for the asthmatic patients’ height and weight percentiles were 50% & 6% and 56% * 7%, respectively, while those for the control population were 44% 2 6% and 47% ? 6%. These data show that mild to moderately severe asthma in the 4- to Wyr-old, nonsteroid-dependent asthmatic child is not associated with significant growth retardation or nutritional deficiencies.
and/or local antibodies account for development or waning of disease. Class-specific IgG and IgA antiovalbumin (GA) antibodies were measured in serum and alveolar washes by an amplified enzyme-linked immunosorbent assay (ELISA). Four groups were included in both acute and chronic experiments: (1) immunized-challenged; (2) immunized-not challenged; (3) unimmunized-challenged; (4) normal rabbits. Higher levels of serum IgG anti-OA and alveolar IgG and IgA anti-OA were found in chronically than in acutely challenged animals. Chronically challenged animals not preimmunized developed serum IgG anti-O.4 levels comparable with immunized animals and developed more alveolar IgG anti-OA than immunized unchallenged controls. Alveolar IgA antibody levels were highest in immunized chronically challenged animals. Thus, neither IgG nor IgA anti-OA in serum or alveolar fluid correlate with disease; local IgA anti-OA may be protective but further studies are needed.
1w.
rowth
of chronic
asthmatic
children.
Kuo C. Chang, M.D., Donald Miklich, Ph.D., Gale Barwise, B.S., and Hyman Chai, M.D., Denver, Cola. The effects of asthma per se and various steroid treatment schedules on linear growth of 231 chronic asthmatic children, 6 to 16 yr of age, were evaluated with the use of subject’s matched healthy sibling parent-pair and norm as controls. The asthmatic children who had never received steroids had significant growth retardation, averaging l.QO standard deviation (SD) below normative mean (p < 0.001). Children who had received occasional steroids also manifested comparable growth retardation (0.92 SD below normative mean, p < 0.0001). Those who were Freated with alternate-day or daily steroids for 2 yr or longer had growth retardation averaging 1.91 and 1.95 SD below the normative mean, respectively (p < 0.0001). Growth stunting intermediate in severity was found in those who were treated with frequent intermittent steroids (1.26 SD below normative mean, p < 0.0001). Regardless of which control system was used, results were similar. The subjects’ matched siblings and parents had heights comparable with those of the normal population. These data suggest that genetic and socioeconomic factors played no role in the growth retardation in our asthmatic patients” Growth retardation found in chronic asthmatic children appears due to the disease itself and is accelerated by steroid therapy.
ocal and systemic IgG and IgA antibodies in experimental hypersensitivity eumonitis. J. E. Butler, Ph.D., P. Swanson, S., H. Ratajczak, Ph.D., and H. B. Richerson, D., Iowa City, Iowa. A rabbit model of hypersensitivity pneumonitis was used to study humoral immunologic responses following inhalation of aerosolized antigen. Animals immunized and chal-
104. Circulating hypersensitivity
immune cQm~lexes pneumonitis. (3.
W. H. Yang, M.D., R. l-i. Khan, Ph.D., C. K. Osterland, M.D., and Jo H. Toqood, Montreal, Quebec, and London, Ontario,
in
Canada.
In an attempt to better understand the immunopathogenesis of hypersensitivity pneumonitis (HP), circulating immune complexes (IC) were measured in sera from 10 patients with ascertained bird fancier’s disease (BF) vs 10 individuals with exposure to avian droppings and serologically detectable relevant precipitins but without clinical, radiologic or pulmonary function abnormalities (ABF). Eleven documented farmer’s lung (FL) were also studied. Heat-decomplemented sera were reacted with Fc receptor-bearing cells (“modified” Raji cells and, in parallel, L-1210 murine tumor cells, selected for a high density of surface Fc receptor); after washing, the absorbed IgG IC were quantitated by fixation of radiolabelled protein A. Controls included human aggregated IgG (HAGG), preformed complexes, and sera from normal: a-gammaglobulinemia and vasculitis individuals. 30th assays (Raji and L-1210) gave identical results which are herein expressed as equivalent units HAGG @g/ml). No significant difference in the frequency of IC was observed between BF and ABF (2 positives in each group); the positive BF had, however, much higher values (143 and 274 vs 34 and 67 for ABF). Only I FL had barely detectable IC (20; upper limits of normal for the tests - 20). From these results, it is concluded that the presence of circulating IgG IC is not a hallmark of HP; local pulmonary immune responses may be more relevant to me pathogenesis.