Malignancy creatine kinase

A marked increase in creatine kinase activity without neuroleptic malignant syndrome has been previously described (SEDA-21, 48) and, another report has further emphasized this possibility (525). 

A 19-year-old schizophrenic patient taking risperidone 6 mg/day and olanzapine 20 mg/day had a creatine kinase activity of 6940 U/l without clinical manifestations of neuroleptic malignant syndrome when he switched to clozapine (dose not stated) the creatine kinase fell to about 300 U/l. Because he developed granulocytopenia, he was given quetiapine instead, and the creatine kinase again rose to 3942 U/l but fell after 4 days to 389 U/l without withdrawal of quetiapine. 

Neuroleptic malignant syndrome has been associated with clozapine (SEDA-22, 58) (98), although some doubts were expressed about the features of earlier cases. The presentation can be different from that associated with traditional antipsychotic drugs for example, the patient may not develop rigidity or a rise in creatine kinase activity (SEDA-25, 62). In the light of two cases, a 35-year-old man and a 62-year-old woman, the literature was comprehensively reviewed and the characteristics of neuroleptic malignant syndrome due to clozapine and typical neuroleptic drugs were compared (99). Causation with clozapine... 

Neuroleptic malignant syndrome and subsequent acute interstitial nephritis has been reported in a 44-year-old woman (102). This patient met the main criteria for neuroleptic malignant syndrome, although she did not develop rigidity or a rise in creatine kinase activity. On the other hand, abnormal creatine kinase activity and signs of myotoxicity were respectively found in 14% and 2.1% of patients who took clozapine for an average of 18 months (n = 94) (103). 

A 22-year-old man developed atypical neuroleptic malignant syndrome while taking clozapine (104). He vomited and was sweating and agitated but afebrile, with mild hypertension (maximum 156/96 mmHg) and a tachycardia, with marked increases in white blood cell count (32 x 109/1), neutrophils (25 x 109/1), and creatine kinase (1442 IU/1) a similar syndrome occurred while he was taking haloperidol. 

A 67-year-old man with bipolar disorder became confused, delirious, and manic (99). His only medications were olanzapine 10 mg/day and divalproex sodium 500 mg bd. On day 6, typical neuroleptic malignant syndrome developed. He had a fever (39.9°C), obtundation, rigidity, tremor, sweating, fluctuating pupillary diameter, labile tachycardia and hypertension, hypernatremia, and raised serum creatine kinase. Olanzapine was withdrawn and the syndrome resolved by day 12. 

A 23-year-old woman had some of the features of the serotonin syndrome (mental status changes, sweating, tremor, and fever) however, the large rise in creatine kinase activity, extreme lead-pipe rigidity, and the abrupt onset suggested neuroleptic malignant syndrome rather than the serotonin syndrome (104). 

A 30-year-old man who had taken olanzapine 20 mg/ day for 10 days developed typical neuroleptic malignant syndrome with raised body temperature (39.7°C), obtundation, tremor, rigidity, sweating, fluctuating pupillary diameter, tachycardia, labile hypertension, raised serum creatine kinase activity, and severe hypernatremia (190 mmol/1) (108). 

A 50-year-old man who was treated with ziprasidone 40 mg bd for 3 weeks had a substantial rise in creatine kinase activity without any evidence of muscle trauma, stiffness, or swelling or any signs of neuroleptic malignant syndrome (29). There was no renal insufficiency or compartment syndrome. 

Raised plasma creatine kinase concentration and white cell count are suggestive (but not conclusive) of neuroleptic malignant s)mdrome. There is some clinical overlap with the serotonin syndrome (see... 

The authors believed that symptoms in this case resembled the neuroleptic malignant syndrome, based on the combination of muscle rigidity, pyrexia, signs of autonomic disturbance, and altered consciousness. They did not think that the raised serum creatine kinase activity was associated with rhabdomyolysis. 

The procedure was continued with a propofol infusion. No treatment for malignant hyperpyrexia was undertaken and no other markers for malignant hyperpyrexia were observed. She made a normal recovery from anesthesia. Creatine kinase activities were raised at 2370 U/1 intraoperatively and 18 046 U/1 at 20 hours postoperatively. 

Malignant hyperthermia is probably due to the inability of certain individuals to control calcium concentrations in the muscle fiber and may involve a generalized alteration in cellular or subcellular membrane permeability, as suggested from research on pigs. This anomaly is genetically determined, but pre-anesthetic evaluation of susceptibility to malignant hyperthermia is a matter of controversy measurement of blood creatine kinase, ATP muscle depletion, or myophosphorylase A, histological... 

There is an association between (latent) muscular dystrophy (usually of the Duchenne or Becker type) and the production of rhabdomyolysis by suxamethonium (84,85,89,90). Suxamethonium can cause excessive muscle damage in these patients, as manifested not only by severe myoglobinemia and raised serum creatine kinase activity but also by acute exacerbation of muscle weakness postoperatively (SEDA-11, 121) (7,29,84,91,92). Massive potassium release can result in hyperkalemic cardiac arrest. Such patients may also develop features suggestive of the syndrome of malignant hyperthermia (93,94). Suxamethonium should not be used in patients with Duchenne muscular dystrophy or who have a family history suspect for the condition. 

A Glycophase DEAE-CPG column has been used to resolve arylsulfa-tase isoenzymes in serum and in concentrated urine samples from healthy controls, patients with colorectal cancer, and patients with malignant melanoma (B16). Creatine kinase MM and BB isoenzymes in brain and in muscle extracts have been resolved by anion exchange, but the MB isoenzyme was not detected either because of denaturation in the chromatographic process or because of adsorption to the column (KI8). The MB isoenzyme has been successfully detected on a DEAE-Glyco-phase column in the serum of a patient who had suffered a myocardial... 

Fishbein, W.N., V.W. Armbrustmacher, and J.L. Griffin. 1980. Skeletal muscle adenylate deaminase, adenylate kinase, and creatine kinase in myoadenylate deaminase deficiency and malignant hyperthermia. Clin. Res. 28 288A. 

Neuroleptic malignant syndrome is characterised by hyperthermia, severe muscle rigidity, autonomic dysfunction and altered mental state. A study of 24 patients who had received a variety of antipsychotics (chlorpromazine, zotepine, paliperidone, bromperidol, supliride, risperidone, thioridazine, olanzapine, fluphenazine, haloperidol, levoproma-zine) demonstrated a temporal relationship of muscle rigidity and elevated creatine kinase to fever [46 ]. 

Nisijima K, Shioda K. Temporal changes in serum creatine kinase concentration and degree of muscle rigidity in 24 patients with neuroleptic malignant syndrome. Neuropsychiatr Dis Treat 2013 9 853-9. 

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