Carbonic anhydrase inhibitors can cause nephrolithiasis. We studied 20 patients receiving long-term carbonic anhydrase inhibitor treatment for periodic paralysis and myotonia. Three patients on acetazolamide (15%) developed renal calculi. Extracorporeal lithotripsy successfully removed a renal calculus in one patient and surgery removed a staghorn calculus in another, permitting continued treatment. Renal function remained normal in all patients. Nephrolithiasis is a complication of acetazolamide but does not preclude its use.
"The renal compensation for metabolic acidosis generates hypocitraturia which further augments the risk of crystalluria (Lamb et al., 2004; Go, 2005; Welch et al., 2006). TPM and ZNS monotherapy have been associated with rates of urolithiasis ranging from 1.5 to 3.7% (Leppik et al., 1993; Shorvon, 1996; Leppik, 1999; Wroe, 2007), whereas the stronger CA-I activity of AZM may account for its substantially higher rate of associated stone disease (reported as high as 15% (Tawil et al., 1993)). "
[Show abstract][Hide abstract] ABSTRACT: Children with refractory epilepsy who are co-treated with the ketogenic diet (KD) and carbonic anhydrase inhibitor (CA-I) anti-epileptic medications including topiramate (TPM) and zonisamide (ZNS) are at risk for urolithiasis. Retrospective chart review of all children treated with ketogenic therapy at our institution was performed in order to estimate the minimal risk of developing signs or symptoms of stone disease. Children (N=93) were classified into groups according to KD+/-CA-I co-therapy. Fourteen patients had occult hematuria or worse, including 6 with radiologically confirmed stones. Three of 6 calculi developed in the KD+ZNS group of 17 patients who were co-treated for a cumulative total of 97 months (3.1 stones per 100 patient months). One confirmed stone was in the KD+TPM group of 22 children who were co-treated for a cumulative total of 263 months (0.4 stones per 100 patient months). All six patients had at least three of five biochemical risk factors including metabolic acidosis, concentrated urine, acid urine, hypercalciuria and hypocitraturia. Standard of care interventions to minimize hypercalciuria, crystalluria and stone formation used routinely by pediatric nephrologists should also be prescribed by neurologists treating patients with combination anti-epileptic therapy. Non-fasting KD initiation, fluid liberalization, potassium citrate prophylaxis as well as regular laboratory surveillance are indicated in this high risk population.
Epilepsy research 06/2010; 90(1-2):151-6. DOI:10.1016/j.eplepsyres.2010.04.005 · 2.02 Impact Factor
"Others complain of paresthesias and cognitive impairment (described by patients as mental dullness, fogginess, inability to concentrate, or confusion) from acetazolamide. Acetazolamide-induced nephrolithiasis (calcium phosphate stones) is not uncommon [7,8] and can often be controlled with dose reduction and appropriate hydration under consultation with a urologist. "
[Show abstract][Hide abstract] ABSTRACT: Management considerations in hypokalemic periodic paralysis include accurate diagnosis, potassium dosage for acute attacks, choice of diuretic for prophylaxis, identification of triggers, creating a safe physical environment, peri-operative measures, and issues in pregnancy. A positive genetic test in the context of symptoms is the gold standard for diagnosis. Potassium chloride is the favored potassium salt given at 0.5-1.0 mEq/kg for acute attacks. The oral route is favored, but if necessary, a mannitol solvent can be used for intravenous administration. Avoidance of or potassium prophylaxis for common triggers, such as rest after exercise, high carbohydrate meals, and sodium, can prevent attacks. Chronically, acetazolamide, dichlorphenamide, or potassium-sparing diuretics decrease attack frequency and severity but are of little value acutely. Potassium, water, and a telephone should always be at a patient's bedside, regardless of the presence of weakness. Perioperatively, the patient's clinical status should be checked frequently. Firm data on the management of periodic paralysis during pregnancy is lacking. Patient support can be found at http://www.periodicparalysis.org.
Journal of Translational Medicine 02/2008; 6(1):18. DOI:10.1186/1479-5876-6-18 · 3.93 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A thorough assessment of vision with special attention to formal visual field testing is the cornerstone to decision making
in idiopathic intracranial hypertension. After the diagnosis of idiopathic intracranial hypertension has been established,
vision should be thoroughly assessed. If there is no visual loss, the patient can be followed carefully. In patients with
symptoms and only a few signs (eg, mild blind-spot enlargement), acetazolamide, 1 to 2 g, or another diuretic should be initiated.
In patients with progressive visual loss in whom maximal diuretic therapy fails and in those who on initial evaluation have
significant recent visual loss that does not respond to maximal diuretic therapy, optic nerve sheath decompression or lumbar
peritoneal shunting should be carried out. With all treatments, weight loss should be encouraged. All patients should be evaluated
regularly with visual field testing.
Current Treatment Options in Neurology 02/1999; 1(1):74-81. DOI:10.1007/s11940-999-0035-3 · 1.94 Impact Factor
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