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What is the worse galactocemia galactocemia type 1 2 or 3?

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Anonymous
Answered
2020-08-14 01:37:50
2020-08-14 01:37:50

what's eoe's?

what's wors: galactocemia. eoe's. or pku's?

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Anonymous
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2020-08-07 23:25:41
2020-08-07 23:25:41

1. Classic galactosemia (type 1) - the most common and severe type, caused by mutations in the GALT gene, and characterized by a complete deficiency of an enzyme called galactose-1-phosphate uridyl transferase (GALT).

vs/

2. Clinical variant galactosemia, which can result in life-threatening complications including feeding problems, failure to thrive, hepatocellular damage including cirrhosis, and bleeding in untreated infants. This is exemplified by the disease that occurs in African Americans and native Africans in South Africa.

difference: Almost all females with classic galactosemia manifest premature ovarian insufficiency (POI). Clinical variant galactosemia, which can result in life-threatening complications including feeding problems, failure to thrive, hepatocellular damage including cirrhosis, and bleeding in untreated infant's.

what's wors: classic galactocemia (cg) or clinical virant galactocemia (cvg)?

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Anonymous
Answered
2020-06-24 13:22:28
2020-06-24 13:22:28

classic galactosemia| sever type1 classic galactosemia

epimerase deficiency galactosemia.

galactokinase deficiency disease.

galactose-1-phosphate uridyl-transferase deficiency disease.

galactose epimerase deficiency.

GALE deficiency.

GALK deficiency.

GALT deficiency.

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Anonymous
Answered
2020-06-24 13:24:09
2020-06-24 13:24:09

Individuals with intermediate epimerase deficiency galactosemia are typically treated with dietary galactose/lactose restriction

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Anonymous
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2020-06-24 13:26:34
2020-06-24 13:26:34

classic| Classic galactosemia (type 1) - the most common and severe type, caused by mutations in the GALT gene, and characterized by a complete deficiency of an enzyme called galactose-1-phosphate uridyl transferase (GALT). Classic galactosemia, also known as type I, is the most common and most severe form of the condition. If infants with classic galactosemia are not treated promptly with a low-galactose diet, life-threatening complications appear within a few days after birth.

epimerase| Individuals with intermediate epimerase deficiency galactosemia are typically treated with dietary galactose/lactose restriction

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Anonymous
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2020-06-25 17:29:31
2020-06-25 17:29:31

Etiology

Classic galactosemia is caused by mutations in the GALT gene encoding the enzyme. Mutations that severely impair enzyme activity result in the classic galactosemia. The so-called variants are mutations associated with higher residual enzyme activity resulting in milder or no features of galactosemia such as the Duarte variant (GALT gene).

Management and treatment

Treatment is based primarily on galactose restriction in the diet. Infant's should be fed with soy formula or other lactose-free formula. Patients are advised to follow a lifelong diet. To prevent a diminished bone mass, calcium, vitamin D and vitamin K supplements are recommended if dietary intake does not meet the recommended daily allowance. Monitoring of cognitive and motor development, gonadal function and bone mass is mandatory. Eye examinations are recommended in case of neonatal cataracts or in case of poor dietary compliance. Despite dietary treatment long-term complications occur.

Prognosis

Prognosis is dependent on age of diagnosis, disease severity and compliance with dietary restrictions, which affects the onset and course of secondary complications.

Duarte galactosemia is a mild variant of classic galactosemia, a condition that affects how the body processes galactose (a simple sugar found in milk, dairy products, and other foods). Unlike the other forms of galactosemia, most affected infants do not develop any concerning signs or symptoms even when breastfed or on a galactose-containing formula. Some may develop jaundice, but this symptom typically resolves quickly when the baby is switched to a low-galactose formula. duarte classic galactosemia is caused by changes in the GALT gene and is inherited in an autosomal recessive manner. People with Duarte galactosemia, specifically, typically have one severe GALT gene and one milder GALT gene mutation, known as the "Duarte classic variant." Experts disagree regarding the risks and long-term complications of duarte classic galactosemia and whether or not dietary interventions are needed. As a result, there is no standard treatment for infants with the condition. Some healthcare providers recommend partial to complete dietary restriction of milk and other high galactose foods for affected infants, but others do not.

