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For hours, walk-ins and appointments.3 - 8 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Serum
0.5 mL
0.4 mL (Note: This volume does not allow for repeat testing.)
Red-top tube or gel-barrier tube
Serum should be separated from cells within one hour and transferred to a plastic transport tube.
Room temperature
Temperature | Period |
---|---|
Room temperature | 14 days |
Refrigerated | 14 days |
Frozen | 14 days |
Freeze/thaw cycles | Stable x3 |
Patient should have no radioactive isotopes administered 24 hours prior to venipuncture.
Nonserum specimen; gross hemolysis; gross lipemia
Measurement of P/Q-type voltage-gated calcium channel (VGCC) antibodies as an aid in the diagnosis of Lambert-Eaton myasthenic syndrome (LEMS)
Radioimmunoassay (RIA)
0.0–30.0 pmol/L
Voltage-Gated Calcium Channels (VGCCs) are transmembrane protein structures that are activated by changes in local electrical membrane potential.1 Multiple types of VGCCs have been described in both the central nervous system and peripheral tissue.1,2 Activation induces changes in protein conformation allowing the influx of calcium ions into cells. VGCCs are classified according to their pharmacological properties as P/Q-, N-, L-, T- or R-type channels.3 P-type VGCCs are associated with Purkinje neurons of the cerebellum and Q-type VGCCs with cerebellar granule neurons.1 Together, P/Q-type VGCCs are primarily involved in acetylcholine release from motor nerve terminals.2,4
Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder of neuromuscular transmission with distinctive pathophysiological, clinical, electrophysiological and laboratory features.4-8 Pathologic antibodies cause a down-regulation of P/Q-type VGCCs diminishing the acetylcholine-mediated transmission of the signal from the presynaptic nerve to skeletal muscles and thus, impairing muscle contraction.4,6-10 Patients with LEMS invariably experience progressive proximal muscle weakness, often accompanied by general fatigue, autonomic symptoms and areflexia.5,6 The majority of cases occur as a paraneoplastic disorder (P-LEMS) associated with a malignant tumor that is most frequently a small cell lung cancer (SCLC).4-7,9,11 Other malignancies that have occasionally been associated with Lambert-Eaton myasthenic syndrome including non-small cell and mixed lung carcinoma, prostate cancer, thymoma and lymphoproliferative disorders.7,13 SCLC is a poorly differentiated, neuroendocrine tumor that expresses P/Q-type (as well as N- and L-type) VGCC.4,7,10-14 In P-LEMS, the initial humoral autoimmune response is generated against the VGCC of tumor cells and engenders pathologic antibodies that cross-react with VGCC of presynaptic nerve endings. 4,6,7,10,12 The onset of neurological symptoms in LEMS patients will often predate the detection of the tumor, and the survival time of the P-LEMS patients is significantly longer than that of those with SCLC without neurological dysfunction.6,7,13,15,16 Prognosis is related to the presence of cancer or autoimmune disease and the severity/distribution of muscle weakness.6 Cause of death in patients with SCLC associated LEMS is typically tumor progression, whereas LEMS that is not associated with malignancy does not reduce life expectancy.6
Order Code | Order Code Name | Order Loinc | Result Code | Result Code Name | UofM | Result LOINC |
---|---|---|---|---|---|---|
140640 | VGCC Antibody | 31024-3 | 000000 | |||
140640 | VGCC Antibody | 140686 | VGCC Antibody | pmol/L | 31024-3 |
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