Hyperamylasemia in acute carbon monoxide poisoning.
Of patients with acute carbon monoxide poisoning admitted to the Trauma Intensive Care Unit of the Osaka University Hospital 39.5% (17/43) manifested hyperamylasemia. Iszyme studies in 16 such patients revealed 87.5% to be of the salivary type. Two patients presented with hyperamylasemia of the pancreatic-salivary type. There was no pancreatic type hyperamylasemia among these patients, negating the possible involvement of the pancreas in hyperamylasemia from carbon monoxide poisoning. There was a statistically significant difference in amylase levels between the arterial and the external jugular venous blood, indicating the salivary gland as the organ mainly responsible for hyperamylasemia in carbon monoxide poisoning. Amylase levels coincided well with the level of consciousness and the base excess. The amylase levels correlated significantly with beta-glucuronidase levels, suggesting the hyperpermeability of cell membranes of the salivary gland as the chief factor in hyperamylasemia secondary to acute carbon monoxide poisoning.[1]References
- Hyperamylasemia in acute carbon monoxide poisoning. Takahashi, M., Maemura, K., Sawada, Y., Sugimoto, H., Ohashi, N., Yoshioka, T., Sugimoto, T. The Journal of trauma. (1982) [Pubmed]
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