GALACTOKINASE DEFICIENCY print. Galactokinase deficiency. Other Names: GALK deficiency; Galactosemia 2; Hereditary galactokinase deficiency; Galactokinase deficiency galactosemia; GALK-D; Galactosemia type 2

Galactokinase deficiency (GALK), a mild type of galactosemia, is an inherited disorder that impairs the body's ability to process and produce energy from a simple sugar called galactose. If babies with GALK eat foods containing galactose, undigested sugars build up. Children with GALK who are not treated with dietary therapy develop cataracts in the eyes, but otherwise they typically do not have long-term health problems. Rarely, a child with GALK will have pseudotumor cerebri, a condition which mimics the symptoms of a large brain tumor when no brain tumor is present. This is thought to be caused by increased pressure in the brain from cerebrospinal fluid (CSF) due to elevated levels of a galactose product in the CSF. The severe medical problems that occur with "classic" galactosemia (type 1), such as liver, kidney, and brain damage, typically are not present in people with GALK. GALK is caused by mutations in the GALK1 gene and inheritance is autosomal recessive. The disorder may be suspected in babies with an abnormal newborn screening result, or in babies with cataracts. The diagnosis can be confirmed with biochemical and molecular genetic testing. The treatment is dietary therapy, which involves taking calcium supplements and restricting galactose in the diet throughout life to prevent cataracts. If cataracts develop, they usually resolve with dietary therapy. Children with GALK should have their growth monitored, and both children and adults should consult with a dietitian and have regular eye exams.

Other Names: UDP-Galactose-4-epimerase deficiency; GALE deficiency; Galactosemia 3; Epimerase deficiency galactosemia; Galactosemia type 3; GALE-D; Uridine diphosphate galactose-4-epimerase deficiency. A very rare, moderate to severe form of galactosemia characterized by moderate to severe signs of impaired galactose metabolism. Epidemiology. Overall prevalence is not known but the disorder is thought to be very rare. Annual incidence is not known.

severities

classic (type1)

type4

type3

type2

durate

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Anonymous
Answered
2020-06-25 23:15:34
2020-06-25 23:15:34

sever type1 classic galactosemia| very sever. type4 moderate/severe. type3 mild/severe. type2 mild/moderate. or durate| mild?

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Anonymous
Answered
2020-08-07 21:15:14
2020-08-07 21:15:14

galactocemia severities classic galactocemia is the most sever type of galactocemia.

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Anonymous
Answered
2020-08-07 22:35:41
2020-08-07 22:35:41

what's wors?

galactocemia. gi issue's. gerd disorder's. eoe's. or: lactose intolerance. or: anaphylexis?

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Anonymous
Answered
2020-08-07 22:42:22
2020-08-07 22:42:22

galactocemia. pku's. gi issue's. gerd disorder's. eoe's. or: lactose intolerance. or: anaphylexis?

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Anonymous
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2020-08-07 22:51:47
2020-08-07 22:51:47

