Biomedical subjects

K N Bhat

Publications and source records attributed to K N Bhat.

5 recordsLinked to original sources

PubMed1977

Hypocomplementemia in chronic idiopathic urticaria.

A discrete evoking factor or presumed pathophysiologic mechanism is not recognized in the majority of patients with chronic urticaria or angioedema. Two cases are reported in which chronic urticaria was the main manifestation of an immune cutaneous vasculitis associated with hypocomplementemia attributable to classic and alternative mechanisms of complement activation. Among 72 consecutive patients evaluated for chronic urticaria, 10 additional patients with idiopathic urticaria were found to have hypocomplementemia. Of these, two had evidence of classic and alternative mechanisms of complement activation, five had evidence of only classic pathway activation, and three evidence of predominately or exclusively alternative pathway activation. Circulating immune complexes were found in the majority of patients with classic pathway activation. Hypocomplementemia may provide clues to pathophysiologic mechanisms operative in some patients with chronic urticaria.

Adult↗

PubMed1976

Plasma histamine changes during provoked bronchospasm in asthmatic patients.

Seven patients with bronchial asthma underwent bronchial inhalation challenge with aerosolized allergen extracts and methacholine. Simultaneously, venous blood samples were collected and histamine was measured. Each patient was challenged on successive days with an allergen extract to which he had no skin-sensitizing antibody (skin test-negative allergen), followed by methacholine and skin test-positive allergen. Bronchospasm was not induced by inhalation of skin test-negative allergens but was observed in all patients after methacholine and in the majority of patients after skin test-positive allergens. No changes in plasma histamine were detected after challenges with methacholine and skin test-negative allergens. After challenge with skin test-positive allergens, significant rises in plasma histamine were detected in 5 of 7 patients. Plasma histamine was elevated within the first 5 min after inhalation of aerosolized allergen, and elevations persisted as long as 30 min. These studies showing that histamine increases significantly in the plasma during allergen-induced asthma in man suggest that histamine should be considered as at least one of the mediators of bronchospasm in allergic asthma. Bronchospasm induced by the cholinergic drug methacholine, unlike allergen-induced bronchospasm, is not associated with changes in plasma histamine.

Administration, Intranasal↗

PubMed1976

Oral aspirin challenges in asthmatic patients: a study of plasma histamine.

Under carefully controlled conditions, seven aspirin-intolerant asthmatic patients were challenged with oral aspirin and experienced respiratory tract reactions with a decline in forced expiratory volume in 1 sec (FEV1) ranging from 26 to 64%. Venous blood samples, which were collected during the challenges, showed a rise in plasma histamine in all seven patients. The increase in plasma histamine occurred at the onset of their respiratory reactions and those patients with the most severe asthmatic responses were found to have the highest and most prolonged levels of plasma histamine. The aspirin-intolerant asthmatic patients were able to ingest Maalox or sodium salicylate without untoward effects, decline in FEV1 values or changes in plasma histamine levels. Ten non-asthmatic individuals and eight out of ten asthmatic control patients were able to ingest aspirin without any reactions or changes in their plasma histamine levels. However, two asthmatic control individuals, with severe asthma requiring treatment with moderate dosages of corticosteroids, were found to have elevated pre-challenge plasma histamine levels which increased during their ASA challenges despite the absence of respiratory reactions or changes in FEV1 values. It is possible that these two individuals were unsuspected aspirin-intolerant asthmatics. These studies demonstrate that asthmatic reactions to acetylsalicylates are associated with release of histamine into plasma in the subgroup of asthmatic patients with the aspirin-intolerance syndrome. Such a finding suggests that histamine may be one of the mediators of bronchospasm in aspirin-induced asthma.

Administration, Oral↗

PubMed1976

Reaction to radiographic contrast agents: new developments in etiology.

Although a significant amount of histamine is released into plasma during contrast media injections, there still is no evidence to support an immunologic basis underlying contrast media reactions. This study supports previous observations that suggest in vitro leucocyte challenge may be of predictive value in contrast media reactions. Lassar's study in dogs and this study in humans clearly shows that complement activation by alternative pathway occurs during contrast agent administration. However, pathophysiological significance of this observation is not clear.

Adult↗

PubMed1976

Activation of the alternative pathway of the complement system by radiographic contrast media.

Nine patients who underwent radiographic contrast media (RCM) infusion for diagnostic purposes were studied. Simultaneously, venous blood samples were collected and complement was measured. None of the patients had a clinical history of allergy to previous infusion of RCM. A significant drop in plasma complement (CH50) levels was detected in five of nine patients. The drop in CH50 was observed within the first 20 min after the initiation of RCM infusion. All five patients in whom a drop in complement was found showed a decrease in hemolytic C3, properdin, and factor B. In addition, by radial immunodiffusion low levels of C3, C6, properdin, and factor B were observed and split products of C3 and factor B were identified by immunoelectrophoresis. No significant changes in C1q and C4 were detected by radial immunodiffusion during the study of these five patients. This study strongly suggested that in some patients undergoing RCM infusion, activation of the complement system occurred and this activation appears to be through the alternative pathway.

Complement C1↗