IgE suppressor T cells and atopy.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to G W Brasher.
Explore the source record for details and available documents.
In 21 affected members from 4 kindreds with hereditary angioedema, serum C1q levels generally were in the lower part of the normal range, with some values clearly below the lower limit of normal. The serum C1q levels in patients with hereditary angioedema were significantly depressed when compared with those in unaffected family members (p less than 0.001) and healthy control subjects (p less than 0.05). serum C1q levels were significantly (p less than 0.01) related to serum C4 levels which have been used as an indicator of disease activity in individual patients. C1q was stable during storage of serum samples at --20 degrees C for 60 days compared to storage at --70 degrees C. These studies indicate that depressed serum C1q concentrations may be seen in patients with hereditary angioedema and that the finding of this abnormality does not exclude the diagnosis.
Infantile asthama is an important pediatric problem and may cause substantial morbidity and mortality in this age group. The pathophysiology of allergic asthma involves a type I hypersensitivity reaction that is mediated by reaginic antibodies of the IgE class. Various factors predisposing to infantile asthma have been suggested but not confirmed. The differential diagnosis of infantile wheezing is of particular importance in this very young age group. An appreciation of the natural history and clinical characteristics of the disease, and of the important causative factors (foods, environmental inhalants, and respiratory infections), will aid the physician in the management of this problem.
It is postulated that both the initiation and the perpetuation of atopic disease occur as a result of a complex interaction of a genetically determined IgE response, increased permeability of the gastrointestinal and respiratory tracts, and an inherent metabolic instability that may be either localized or generalized. These three factors vary as a function of age and serve to explain the complicated natural history of allergic manifestations in atopic persons.
The role of T lymphocytes in atopic disease is of considerable importance because animal studies indicate that cells of this lymphoid series may influence reaginic antibody response. T lymphocyte subpopulations were studied in a group of 76 children with allergic respiratory disease. There was no statistical difference between atopic children with asthma and those with allergic rhinitis as compared with an age-matched control population of 20 non-atopic children in terms of levels of active T lymphocytes or total T lymphocytes. The results of this study do not support the concept of a T cell immunodeficiency in children with allergic respiratory disease.
A cerebral infarction occurred in a 37-year-old man following wasp stings. Computerized axial tomography documented the neurologic lesion.
Explore the source record for details and available documents.
In a group of 83 infants with asthma the major etiologic factors were found to be foods, environmental inhalants and respiratory infections. Airborne pollens and molds were found to be important in a small number of patients during the latter part of infancy. IgA deficiency and general anesthesia under the age of two years played a less well defined role in the pathogenesis of infantile asthma.
Human pancreatic fluid obtained from 2 subjects, each with a traumatic pancreatic fistula, contained detectable levels of IgG, IgA, IgM, IdD, and IgE. Although the mean IgG/IgA ratio for 10 random specimens was 1.63, the relative concentration was estimated to be less than unity when extreme values were eliminated. The molecular weight of IgA in pancreatic fluid was found to be comparable to that of the IgA molecule in serum. The absence of secretory component in pancreatic IgA provides further evidence that pancreatic IgA and serum IgA are similar. Serial determinations of the immunoglobulins stored at 4 degrees C showed a progressive decrease of all immunoglobulins, the order of stability being IgG approximately equal to IgA larger than IgM approximately equal to IgD. The demonstrated proteolytic activity in the specimens could account for the immunoglobulin decay and for the variable detection of IgM and IgD in pancreatic-fluid specimens.
The concept that hereditary angioedema assumes a benign form in some families is supported by documented disease in a 37-year-old man who had had recurrent attacks for one year but has been without symptoms for 14 years. Although numerous members of the patient's family have been affected during the past five generations, known causes of death have not been directly related to angioedema.
The role of IgA in the pathogenesis of infantile atopic disease was examined to determine whether the presence or absence of IgA in umbilical cord serum at birth could be correlated with the subsequent development of asthma and atopic eczema. Asthma occurred in four of the 50 infants without detectable IgA and in four of the 21 infants with detectable IgA. Atopic eczema occurred in three of the 50 infants without detectable IgA and in none of the 21 infants with detectable IgA. The difference in the incidence of atopic disease in the two groups was not statistically significant. The results of this study suggest that IgA deficiency in early infancy does not play a causal role in the development of atopy.
Complement component analysis is valuable for differentiating the various types of angioedema. Patients with hereditary angioedema have decreased levels of C1 esterase inhibitor and C4 in the presence of normal amounts of C3 and C1q. Acquired C1 esterase inhibitor deficiency secondary to malignant disease is also manifested by depressed C1 esterase inhibitor and C4, but decreased C1q levels distinguish it from hereditary angioedema. Normal values for these complement components are found in persons with allergic angioedema.
Infantile asthma presents a major therapeutic challenge to the practicing physician. The typical infant with asthma is a 14-month-old boy with recurrent episodes of wheezing since the age of seven months. Nasal eosinophilia is found less often than in older allergic children; however, 47 percent of infants with asthma will have either peripheral blood or nasal secretion eosinophilia to aid in the recognition of their atopic diathesis. The younger the infant (both at age of onset and at age of evaluation) the more likely are foods to be important factors in his allergic respiratory disease. His disease is unlikely to interfere with growth during infancy but may do so later in life. Hyposensitization is more likely to be required later in childhood if he does not respond to dietary manipulation. Despite appropriate therapy, wheezing may continue to be a problem during childhood and this is significantly correlated with the presence of a positive nasal smear at the time of initial allergy evaluation.