Phenylketonuria (PKU) is an autosomal recessive metabolic genetic disorder due to a mutation in the phenylalanine hydroxylasegene gene. PKU is an autosomal recessive genetic disorder that occurs due to a mutation in phenylalanine hydroxylase gene, which makes this enzyme non-functional. Phenylalanine hydroxylase is the enzyme that is necessary for the conversion of the amino acid phenylalanine (Phe) to the amino acid tyrosine. Phenylalanine is a large, neutral amino acid (LNAA), which can compete for transport across the blood โ€“ brain barrier (BBB) via the large neutral amino acid transporter (LNAAT). Untreated PKU can lead to mental retardation, seizures, and other serious medical problems. Therefore, PKU is commonly included in the newborn screening panel of most countries, with varied detection techniques. The mainstream treatment for classic PKU patients is a strict PHE-restricted diet supplemented by a medical formula containing amino acids and other nutrients. PKU is an autosomal recessive genetic disorder. autosomal recessive. Phenylketonuria. or: phenylalanine. Phenylketonuria (PKU) is an autosomal recessive metabolic genetic disorder characterized by a mutation in the gene for the hepatic enzyme phenylalanine hydroxylase (PAH), rendering it nonfunctional. Other non-PAH mutations can also cause PKU. This is an example of non-allelic genetic heterogeneity. The PAH gene is located on chromosome 12 in the bands 12q22-q24.1. More than 400 disease-causing mutations have been found in the PAH gene. PAH deficiency causes a spectrum of disorders, including classic phenylketonuria and hyperphenylalaninemia (a less severe accumulation of phenylalanine). Because PKU is an autosomal recessive genetic disorder, both parents must have at least one mutated allele of the PAH gene. The child must inherit both mutated alleles, one from each parent. Therefore, it is possible for a parent with the disease to have a child without it if the other parent possesses one functional allele of the gene for PAH. Yet, a child from two parents with PKU will inherit two mutated alleles every time, and therefore will also inherit the disease. Inheritance of PKU: Phenylketonuria is inherited in an autosomal recessive fashion. PAH enzyme is necessary for the metabolism of the amino acid phenylalanine (Phe) to the amino acid tyrosine. When PAH activity is reduced, phenylalanine accumulates. Excessive phenylalanine can be metabolized into phenylketones through the minor route, a transaminase pathway with glutamate. Metabolites include phenylacetate, phenylpyruvate, and phenethylamine. Elevated levels of phenylalanine in the blood and detection of phenylketones in the urine is diagnostic. Phenylalanine is a large, neutral amino acid (LNAA). LNAAs compete for transport across the bloodโ€“brain barrier (BBB) via the large neutral amino acid transporter (LNAAT). If phenylalanine is in excess in the blood, it will saturate the transporter. Excessive levels of phenylalanine tend to decrease the levels of other LNAAs in the brain. However, as these amino acids are necessary for protein and neurotransmitter synthesis, Phe buildup hinders the development of the brain, causing mental retardation. Treatment: The mainstream treatment for classic PKU patients is a strict PHE-restricted diet supplemented by a medical formula containing amino acids and other nutrients. In the United States, the current recommendation is that the PKU diet should be maintained for life. Patients who are diagnosed early and maintain a strict diet can have a normal life span with normal mental development. However, recent research suggests that neurocognitive, psychosocial, quality of life, growth, nutrition, and bone pathology are slightly suboptimal. Detection: PKU is commonly included in the newborn screening panel of most countries, with varied detection techniques. Most babies in developed countries are screened for PKU soon after birth.

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Anonymous
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2020-08-07 22:52:04
2020-08-07 22:52:04

Screening for PKU is done with bacterial inhibition assay (Guthrie test), immunoassays using fluorometric or photometric detection, or amino acid measurement using tandem mass spectrometry (MS/MS). Measurements done using MS/MS determine the concentration of Phe and the ratio of Phe to tyrosine, both of which will be elevated in PKU. Incidence: A rarer form of hyperphenylalaninemia occurs when PAH is normal, but there is a defect in the biosynthesis or recycling of the cofactor tetrahydrobiopterin (BH4) by the patient. This cofactor is necessary for proper activity of the enzyme. The coenzyme (called biopterin) can be supplemented as treatment. Those who suffer from PKU must be supplemented with tyrosine to account for PAH deficiency in converting phenylalanine to tyrosine sufficiently. Dihydrobiopterin reductase activity is to replenish quinonoid-dihydrobiopterin back into its tetrahydrobiopterin form, which is an important cofactor in many metabolic reactions in amino acid metabolism. Those with this deficiency may produce sufficient levels of PAH, but since tetrahydrobiopterin is a cofactor for PAH activity, deficient dihydrobiopterin reductase renders any PAH enzyme non-functional. Tetrahydrobiopterin is also a cofactor in the production of L-DOPA from tyrosine and 5-hydroxy-l-tryptophan from tryptophan, which must also be supplemented as treatment in addition to the supplements for classical PKU. Levels of dopamine can be used to distinguish between these two types. Low levels of dopamine lead to high levels of prolactin. By contrast, in classic PKU, prolactin levels would be relatively normal. Tetrahydrobiopterin deficiency can be caused by defects in four different genes.

