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Biomedical subjects

H G Morris

Publications and source records attributed to H G Morris.

At least 55 records · Page 3Linked to original sources

Short-term efficacy and side effects of cloprednol in children with asthma.

Efficacy and safety of alternate-day prednisolone compared to single daily cloprednol were evaluated over a six-week period in 11 children with severe asthma requiring in-residence medical supervision and long-term corticosteroid therapy. Clinical indices of efficacy, including daily pulmonary symptom scores, number of asthma attacks, asthma severity scores, and bronchodilator usage, all favored cloprednol. Afternoon pulmonary function tests (FEV1, FVC, and PEFR) were all significantly improved during the cloprednol period. Although plasma cortisol values remained within the broad range of normal during the cloprednol period, mean values were consistent with partial pituitary-adrenal suppression similar in degree to that observed 24 hours after administration of an alternate-day program of prednisolone therapy. The results of this trial showed cloprednol in single daily doses to be more effective than prednisolone in alternate doses for the treatment of children with severe asthma.

Adolescent↗

Leukocyte cyclic adenosine monophosphate in asthmatic children. Effects of adrenergic therapy.

Blood specimens for measurement of leukocyte cyclic adenosine monophosphate (AMP) were obtained at weekly intervals from asthmatic children who were participating in a double-blind, crossover study to compare the effects of two adrenergic agents and a placebo. When patients were treated with the placebo, the basal measurements and the cyclic AMP responses of leukocytes to in vitro stimulation with epinephrine (10(-4) M) were similar to those of normal subjects but within one week after initiation of treatment with an adrenergic bronchodilator, leukocyte cyclic AMP responses to adrenergic stimulation in vitro decreased and remained low during the remainder of the treatment period. Within one week after discontinuation of adrenergic therapy, leukocyte cyclic AMP responses returned to the control level. Our results indicate that the alterations in leukocyte cyclic AMP metabolism which have been observed previously in asthmatic patients may result from medications used for treatment of asthma.

Adolescent↗

Adrenergic desensitization in leukocytes of normal and asthmatic subjects.

Cyclic AMP was measured in leukocytes of normal and asthmatic subjects before and after one week of treatment with equal amounts of ephedrine. During the control and placebo periods, the measurements of cyclic AMP in leukocytes of asthmatic subjects were similar to those of normal individuals. After one week of treatment with ephedrine, both groups exhibited suppression of the leukocyte cyclic AMP response to adrenergic stimulation in vitro: however, the suppression of response was significantly greater in asthmatic subjects (p less than .u1). Subcutaneous administration of epinephrine was followed by further suppression of the leukocyte cyclic AMP response to in vitro stimulation which was similar in both groups during all treatment periods. The results indicate that in vivo exposure to adrenergic medications is followed by desensitization of the leukocyte responses to subsequent adrenergic stimulation in vitro. After administration of small doses of medication, the severity and/or duration of desensitization is significantly greater in asthmatic leukocytes.

Adolescent↗

Growth of asthmatic children during treatment with alternate-day steriods.

The effects of specific doses of alternate-day treatment with prednisone on linear growth were evaluated in children with severe asthma. It was found that even the control patients who did not receive steroid therapy had heights that were significantly lower than those of normal children of the same age and sex. The average severity of growth suppression in children who received alternate-day or intermittent treatment with steriods did not differ from that of asthmatic control patients. However, evaluation of individual patterns of growth during the follow-up period revealed that children who received small doses of alternate-day treatment (mean dose of prednisone, 9 mg. q.o.d.; range, 2.5 to 14 mg.) had acceleration of growth, whereas children who received larger treatment doses (mean dose of prednisone, 30 mg. q.o.d.; range, 18 to 58 mg.) had further suppression of growth during the period of study. Additionally, patients who had previously been treated with daily corticosteroids failed to demonstrate "catch-up" growth after introduction of an alternate-day program (mean dose of prednisone, 17 mg. q.o.d.).

Age Factors↗

Growth and skeletal maturation in asthmatic children: effect of corticosteroid treatment.

The effects of corticosteroid treatment on growth and skeletal maturation were evaluated in 189 children with severe asthma who were referred for care at a residential treatment center. Height age on admission was significantly retarded in 8-10% of patients who had received little corticosteroid treatment previously and in 35% of patients who had taken steroids daily for more than 2 years. Children who had been treated with steroids intermittently or on alternate days were comparable to those who had taken steroids rarely. During an average residential period of 17 months, patients whose daily steroid treatment was discontinued had a relative gain in height age of 5 months; children who were started on daily steroids had a 5-month delay in growth. Evaluation of skeletal maturation at the time of admission revealed that skeletal age was more retarded than height age in the boys and less retarded than the height age in the girls. During the period of residence, the changes in bone age paralleled the changes in height age.

Adolescent↗

Plasma growth hormone concentration in corticosteroid-treated children.

Endogenous plasma growth hormone concentrations were measured in 23 children who were receiving daily corticosteroid therapy and in 10 control asthmatic children who had not received steroids for at least 8 months. The growth hormone concentrations were similar in the two groups of patients both during the fasting state and after insulin-induced hypoglycemia. 12 children, who were studied while receiving a large dose of prednisone and again 2 wk after steroid withdrawal, also showed no change in growth hormone concentration in relation to corticosteroid therapy. These findings suggest that deficiency of growth hormone is not the major mechanism responsible for the dwarfism of corticosteroid-treated children.

Adolescent↗

Metabolic effects of human growth hormone in corticosteroid-treated children.

The effects of administered human growth hormone (HGH) were evaluated in dwarfed, prepubertal children who were receiving long-term corticosteroid therapy for a chronic disease. During 11 complete metabolic balance studies, the eight corticosteroid-treated children demonstrated impaired response to large doses of HGH with minimal nitrogen and no phosphorus retention. In contrast, two hypopituitary subjects and two asthmatic children not receiving corticosteroid responded to the same preparations of HGH with nitrogen, potassium, and phosphorus retention. Six corticosteroid-treated children were given large doses of HGH (40-120 mg/wk for 4 to 8 months and showed no improvement in their retarded rate of growth, whereas the hypopituitary subjects showed accelerated growth during administration of 10-15 mg of HGH/wk. It is concluded that dwarfism in steroid-treated children results from corticosteroid-induced antagonism of the effects of HGH at the peripheral tissue level.

Adolescent↗