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Citrullinemia is an autosomal recessive urea cycle disorder that causes ammonia and other toxic substances to accumulate in the blood. [1] Two forms of citrullinemia have been described, both having different signs and symptoms, and are caused by mutations in different genes. Citrullinemia belongs to a class of genetic diseases called urea ...
An accumulation of ammonia during the first few days of life leads to poor feeding, vomiting, seizures, and the other signs and symptoms of type I citrullinemia. Treatment for this defect includes a low-protein diet and dietary supplementation with arginine and phenylacetate. Arginine allows the urea cycle to complete itself, creating the ...
As one of the urea cycle disorders, citrullinemia type I needs to be distinguished from the others: carbamoyl phosphate synthetase deficiency, argininosuccinic acid lyase deficiency, ornithine transcarbamylase deficiency, arginase deficiency, and N-Acetylglutamate synthase deficiency. Other diseases that may appear similar to CTLN1 include the ...
The drug or other substance has a high potential for abuse. The drug or other substance has a currently accepted medical use in treatment in the United States or a currently accepted medical use with severe restrictions. Abuse of the drug or other substances may lead to severe psychological or physical dependence.
Citrullinemia type II [1] Inborn errors of organic acid metabolism. Methylmalonic acidemia (Cbl C,D) [1] Malonic acidemia [1] 2-Methyl 3-hydroxy butyric aciduria [1] Isobutyryl-CoA dehydrogenase deficiency [1] 2-Methylbutyryl-CoA dehydrogenase deficiency [1] 3-Methylglutaconyl-CoA hydratase deficiency [1] Glutaric acidemia type II
Hemolytic disease of the newborn (anti-Rhc) can range from a mild to a severe disease. It is the third most common cause of severe HDN. Rh disease is the most common and hemolytic disease of the newborn (anti-Kell) is the second most common cause of severe HDN. It occurs more commonly in women who are Rh D negative. [citation needed]
Pulmonary surfactant is used as a medication to treat and prevent respiratory distress syndrome in newborn babies. [1] Prevention is generally done in babies born at a gestational age of less than 32 weeks. [1] It is given by the endotracheal tube. [1] Onset of effects is rapid. [2] A number of doses may be needed. [2]
The need for treatment depends on bilirubin levels, the age of the child, and the underlying cause. [1] [3] Treatments may include more frequent feeding, phototherapy, or exchange transfusions. [1] In those who are born early more aggressive treatment tends to be required. [1] Physiologic jaundice generally lasts less than seven days. [1]