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Anonymous
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2020-08-07 22:52:41
2020-08-07 22:52:41

The mean incidence of PKU varies widely in different human populations. Caucasians are affected at a rate of 1 in 10,000. Turkey has the highest documented rate in the world, with 1 in 2,600 births, while countries such as Finland and Japan have extremely low rates with fewer than one case of PKU in 100,000 birth's.

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Anonymous
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2020-08-07 22:58:05
2020-08-07 22:58:05

Galactosemia and Glycogen Storage Disease. Galactosemia and GSD are two diseases that are caused by improper carbohydrate metabolism. Differentiate between galactosemia and glycogen storage disease. Galactosemia follows is a rare genetic metabolic disorder that affects an individualโ€™s ability to metabolize the sugar galactose properly.

Infants affected by galactosemia typically present with symptoms of lethargy, vomiting, diarrhea, failure to thrive, and jaundice.

A galactosemia test is a blood test (from the heel of the infant) or urine test that checks for three enzymes that are needed to change galactose sugar that is found in milk and milk products into glucose, a sugar that your body uses for energy. The only treatment for classic galactosemia is eliminating lactose and galactose from the diet. Glycogen storage disease (GSD, also glycogenosis and dextrinosis) is the result of defects in the processing of glycogen synthesis or breakdown within muscles, liver, and other cell types. The only treatment for classic galactosemia is eliminating lactose and galactose from the diet. There are eleven (11) distinct diseases that are commonly considered to be glycogen storage diseases. enzyme: A globular protein that catalyses a biological chemical reaction. glycogen: A polysaccharide that is the main form of carbohydrate storage in animals; converted to glucose as needed. Galactosemia (British Galactosaemia) is a rare genetic metabolic disorder that affects an individualโ€™s ability to metabolize the sugar galactose properly. Although the sugar and lactose metabolizes to galactose, galactosemia is not related to and should not be confused with lactose intolerance. Galactosemia follows an autosomal recessive mode of inheritance that confers a deficiency in an enzyme responsible for adequate galactose degradation. Its incidence is about one per 60,000 births for Caucasians. In other populations the incidence rate differs. Lactose in food (such as dairy products) is broken down by the enzyme lactase into glucose and galactose. In individuals with galactosemia, the enzymes needed for further metabolism of galactose are severely diminished or missing entirely, leading to toxic levels of galactose 1-phosphate in various tissues as in the case of classic galactosemia, resulting in hepatomegaly (an enlarged liver), cirrhosis, renal failure, cataracts, and/ or: brain damage, Without treatment, mortality in infants with galactosemia is about 75%. Detection of the disorder through newborn screening (NBS) does not depend on protein or lactose ingestion, and, therefore, it should be identified on the first specimen unless the infant has been transfused. A specimen should be taken prior to transfusion. The enzyme is prone to damage if analysis of the sample is delayed or exposed to high temperatures. Treatment: The only treatment for classic galactosemia is eliminating lactose and galactose from the diet. Even with an early diagnosis and a restricted diet, however, some individuals with galactosemia experience long-term complications such as speech difficulties, learning disabilities, neurological impairment (e.g., seizure's. tremors, etc.), and ovarian failure in females. Infants with classic galactosemia cannot be breast-fed due to lactose in human breast milk and are usually fed a soy-based formula. Galactosemia is sometimes confused with lactose intolerance, but galactosemia is a more serious condition. Lactose intolerant individuals have an acquired or inherited shortage of the enzyme lactase, and experience abdominal pains after ingesting dairy products, but no long-term effects. In contrast, a galactosemic individual who consumes galactose can cause permanent damage to their bodies. Glycogen Storage Disease. Glycogen storage disease (GSD, also glycogenosis and dextrinosis) is the result of defects in the processing of glycogen synthesis or breakdown within muscles, liver, and other cell types. GSD has two classes of cause: genetic and acquired. Genetic GSD is caused by any inborn error of metabolism (genetically defective enzymes) involved in these processes. In livestock, acquired GSD is caused by intoxication with the alkaloid castanospermine. Overall, according to a study in British Columbia, approximately 2.3 children per 100,000 births (one in 43,000) have some form of glycogen storage disease. In the United States, they are estimated to occur in one per 20,000โ€“25,000 births. A Dutch study estimated it to be one in 40,000. There are 11 distinct diseases that are commonly considered to be glycogen storage diseases (some previously thought to be distinct have been reclassified).

