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Phenylketonuria (PKU)-like symptoms, including more pronounced developmental defects, skin irritation, and vomiting, may appear when phenylalanine levels are near 20 mg/dL (1200 mol/L). [1] Hyperphenylalaninemia is a recessive hereditary metabolic disorder that is caused by the body's failure to convert phenylalanine to tyrosine as a result of ...
PKU was the first disorder to be routinely diagnosed through widespread newborn screening. Robert Guthrie introduced the newborn screening test for PKU in the early 1960s. [67] With the knowledge that PKU could be detected before symptoms were evident, and treatment initiated, screening was quickly adopted around the world.
At around age 4, children develop an adult-like pattern of bowel movements (1-2 stools/day). The median onset of functional constipation in children is at 2.3 years old, with girls and boys being similarly affected. [2] Children benefit from scheduled toilet breaks, once early in the morning and 30 minutes after meals.
After the discovery of PKU as a cause of mental retardation, Horst Bickel and colleagues discovered that it could be treated successfully with a diet low in phenylalanine. [7] The main drawback in successful treatment of PKU was the delay in identifying affected individuals. The common test for PKU at the time was mixing urine with ferric chloride.
It shares history with PKU and hyperphenylalaninemia (HPA) . Asbjørn Følling, a physician studying metabolic diseases, identified an excess of phenylpyruvate as the cause of a strange, musty odor from the urine of two Norwegian children. [13] Further research by Penrose in 1935 lead to the coining of the term, "phenylketonuria". The ...
Constipation is more concerning when there is weight loss or anemia, blood is present in the stool, there is a history of inflammatory bowel disease or colon cancer in a person's family, or it is of new onset in someone who is older. [12] Treatment of constipation depends on the underlying cause and the duration that it has been present. [4]