The maximum infusion rate for Cleviprex is 32 mg/hour. Most patients in clinical trials were treated with doses of 16 mg/hour or less. Because of lipid load restrictions, no more than 1000 mL (or an average of 21 mg/hour) of Cleviprex infusion is recommended per 24 hours. In clinical studies, no significant changes occurred in serum triglyceride levels in the Cleviprex treated patients. There is little experience with infusion durations beyond 72 hours at any dose. The infusion can be reduced or discontinued to achieve desired blood pressure while appropriate oral therapy is established. Safety information
Cleviprex is intended for intravenous use. Titrate drug depending on the response of the individual patient to achieve the desired blood pressure reduction. Monitor blood pressure and heart rate continually during infusion, and then until vital signs are stable. Patients who receive prolonged Cleviprex infusions and are not transitioned to other antihypertensive therapies should be monitored for the possibility of rebound hypertension for at least 8 hours after the infusion is stopped. In clinical trials, the safety profile of clevidipine was generally similar to sodium nitroprusside, nitroglycerin, or nicardipine in patients undergoing cardiac surgery.Cleviprex is contraindicated in patients with allergies to soybeans, soy products, eggs, or egg products; defective lipid metabolism such as pathologic hyperlipemia (rare genetic disorders characterized by abnormal triglyceride metabolism), lipoid nephrosis, or acute pancreatitis if it is accompanied by hyperlipidemia; and in patients with severe aortic stenosis. Hypotension and reflex tachycardia are potential consequences of rapid upward titration of Cleviprex.
Hereditary pyropoikilocytosis (HPP) is an autosomal recessive form of hemolytic anemia characterized by an abnormal sensitivity of red blood cells to heat and erythrocyte morphology similar to that seen in thermal burns or from prolonged exposure of a healthy patients blood sample to high ambient temperatures. Patients with HPP tend to experience severe hemolysis and anemia in infancy that gradually improves, evolving toward typical elliptocytosis later in life. However, the hemolysis can lead to rapid sequestration and destruction of red cells. Splenectomy is curative when this occurs. HPP has been associated with a defect of the erythrocyte membrane protein spectrin and with spectrin deficiency. It was characterized in 1975. It is considered a severe form of hereditary elliptocytosis. Causes
Mutations of the alphaspectrin gene causes this disease. HPP can be considered as a subset of hereditary elliptocytosis. Diagnosis
Genetic testing for the presence of mutations in protein molecules is considered to be a confirmatory testing technique. It is important to know the risks regarding the transmission and dangers of HPP. Treatment
Splenectomy is a possible treatment

See also
Erythrocyte
Poikilocytosis
List of hematologic conditions

References


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