Do shrimp-allergic individuals tolerate shrimp-derived glucosamine?

BACKGROUND: There is concern that shrimp-allergic individuals may react to glucosamine-containing products as shrimp shells are a major source of glucosamine used for human consumption. OBJECTIVE: The purpose of this study was to determine whether shrimp-allergic individuals can tolerate therapeutic doses of glucosamine. METHODS: Subjects with a history of shrimp allergy were recruited and tested for both shrimp reactivity via a prick skin test and shrimp-specific IgE by an ImmunoCAP assay. Fifteen subjects with positive skin tests to shrimp and an ImmunoCAP class level of two or greater were selected for a double-blind placebo-controlled food challenge (DBPCFC) using glucosamine-chondroitin tablets containing 1,500 mg of synthetically produced (control) or shrimp-derived glucosamine. Immediate reactions, including changes in peak flow and blood pressure, and delayed reactions (up to 24 h post-challenge) via questionnaire were noted and assessed. RESULTS: All subjects tolerated 1,500 mg of both shrimp-derived or synthetic glucosamine without incident of an immediate hypersensitivity response. Peak flows and blood pressures remained constant, and no subject had symptoms of a delayed reaction 24 h later. CONCLUSION: This study demonstrates that glucosamine supplements from specific manufacturers do not contain clinically relevant levels of shrimp allergen and therefore appear to pose no threat to shrimp-allergic individuals.

Thromboxane and prostacyclin in acute lung injury caused by venous air emboli in unanesthetized sheep.

In 4 unanesthetized sheep with lung lymph fistulas we studied the role of thromboxane A2 (TxA2) in the lung microvascular injury caused by 4 h of venous air embolism. In each sheep, we did paired air embolism experiments: control and after giving the TxA2-synthetase inhibitor, U63,557A. Inhibition of TxA2-synthetase did not affect the hemodynamic response to air emboli; lung lymph flow increased slowly but to the same final rate as with air alone. The pulmonary production of TxA2, estimated as the lymph concentration of thromboxane B2 (TxB2) X lymph flow, increased during air embolism in the control experiment but increased much less when TxA2-synthetase was inhibited. Similarly, prostacyclin (PGI2) production increased during air embolism but was reduced when TxA2-synthetase was inhibited. Our results suggest that TxA2 does not mediate the pulmonary hypertension caused by venous air emboli, but it might modulate the increase in lymph flow by acting on the lymphatic pump or affecting hemodynamics in the pulmonary microcirculation. Our results do not support that TxA2 mediates the injury caused by venous air embolism. Pulmonary production of PGI2 seems to depend on the pulmonary production of TxA2, as shown by the parallel changes of their metabolites during air embolization.