| pubmed-article:14981639 | pubmed:abstractText | Calcemic fluxes with hypocalcemia leading to hypercalcemia in acute rhabdomyolisis are poorly understood. Analyses in the literature of the factors modulating the blood calcium level include 2, possibly 3 systems. Conflicting results implicate the parathyroid hormone and vitamin D metabolites, but additional contribution from skeletal and muscle calcium ion deposition and dissolution have been cited in some cases, potentially even dominating control of blood calcium during recovery. We have had the opportunity to study in detail a patient presenting with the most severe rhabdomyolisis, serum creatine phosphokinase levels exceeding 10(6) U/L, thus providing an analysis that delineates major changes in regulatory factors controlling calcium status. We found an exaggerated and clearly defined, phasic sequence of changes in these factors that led to ostensibly atypical, biphasic hypercalcemia juxtaposing the transient and well-described hypocalcemia in such patients. Our conclusions help to clarify the controversy, adding substance to the argument that there is no disruption in the parathyroid hormone-vitamin D axis regulating blood calcium levels in this rare disease. | lld:pubmed |
