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• W1565411512 abstract "To the Editor: We describe a 70-year-old, well-educated woman with rapidly progressive dementia (RPD) with parkinsonism. Her medical history revealed a generalized epileptic insult of unknown cause in 2004, with a normal electroencephalogram and magnetic resonance imaging of the cerebrum. In January 2008, she was diagnosed with systemic lupus erythematosus (SLE) with severe renal insufficiency (renal clearance of 29 mL/min) owing to lupus glomerulonephritis class IV for which she was treated with prednisone and cyclophosphamide. During treatment, three generalized insults took place, for which she was treated with maintenance valproate monotherapy (500 mg two times a day), after which no epileptic insult occurred. A few months later, there was partial remission of the SLE; laboratory tests for lupus disease activity had improved. In contrast, cognition and gait rapidly deteriorated. Symptoms consisted of loss of interest, bradyphrenia, perseveration, apraxia, aphasia, agnosia, disorientation, and loss of memory. She did not appear depressed, and no hallucinations were observed. Performance on the Clock-Drawing Test, which is used to identify cognitive dysfunction, particularly constructional apraxia and executive function, was impaired (Figure 1A). Her cognitive screening test (CST) score (on a Dutch screening test comparable to the Mini-Mental State Examination) was 15 out of 20, indicating moderate cognitive impairment. All primitive reflexes were positive, and there was rigidity and tremor of the arms. She had difficulty with initiating gait. Her gait was slow, wide based, and short stepped. She had impairment of postural reflexes and a strong tendency to fall. For the Clock-Drawing Test, the patient is asked to draw a clock, put in all the numbers, and set the hands at 10 minutes past 11 o'clock. (A) Clock drawn in July 2008, after treatment with cyclophosphamide and 10 weeks of treatment with valproate. Inaccurate representation of 10 minutes past 11 o'clock with visuospatial organization well done. (B) Clock drawn in August 2008, after treatment with methylprednisolone and 17 weeks of treatment with valproate. Inability to make any reasonable representation of a clock. (C) Clock drawn in October 2008, 4 weeks after valproate was discontinued. Improvement of the Clock-Drawing Test. (D) Clock drawn 5 weeks after valproate was discontinued. Normal Clock-Drawing Test. RPD can develop subacutely over months, weeks, or even days and be quickly fatal. Because many RPDs are treatable, it is of paramount importance to evaluate and diagnose these patients quickly.1 The differential diagnosis of RPD includes neurodegeneration, encephalitis or meningitis, autoimmune disease, (para)neoplastic limbic encephalitis, and toxic-metabolic conditions.1 Total serum valproate levels were below therapeutic ranges, varying between 44 and 48 mg/L (therapeutic range 50–100 mg/L), and her serum ammonia level (12 μmol/L) was not high, making valproate intoxication and valproate-associated hyperammonemic encephalopathy unlikely. After extensive investigation, other causes of RPD were excluded, and it was assumed that the patient had neuropsychiatric SLE (NPSLE).2 She was treated with intravenous methylprednisolone for 3 days, followed by oral prednisone combined with mycophenolate mofetil. Meanwhile, cognition and gait further deteriorated. She became apathic, bedridden, and unable to perform any activity of daily life without help. Performance on the Clock-Drawing Test worsened (Figure 1B), and her CST dropped to 2, indicating severe cognitive dysfunction. Because NPSLE in general improves with immunosuppressive therapy,2, 3 this diagnosis was regarded as increasingly unlikely, and treatment with valproate was discontinued.4-8 Cognitive function and gait improved considerably after 2 weeks and were normal after 5 weeks. Performance on the Clock-Drawing Test 4 and 5 weeks after discontinuing valproate is shown in Figure 1C and D. Her CST score became normal (20/20). With hindsight, several hypotheses might explain the dramatic effects of valproate. First, valproate has high protein binding, more than 80%, mainly to albumin. Only free drug can cross the plasma membrane and bind with the receptor for pharmacological action. Free valproate concentrations mirror cerebral spinal fluid concentration. Valproate has a narrow therapeutic index, and toxicity may be encountered slightly above the upper end of the therapeutic range. For instance, a lowering of serum albumin from 40 to 30 g/L may double the amount of free valproate.9 In this patient, serum albumin was 24 g/L. Second, in renal failure, unknown compounds displace valproate from protein-binding sites and may increase the free fraction up to 20% to 30% (normally 10%).9 This patient had a toxic free fraction and concentration in the serum of 24% and 11 mg/L (normal range 5–10 mg/L) and liquor of 22% and 10 mg/L (normal range 5–10 mg/L). Third, mycophenolate is also a strongly protein-bound drug (92–98%) and may have further increased the free valproate level. Finally, this patient had an intermediate-metabolizer (CYP2C9*3) heterozygous genotype, which can also lead to a higher free valproate level.9 It was concluded that valproate intoxication caused by a too-high (toxic) free concentration could entirely explain the RPD. The subtherapeutic total serum valproate level was initially misleading. Neurotoxicity has been described only in patients with normal or high total levels of valproate.4-8 Conditions such as hypoalbuminemia and renal failure can lead to a significant increase in free concentrations, resulting in (neuro)toxicity even if the total valproate level is within or below therapeutic range. In patients with renal failure, hypoalbuminemia, or prescription of highly protein bound medication, monitoring of free valproate concentration is recommended. Free drug concentration of valproate is easily measured in clinical laboratories, and this method is widely available. Conflict of Interest: The editor in chief has reviewed the conflict of interest checklist provided by the authors and has determined that the authors have no financial or any other kind of personal conflicts with this paper. Author Contributions: MS, EH: Acquisition of data, concept, design and writing of the manuscript. JB, WH: Concept and design of the manuscript. JC, DH, PD, JB, JV: Concept of the manuscript. Sponsor's Role: None." @default.
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• W1565411512 date "2010-04-01" @default.
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• W1565411512 title "Reversible Rapidly Progressive Dementia with Parkinsonism Induced by Valproate in a Patient with Systemic Lupus Erythematosus" @default.
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• W1565411512 doi "https://doi.org/10.1111/j.1532-5415.2010.02795.x" @default.
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