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Regardless, median galactose-1-phosphate levels act as the most accurate predictors of the severity of symptoms associated with Type III galactosemia. [10] Blockage of the Leloir pathway by GALE deficiency or dysfunction activates alternate pathways of glucose metabolism and leads to galactitol and galactonate formation.
Patients with higher levels of residual enzyme activity can typically tolerate higher levels of galactose in their diets. As patients get older, dietary restriction is often relaxed. [2] With the increased identification of patients and their improving outcomes, the management of patients with galactosemia in adulthood is still being understood.
The only treatment for classic galactosemia is eliminating lactose and galactose from the diet (e.g. exclusion of dairy products containing lactose). [ 9 ] [ 20 ] [ 21 ] Lactose-restricted diet is efficient in resolving acute complications; however, it is not sufficient to prevent long-term complications affecting the brain and female gonads ...
Therefore, creatinine concentrations in blood and urine may be used to calculate the creatinine clearance (CrCl), which correlates approximately with the glomerular filtration rate (GFR). Blood creatinine concentrations may also be used alone to calculate the estimated GFR (eGFR). The GFR is clinically important as a measurement of kidney function.
The treatment for galactosemic cataract is no different from general galactosemia treatment. In fact, galactosemic cataract is one of the few symptoms that is actually reversible. Infants should be immediately removed from a galactose diet when symptoms present, and the cataract should disappear and visibility should return to normal. [12]
Specifically, when exposed to high levels of dietary galactose, a sugar abundant in breast milk, milk formula, and most dairy products, [5] infants with DG may show elevated levels of galactose and galactose metabolites such as galactose-1-phosphate (Gal-1P) and galactitol in blood and urine, respectively.
The development of early cataracts in homozygous affected infants is fully preventable through early diagnosis and treatment with a galactose-restricted diet. Some studies have suggested that, depending on milk consumption later in life, heterozygous carriers of galactokinase deficiency may be prone to presenile cataracts at 20–50 years of age.
The age term is (140 – age). This means that a 20-year-old person (140 – 20 = 120) will have twice the creatinine clearance as an 80-year-old (140 – 80 = 60) for the same level of serum creatinine. The C-G equation assumes that a woman will have a 15% lower creatinine clearance than a man at the same level of serum creatinine.
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