Nephrolithiasis and Nephrocalcinosis From Topiramate Therapy in Children With Epilepsy.

INTRODUCTION: Adults treated with topiramate may develop nephrolithiasis, but its frequency in children on topiramate is unknown. Topiramate inhibits renal carbonic anhydrase, which can lead to renal tubular acidosis and hypercalciuria. We studied 40 consecutive children who initiated topiramate therapy for seizures between January 1997 and February 2003, followed for a mean of 36 months. METHODS: Serum electrolytes, urinary calcium/creatinine ratios, and renal ultrasonography were performed before topiramate and every 6 months thereafter. RESULTS: Four children developed nephrolithiasis and/or nephrocalcinosis, which resolved on discontinuation of topiramate. In 40 patients, the mean urinary calcium/creatinine ratio increased over time (P < 0.001). The mean serum bicarbonate in 40 patients decreased over time (P < 0.01). Twenty-three children had urinary calcium/creatinine ratios before topiramate. Nine children with baseline hypercalciuria (defined as urinary calcium/creatinine >0.21) were compared with the 14 children with baseline normal urinary calcium excretion. A greater increase in urinary calcium/creatinine ratios occurred in hypercalciuric children (P < 0.001) and a greater decrease in serum bicarbonate levels occurred in the hypercalciuric children (P < 0.05) compared with children with baseline normal calcium excretion. Greater urinary calcium excretion was associated with increasing doses of topiramate (P = 0.039). CONCLUSION: Our study shows that long-term therapy with topiramate in children is associated with persistent hypercalciuria and metabolic acidosis, which can lead to nephrocalcinosis and/or nephrolithiasis. All children initiating topiramate therapy should have baseline and follow-up urinary calcium/creatinine studies, serum electrolytes, and periodic renal ultrasonography, if the urinary calcium/creatinine ratio increases to a level above normal for age.

Guillain-Barré syndrome.

• Based on strong research evidence, in countries where poliomyelitis has been eliminated, GBS is the most common cause of acquired paralysis in children. (9) • Based on strong research evidence, GBS describes a spectrum of disorders caused by an autoimmune reaction against peripheral nerve components, including the myelin sheath and the axon. (10)(11) • Based on strong research evidence, GBS usually is preceded by a bacterial or viral infection, less likely by vaccination in the 1 to 4 weeks before onset. The strongest relationship is with infection by C jejuni. (12)(13) • Based on strong research evidence, GBS in children most often presents with symmetrical ascending paralysis, diminished or absent reflexes, and often severe pain. Pain may lead to a delay in diagnosis. (2) (3)(9)(14) • Based on strong research evidence, the progressive phase peaks in 7 to 14 days and can lead to various levels of weakness, from abnormal gait to total paralysis, cranial nerve weakness, pain, respiratory compromise, and autonomic instability. (2) • Based on some research evidence and consensus, children require hospitalization and often intensive care until their condition stabilizes because of significant risk of respiratory compromise and autonomic instability. (15) • Based on strong research evidence in adults and some research evidence in children, IVIG and plasma exchange hasten recovery from GBS in patients with impaired ability to ambulate. (4)(6) • Based primarily on consensus, IVIG is the treatment of choice in children with GBS. (6)(9)(15) • Based on strong research evidence, the prognosis for full functional recovery in childhood GBS is excellent. (2)(8)(9).