Calcium channel abs (P/Q type) (Serum (s))

The primary pathophysiological disorder in Lambert-Eaton syndrome (LES) is a reduced release of the neurotransmitter acetylcholine from the nerve endings into the synaptic gap. The cause for this presynaptic defect is autoantibodies against voltage-dependent calcium channels (VGCC) localized in the membrane of the nerve cell. The VGCC control the neurotransmitter release at the neuromuscular junction and are the target antigens of the autoantibodies. In most people with Lambert-Eaton syndrome (LES) there is a malignant tumor, often a small-cell bronchial carcinoma, occasionally a prostate carcinoma, a thymoma or a lymphoproliferative disease. The LES belongs to the paraneoplastic syndromes and can occur at an early stage before the tumor is known. There is no malignant tumor in some of the patients. This idiopathic form is often associated with other autoimmune diseases, especially systemic lupus erythematosus, especially in patients under 30 years of age.

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