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Anonymous
Answered
2020-08-07 23:21:10
2020-08-07 23:21:10

galactocemia

1. type1 (classic galactocemia): Results in classic galactosemia, in which homozygotes have less than 5% enzyme activity. If untreated, severe damage of body systems can occur; if undetected, death.| GALT deficiency causes the most common and severe form of galactosemia and will be the focus of the following discussion.

2. type4 (gale): Either results in deficiency that is found only in red blood cells and no symptoms occur, or a deficiency that affects most tissues and results in symptoms similar to those found in classic galactosemia. moderate/severe

3. type3 galactocemia. moderate

4. durate galactocemia (dg): Children with Duarte variant galactosemia generally have a residual 10-25% GALT enzyme activity. It occurs when a child inherits a classic mutation from one parent and the Duarte variant from the other. It is similar to Classic galactosemia, but less severe. Depending on severity, no treatment may be needed. mild/severe

5. type2 galactocemia: Results in relatively mild symptoms, although may cause cataracts. Individuals still have normal GALT enzyme activity. mild

Classic galactosemia (galactosemia type I, GALT deficiency, galactose-1-phosphate uridyltransferase deficiency)

Duarte galactosemia (mild galactosemia)

Galactokinase deficiency disease (GALK deficiency, galactosemia type II)

UDP-galactose-4-epimerase deficiency disease (GALE deficiency, galactosemia III)

classic galactocemia (cg) is, the most worst/severe type/type of this disorder

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Anonymous
Answered
2020-08-07 23:30:25
2020-08-07 23:30:25

classic galactocemia or clinical variant galactocemia severities

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Anonymous
Answered
2020-08-10 16:55:12
2020-08-10 16:55:12

1. classic (type1)| severe

2. clinical? (type7)?

3. clinical virant? (type6)?

4. clinical durate virant? (type8)?

5. galactose epimerase deficiency (type4)| modrate/severe

6. GALE deficiency galactocemia (type3)?

7. galactokinase deficiency (type2)?

or# 8. durate (type5)?

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Anonymous
Answered
2020-08-07 23:32:23
2020-08-07 23:32:23

type 1, or classic and clinical variant galactosemia.

type 2, or galactokinase deficiency.

type 3, or epimerase deficiency.

duarte variant galactosemia.

classic

clinical virant

empirase defencese

galk defencise

durate virant

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Anonymous
Answered
2020-08-07 23:37:57
2020-08-07 23:37:57

what's worse galactocemia or what classic/durate galactocemia is wors?

classic galactocemia (cg)

vs/

classical clinical galactocemia (ccg)

vs/

classic virant galactocemia (cvg)

or/

classic durate galactocemia (cdg)

durate galactocemia (dg)

or is it:

durate virant galactocemia (dvg)?

or is it: durate classic galactocemia (dcg)

or clinical classic galactocemia. or durate clinical galactocemia.

or: clinical durate galactocemia?

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Anonymous
Answered
2020-08-08 01:01:05
2020-08-08 01:01:05

can i consume daiya product's if i have: severe type1 classic galactocemia or anytype of: galactocemia. or if i have: celeic deseas. or intolerance to: gluten?

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Anonymous
Answered
2020-08-08 01:02:29
2020-08-08 01:02:29

is daiya safe for: sever type1 classic galactocemia or for anytype of: galactocemia?

