Symptomatic bradycardia probably due to tizanidine hydrochloride in a chronic hemodialysis patient.

A 71-year-old woman was admitted to the Wakayama Medical University Hospital with dizziness and loss of body balance. She had started hemodialysis at the age of 70. During the 33 days before admission, she received oral tizanidine hydrochloride at 3 mg/day for leg cramps. An admission electrocardiogram (ECG) demonstrated sinus bradycardia of 47 bpm. A 24-h ECG showed a total number of heartbeats of 68,779 and an average heart rate of 48 bpm. The maximum RR interval was 3720 msec. The electrophysiology test demonstrated slight sinus node dysfunction. There was no major organic heart disease. We suspected that tizanidine was the cause of bradycardia and stopped administration of this drug. After discontinuation symptoms gradually disappeared. The serum concentration of the tizanidine showed a higher trough of 1.78 ng/mL. In conclusion, because there was a disappearance of symptoms and a lightening of bradycardia due to the discontinuation of this medication, tizanidine was strongly suspected as the cause of severe bradycardia.

Study of plasma exchange for liver failure: beneficial and harmful effects.

Plasma exchange (PE) is often performed in combination with hemodialysis (HD) or hemodiafiltration. However, most methods were developed for the treatment of renal failure, so various problems may arise during treatment of liver failure (LF). In this study, we investigated the impact of PE alone and in combination with HD, and we assessed the complications of using PE + HD for the treatment of LF. After the exchange of 1 L of fresh frozen plasma (FFP), we measured serum electrolytes, HCO(3) (-), citrate, and acetate at 3 points in the circuit: A) the plasma separator inflow; B) after mixing of FFP/the dialyzer inflow; and C) the dialyzer outflow. Serum levels of human hepatocyte growth factor (HGF), acetate, and citrate were also measured before and after PE + HD. The levels of K(+), Ca(++), HCO(3) (-), and acetate were significantly decreased, and citrate was increased, between A and B. K(+) and citrate were decreased, while Ca(++), HCO(3) (-), and acetate showed an increase between B and C. Comparison of A with C revealed insufficient correction of the Ca(++) and citrate levels by HD. After PE + HD, serum levels of acetate and citrate were increased, while HGF was decreased. We concluded that i) when PE is performed, HD is also necessary for correction, but achieves insufficient correction of Ca(++) and citrate, ii) PE is non-selective and not only removes toxins but also beneficial substances such as HGF, iii) accumulation of acetate occurred, even with bicarbonate dialysate, since it also contains acetate for acidification.

Effect of percutaneous calcitriol injection therapy on secondary hyperparathyroidism in uraemic patients.

BACKGROUND: The impetus to develop percutaneous calcitriol injection therapy (PCIT) was the lack of therapeutic tools to treat secondary hyperparathyroidism (2HPT) resistant to medical therapy. METHODS: Nine dialysis patients resistant to intravenous calcitriol or calcitriol analogues underwent daily PCIT 5-10 times consecutively. The PCIT involved the injection of a volume of calcitriol equal to that of the enlarged parathyroid glands (PTGs) under ultrasonographic guidance. All patients had follow-up intravenous calcitriol after PCIT. RESULTS: The serum intact PTH concentration was markedly reduced following PCIT and was maintained for 12 weeks with intravenous calcitriol without significant changes in serum adjusted calcium and phosphorus concentrations. All patients tolerated PCIT without serious adverse events. Serum bone alkaline phosphatase concentrations and the volume of the enlarged PTGs were also significantly reduced. CONCLUSION: PCIT is a safe and effective treatment, which may also suppress parathyroid hyperplasia and improve bone turnover for refractory 2HPT.