Acquired factors that affect plasma cholinesterase activity include pregnancy, liver disease, kidney failure, heart failure, thyrotoxicosis, and cancer, as well as a number of other drugs.If unrecognized by a clinician it could lead to awareness if anesthesia is discontinued whilst still paralyzed or hypoxemia (and potentially fatal consequences) if artificial ventilation is not maintained. Normal treatment is to maintain sedation and ventilate the patient on an intensive care unit until muscle function has returned. Blood testing for cholinesterase function can be performed.Mivacurium, a non-depolarizing neuromuscular blocking drug, is also metabolized via the same route with a similar clinical effect in patients deficient in plasma cholinesterase activity.Deliberate induction of conscious apnea using this drug led to its use as a form of aversion therapy in the 1960s and 1970s in some prison and institutional settings. This use was discontinued after negative publicity concerning the terrifying effects on subjects of this treatment and ethical questions about the punitive use of painful aversion. Mechanism of action
There are two phases to the blocking effect of suxamethonium. Phase 1 block
Phase 1 blocking has the principal paralytic effect. Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptors monovalent cation channel; a disorganized depolarization of the motor end-plate occurs and calcium is released from the sarcoplasmic reticulum. In normal skeletal muscle, acetylcholine dissociates from the receptor following depolarization and is rapidly hydrolyzed by acetylcholinesterase. The muscle cell is then ready for the next signal.
Patients are treated similarly to patients suffering the counterparts those with multiple myeloma except that the focus is treating or preventing kidney damage using chemotherapy to reduce production of the monoclonal light chain and thereby stopping, reversing, or preventing kidney injury. Plasma cell leukemia
Plasma cell leukemia is a form of multiple myeloma in which significant numbers of typically immature appearing plasma cells, i.e. plasmablasts, circulate in the blood. Very small numbers of plasma cells may reach the circulation in non-IgM multiple myeloma, non-IgM SMM, and, exceptionally, non-IgM MGUS. In these plasma cell dyscrasias, the presence of even very small numbers of circulating plasma cells is a poor prognostic indicator. In plasma cell leukemia, however, circulating plasma cells reach far higher numbers and at these circulating levels are associated with exceptionally poor  survival rates. The International Myeloma Working Group has defined the diagnostic criteria for plasma cell leukemia as the presence in blood of >2x109 plasma cells per liter or, alternatively, >20% of nucleated blood cells being plasma cells. More recently, the Group has suggested that values of 0.5x109 or 5%, respectively, may be more appropriate from a therapeutic viewpoint and therefore should be studied as a definitive criterion for the disease. A recent study supported this suggestion in finding that multiple myeloma patients with >5% circulating plasma cells had a prognosis much worse than that for multiple myeloma and similar to that for plasma cell leukemia. Flow cytometry immunophenotyping of blood cells to detect clonal phenotypes of plasma cells seen in multiple myeloma (e.g.