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Anonymous
Answered
2020-08-08 01:10:05
2020-08-08 01:10:05

what's wors: galactocemia. hyper/hypo galactocemia. pku. arfid. feeding tude need's. anemia. anorrexa/bulima. eoe/ige. gerd disorder's. lactose intolerance/issues/reflex or allergies. or reflex issues. sensory issues. lactose sensitive. milk/dairy issues or allergies/sensative's. or: anaphylaxis or: reflex/acid reflex issue's?

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Anonymous
Answered
2020-08-08 01:14:52
2020-08-08 01:14:52

btween: galactocemia or lactose intolerance. or. pku. or even: pseudo-obstruction motility and antral hypomotility disorders, severe gastrointestinal disorder's, what's wors?

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Anonymous
Answered
2020-08-08 01:15:51
2020-08-08 01:15:51

from: "miracle's from heaven" what was anna's rare disorder?

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Anonymous
Answered
2020-08-08 21:46:52
2020-08-08 21:46:52

what's wors: galactocemia. hyper/hypo galactocemia. pku. arfid. feeding tude need's. anemia. anorrexa/bulima. eoe/ige. gerd disorder's. lactose intolerance/issues/reflex or allergies. or reflex issues. sensory issues. lactose sensitive. milk/dairy issues or allergies/sensative's. or: anaphylaxis or: reflex/acid reflex issue's?

severities:

galactocemia

hyper/hypo galactocemia

pku

arfid

feeding tube need's

anemia. anorrexa/bulima

eoe/ige.

gerd disorder's

lactose intolerance/issues/reflex or allergies. or reflex issues+ lactose sensitives

sensory issues.

milk/dairy issues or allergies/sensative's

anaphylaxis

reflex/acid reflex issue's

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Anonymous
Answered
2020-08-08 21:58:38
2020-08-08 21:58:38

can classic galactocemia or anytype of galactocemia have: daiya. or goodness oatmilk nesquik. or no whey product/item's?

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Anonymous
Answered
2020-08-10 03:01:08
2020-08-10 03:01:08

true or fals?

galactocemia type's/severities. galactocemia shortend

name1. classic| type1| severe| GALT|

severe2. uridine diphosphate galactose (udg) epimerase deficiency| type4| GALE| modrate/severe.

3. galactose epimerase deficiency| GALE-D; uridine diphosphate galactose| epimerase deficiency| type3| modrate/severe.

4. duarte galactosemia| type5 | mild/severe.

5. galactokinase deficiency. GALK deficiency. GALK-D. GALK. Galactokinase deficiency galactosemia| type2| mild/modrate.

lactose intolerant. type's/severities.

1) classic|

severe2) developmental| modrate/severe

3) congenital| severe

4) semi lactose intolerance| modrate

5) primary| mild/severe

6) secondary| mild/moderateseverities

1. classic or congenital| severe

2. developmental| modrate/severe

3. semi| modrate

4. primary| mild/severe

5. secondary| mild/moderate

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Anonymous
Answered
2020-08-10 16:41:33
2020-08-10 16:41:33

Subdivisions of Galactosemia

classic galactosemia

clinical variant galactosemia

biochemical variant galactosemia (Duarte variant galactosemia)

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Anonymous
Answered
2020-08-10 16:45:30
2020-08-10 16:45:30

