Atsushi Nomura

Myoclonus after Dextromethorphan Administration in Peritoneal Dialysis

Objective To report a case of myoclonus that developed after administration of dextromethorphan. Case Summary: A 64-year-old man was diagnosed with chronic renal failure due to diabetic nephropathy. The patient started on peritoneal dialysis 6 months before he was hospitalized. Two days before hospitalization, he developed cough and sputum and he visited an outpatient clinic, where dextromethorphan was prescribed. After taking a total of 30 mg of dextromethorphan, the patient developed myoclonus, tremor, agitation, slurred speech, and diaphoresis, which continued after he stopped taking the prescribed medicine. He visited an emergency department and was hospitalized for examination and treatment of myoclonus. Discussion: As the patients dialysis schedule was adequate, these symptoms were likely not due to uremia. The blood concentration of dextromethorphan (2.68 ng/mL) 60 hours after the 30-mg dose was higher than expected, and the blood concentration of dextrorphan, a metabolite, was lower than expected. We suspected that myoclonus was due to dextromethorphan-related symptoms induced by CYP2D6, which primarily metabolizes dextromethorphan. We analyzed the CYP2D6 gene for polymorphisms and identified CYP2D6 *1/*10. The patient had been taking metoprolol 40 mg/day for 2 years. The btood concentration of metoprolol 6 hours after administration was 13 ng/mL, which suggests that it was metabolized normally. Metoprolol has another metabolic pathway, via CYP2C19, and this may have led to its lack of accumulation. Moreover, metoprolol may have bound to active CYP2D6. Thus, affinity for CYP2D6, protein-binding rate, and lipid solubility may influence these drug interactions. Total scores for the Adverse Drug Reaction (ADR) probability scale and the Drug Interaction Probability Scale (DIPS) were 9 (highly probable) and 3 (possible), respectively. Conclusions: Myoclonus and other symptoms in this patient may have been caused by a prolonged high concentration of dextromethorphan due to CYP2D6 polymorphisms and drug interactions.

Rare Cause of Nuchal Pain: Calcification of the Alar Ligament

Calcification of the alar ligament is a rare condition, which usually develops in the elderly and tends to occur following traumatic injury or as a consequence of inflammatory disease. In crowned dens syndrome, calcium pyrophosphate dehydrate crystals deposit on the atlantoaxial joint. A 38-year-old woman with no history of traumatic injury presented with acute-onset neck pain. The patient was diagnosed with rheumatoid arthritis (RA) and …

A Fatal Case of Metformin-associated Lactic Acidosis

A 72-year-old woman with a history of type 2 diabetes mellitus was brought to the ER with metformin-associated lactic acidosis. She received continuous hemofiltration and hemodialysis, but the laboratory analyses showed no improvement. She died 11 hours after admission. Metformin is minimally bound to proteins and is readily dialyzable, but a prolonged period of dialysis is required, because metformin has a very large distribution volume and is distributed to multiple compartments. The peak blood metformin level was 432 mg/L in this case, which is one of the highest metformin concentrations ever reported, and eight hours of hemodialysis were not sufficient to reduce the serum level.

Association Between Staphylococcus aureus Bacteremia and Hospital Mortality in Hemodialysis Patients With Bloodstream Infection: A Multicenter Cohort From Japanese Tertiary Care Centers

Multiple studies have shown that Staphylococcus aureus bacteremia (SAB) has been a major cause of death in hemodialysis patients. We examined whether SAB is a risk for mortality among chronic hemodialysis patients in Japan where the standard vascular access is arteriovenous fistula (AVF). This was a multicenter, retrospective study of maintenance hemodialysis patients with bloodstream infection (BSI) from 2011 to 2013 at tertiary care centers in Japan. The endpoint was hospital mortality. Our cohort contained 32 SAB cases (14 MRSA and 18 MSSA) and 42 non‐SAB cases. Hospital mortality was higher among SAB cases than non‐SAB cases (46.9% vs. 23.8%, P = 0.038). In patients with BSI, SAB was significantly associated with hospital mortality after adjustment for potential confounders, including type of vascular access (OR 3.26). S. aureus was the leading cause of BSI and hospital mortality among this cohort. Therefore, initial empiric treatment should cover for S. aureus.

Ischemic Acute Tubular Necrosis due to Diltiazem Overdose

Diltiazem overdose has a high mortality rate due to cardiotoxicity associated with bradycardia and hypotension. A previous article reported that this type of overdose can cause acute tubular necrosis, which was not pathologically, but rather clinically, diagnosed. We herein report the case of a 55-year-old man who sustained nonoliguric acute kidney injury after taking 60 diltiazem tablets. A kidney biopsy performed six days after admission showed ischemic, not toxic, acute tubular necrosis. The patients kidney function improved spontaneously. In this case report, we clarify the cause of renal impairment caused by diltiazem overdose pathologically. Physicians should therefore consider ischemic acute tubular necrosis as a cause of kidney injury in patients with diltiazem overdose.

Warning: The ECG May Be Normal in Severe Hyperkalemia

A 77-year-old man with chronic kidney disease was admitted to our hospital due to acute kidney injury and hyperkalemia (serum potassium, 8.5 mEq/L) with a normal ECG finding (Picture 1). Hyperkalemia was caused by tumor lysis syndrome from gastric cancer and medications, including enalapril, carvedilol, and spironolactone. His hyperkalemia improved following the discontinuation of these medications and administration of sodium polystyrene sulfonate. The patient selected best supportive care, rather than chemotherapy, for his cancer and was discharged six days after admission. However, he returned five days later due to the deterioration of his general condition and hyperkalemia (serum potassium, 8.6 mEq/L). At this admission, the ECG showed sine-wave ventricular tachycardia (VT) (Picture 2). This case report suggests that ECG changes in hyperkalemia may be established not only by the level of hyperkalemia, but also by the development of hyperkalemia. Therefore, hyperkalemia should not be diagnosed based on ECG findings.

Dr. Takizawa, et al reply.

To the Editor: We appreciate Dr. Rothschild’s comments1 on our paper2. Regarding the diagnosis of rheumatoid arthritis (RA) of this patient, she met the 6 points of the … Address correspondence to Dr. N. Takizawa, Department of Rheumatology, Chubu Rosai Hospital, Minato-ku Komei 1-10-6, Nagoya, Aichi 455-8530, Japan. E-mail: ttkkzzww5959{at}gmail.com