Drug Interactions between Atamet and Ustell

CONTRAINDICATED: Levodopa is the precursor of dopamine, which in turn is converted to norepinephrine. As such, levodopa may precipitate severe hypertensive reactions in patients treated with nonselective monoamine oxidase inhibitors (MAOIs). The mechanism is enhanced peripheral catecholamine availability due to decreased degradation (MAOI activity) and increased synthesis (levodopa effect) of dopamine and probably also norepinephrine.

MANAGEMENT: The concomitant administration of carbidopa has been reported to prevent or blunt the hypertensive response by inhibiting peripheral conversion of levodopa to dopamine. However, some clinicians maintain that, with or without carbidopa, levodopa should not be used concurrently with nonselective MAOIs or other agents that possess MAOI activity (e.g., furazolidone, linezolid, methylene blue, procarbazine). At least 14 days should elapse between discontinuation of MAOI therapy and initiation of treatment with levodopa.

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MONITOR CLOSELY: The following interaction applies only to products containing sodium biphosphate that are used for bowel cleansing. It does not apply to products containing sodium biphosphate that are used for other, non-laxative related purposes.

Coadministration with agents that affect renal function or perfusion such as diuretics, ACE inhibitors, angiotensin receptor blockers, and nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the risk of acute phosphate nephropathy associated with the use of bowel-cleansing phosphate solutions. The risk and/or severity of fluid and electrolyte disturbances may also be increased, which can lead to serious adverse events including cardiac arrhythmias, seizures, and renal impairment. Acute phosphate nephropathy is a rare adverse event that presents as acute renal failure with minimal proteinuria and a bland urine sediment. Renal biopsy findings are consistent with nephrocalcinosis and include acute and/or chronic renal tubular injury, calcium-phosphate crystal deposition in the distal tubules and collecting ducts, and no other pattern of histological injury. The risk of acute phosphate nephropathy stems from the large phosphate load, fluid shifts, and decreased intravascular volume, which can be exacerbated in the presence of medications that affect renal perfusion or function. In reported cases, acute renal failure was typically diagnosed within two to five months of colonoscopy. These cases often resulted in permanent impairment of renal function, some requiring long-term dialysis.

MANAGEMENT: Caution is advised when bowel-cleansing phosphate preparations are prescribed in patients treated with agents that affect renal function or perfusion, particularly if they are frail or elderly. Bowel-cleansing phosphate preparations should not be used in patients who have impaired renal function or perfusion, dehydration, or uncorrected electrolyte abnormalities. In patients at risk for acute phosphate nephropathy, baseline and postprocedure labs including serum electrolytes, calcium, phosphate, BUN, and creatinine should be performed. Patients should be advised not to exceed the recommended dosage of their bowel-cleansing preparation and to drink sufficient quantities of clear fluids during before, during, and after bowel cleansing. Limited data suggest that administration of an electrolyte rehydration solution may attenuate the electrolyte abnormalities and hypovolemia. Hospitalization and intravenous fluid hydration may be appropriate for frail or elderly patients who may be unable to drink an adequate volume of fluid.

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MONITOR: Anticholinergic agents may decrease the absorption and oral bioavailability of levodopa. The proposed mechanism involves increased gastrointestinal transit time due to reduction of stomach and intestinal motility by anticholinergic agents, thereby increasing the gastric degradation of levodopa and reducing the amount available for absorption in the small intestine. In one study, pretreatment with trihexyphenidyl decreased the peak plasma concentration (Cmax) and delayed the time to peak concentration (Tmax) of levodopa in 3 of 6 healthy volunteers and 4 of 6 Parkinson patients. In another study, 42% of patients receiving levodopa with anticholinergic therapy developed abnormal involuntary movements compared to 19% of those treated with levodopa alone. Discontinuation or dosage reduction of anticholinergic therapy resulted in disappearance or amelioration of the symptoms in 9 of 10 cases, although subsequent aggravation of Parkinsonism necessitated resumption of anticholinergic therapy in 5 cases. There is also a case report describing a patient who required large doses of levodopa during concomitant therapy with homatropine. Following discontinuation of homatropine, the patient exhibited symptoms of levodopa toxicity and required a significant decrease in the levodopa dosage. Other studies have reported no effect of anticholinergic agents on levodopa blood levels or pharmacologic effects.

MANAGEMENT: Although certain anticholinergic agents may be used as adjunctive therapy in Parkinson's disease, clinicians should recognize their potential to reduce the oral bioavailability of levodopa in some patients. Pharmacologic response to levodopa should be monitored more closely whenever anticholinergic agents are added to or withdrawn from therapy, and the dosages of the drugs adjusted as necessary.

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