Galactosemia occurs due to disruptions or changes (mutations) in the GALT gene resulting in deficiency of the GALT enzyme. This leads to abnormal accumulation of galactose-related chemicals in various organs of the body causes the signs and symptoms and physical findings of galactosemia. The galactose-1-phosphate uridyl transferase (GALT) enzyme is needed for the breakdown of the milk sugar, galactose. Deficiency of this enzyme results in the accumulation of toxic products: galactose-1-phosphate (a derivative of galactose), and galactitol (an alcohol derivative of galactose). Galactitol accumulates in the lens of the eye where it causes lens swelling and protein precipitation and, subsequently, cataracts. Accumulation of galactose-1-phosphate is thought to cause the other signs and symptoms of disease. Galactosemia is an autosomal recessive genetic disorder. Recessive genetic disorders occur when an individual inherits a non-working gene from each parent. If an individual receives one working gene and one non-working gene for the disease, the person will be a carrier for the disease, but usually will not show symptoms. The risk for two carrier parents to both pass the non-working gene and, therefore, have an affected child is 25% with each pregnancy. The risk to have a child who is a carrier, like the parents, is 50% with each pregnancy. The chance for a child to receive working genes from both parents is 25%. The risk is the same for males and females. Affected Population's: Classic galactosemia is diagnosed in the range of 1/16,000 to 1/48,000 births through newborn screening programs around the world, depending on the diagnostic criteria used by the program. The disorder has been reported in all ethnic groups. An increased frequency of galactosemia occurs in individuals of Irish ancestry. Clinical variant galactosemia occurs most often in African Americans and native Africans in South Africa who have a specific GALT gene mutation. Related Disorders Symptoms of the following disorders can be similar to those of galactosemia. Comparisons may be useful for a differential diagnosis: Galactokinase (GALK) deficiency is associated with cataracts, increased blood concentration of galactose and increased concentration of galactitol in the urine. Galactitol accumulates in the lens of the eye where it causes lens swelling and protein precipitation and, subsequently, cataracts. GALK deficiency is an autosomal recessive genetic disorder caused by mutations in the GALK1 gene and diagnosed by reduced GALK enzyme activity. Uridine diphosphate galactose 4-epimerase (GALE) deficiency is similar to GALT deficiency when it presents in the newborn period. The severe form has been reported in only 8 patients. GALE deficiency is an autosomal recessive genetic disorder caused by mutations in the GALE gene and diagnosed by reduced GALE enzyme activity. Lactose intolerance (LI) is a metabolic disorder characterized by the inability to break down lactose, the predominant sugar found in milk and milk products. People with LI cannot properly digest lactose because they lack or are deficient in the intestinal enzyme, lactase, which is key to the digestion of lactose. Lactose is a complex sugar made up of two different sugar molecules (disaccharide), galactose and glucose, each of which is a simple (monosaccharide) sugar and more readily absorbed in the bodyโ€™s intestines and processed in other organs. Individuals with a deficiency of lactase experience cramps, nausea, bloating, stomach rumbling (Borborygmi), gas (flatus) and/or diarrhea after eating or drinking lactose-rich foods, not all of which are dairy products. Signs are more severe when they occur in a newborn infant. The signs of congenital lactose intolerance are apparent soon after birth and usually include severe diarrhea, vomiting, abnormally low levels of body fluids (dehydration), and failure to thrive. (galactocemia is wors then lactose intolerance is). Neonatal hepatitis is a general term used to denote injury to the liver that occurs shortly before and/or after birth. Neonatal hepatitis may be caused by viruses, metabolic disease or genetic disorders, as well as other rare diseases that affect or impair the function of the liver. In some children, the cause of liver injury is unknown โ€“ these cases are referred to as idiopathic neonatal hepatitis (INH). The signs of idiopathic neonatal hepatitis may vary greatly from one individual to another. Findings common to liver disease often occur including yellowing of the whites of the eyes and the skin (jaundice), enlargement of the liver (hepatomegaly) and unusually dark urine. Most individuals with idiopathic neonatal hepatitis fully recover from the condition; however, some will progress to chronic liver disease. (For more information on this disorder, choose โ€œneonatal hepatitisโ€ as your search term in the Rare Disease Database.)

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Anonymous
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2020-08-10 16:48:44
2020-08-10 16:48:44

galactocemia (galt) diagnoses: Classic galactosemia and clinical variant galactosemia are diagnosed when galactose-1-phosphate is elevated in red blood cells and GALT enzyme activity is reduced. Molecular genetic testing is also available to identify mutations in the GALT gene. Nearly 100% of infants with galactosemia can be diagnosed in newborn screening programs using a blood sample from the heel stick. Infants with clinical variant galactosemia can be missed at newborn screening if GALT enzyme activity is not measured.

Treatment

Infants and children with galactosemia should have a lactose-restricted (dairy-free) diet that contains lactose-free milk substitutes and other foods such as soy bean products.

A lactose tolerance test should NOT be administered to children with galactosemia. Fortunately, the body of an infant with galactosemia can synthesize galactolipids and other essential galactose-containing compounds without the presence of galactose in food. Therefore, satisfactory physical development is largely possible if a strict diet is followed.

Speech therapy may be necessary for children with childhood apraxia of speech or dysarthria. For school age children, individual education plans and/or professional help with learning skills may be necessary for some individuals, depending on psychological developmental assessments. Hormone replacement therapies may also be used in cases of delayed puberty, and later in adolescence for the secondary loss of menstrual periods, termed premature ovarian insufficiency (POI).

Appropriate treatment (i.e., antibiotic drugs) may be used to control infection in the newborn period. The emotional effects of the strict diet may require attention and supportive measures throughout childhood. Genetic counseling is recommended for families with children who have galactosemia.

Following several conferences, a consensus on the treatment and follow-up of patients with galactosemia was published in 2017.

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Anonymous
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2020-06-24 13:21:09
2020-06-24 13:21:09

classic galactosemia, also known as type I, is the most common and most severe

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The herpes virus (type 1 or 2) are so close that there is little difference between them. Neither is worse.

what all: severities, is worst| most sever to less or least severclassic galactocemia/durate galactocemia+ other: galt'spku'sanaphylaxisallergiesor: intolerance

There are 2 types of diabetes. Type 1 is more commonly seen in children. Type 1 is worse than Type 2 as you have to have insulin administered through injections. If you have Type 2 (which is normally seen in adults or people who are overweight) you will just have to take pills.

1. It got worse when it started raining.2. I am worse at maths than her.

depends on the consecence of make the mistake sometimes one is worse then 2 and sometimes its the other way round

Depends if your type 1 or 2. I hate type 2's. Pisses me off that they are even called Diabetic. But if your type 1 ( like me ) get some carb counting scales. Just put the food on, and it tells you how many carbs.

Type 1 diabetes is less common than Type 2, but not necessarily worse. Type 1 diabetes requires the injection of insulin on a regular daily basis. Due to improvements in medical technology, the needles used for this purpose are now extremely fine (very small) to the point that you hardly feel the sting of the needle, if at all. Both forms of diabetes are easily treatable, requiring minimal lifestyle changes, compared to a decade ago.

The question "which type is worse?" is complicated to answer. medically speaking, type 1 is worse, because the pancreas shuts down, whereas in type 2, the pancreas simply functions improperly. However, as a type 1 diabetic patient, I can tell you that Type 1 is BAD. through constant glucose checks and insulin injections, it is a lot to manage and sometimes quite a hassle. But, as complicated as type 1 is, as a teenager, I would much rather have type 1, because type 2 is more heavily dependent on diet change, and although some people can easily make this switch, others cannot. Type 2 is also harder to manage due to insulin resistance.I also have type 1, and yes it is less convenient and maybe a little bit more painful now, but the effects of type 1 diabetes in the future are completely under your personal control. Type 2 diabetics have the problem of having insulin resistance. Yes, their pancreas's still produce insulin, but that does not mean that their body is receiving it. Like type 1's they also have to maintain a strict diet and exercise regularly, but their health is not completely up to them. Type 1's can control their own destinies. Type 2 Diabetes is a more serious disease.

Type one diabetes is a horrible disease that is like Type 2 dietbetes only worse

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HSV-1 usually causes cold sores. HSV-2 usually affects the genitals. You need to decide for yourself which is worse.

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you know what my dad has type 2 diabetes and the type one is way way way worse. type one can kill you but when i was three my dad had type 2 diabetes and it is OK and did you know if your mom or dad had diabetes you are at risk of getting type 2 so say your dad or mom has type one diabetes you are at risk of getting it but if your mom or dad had type 2 diabetes you are at risk of getting type 2 - hope this helped alot

1/2 (type a 1, then a /, then a 2)

I believe that Type 1 is an autoimmune disease and Type 2 is not, so with Type 1 auto antibodies are present and with Type 2 they are not. Therefore, I do not believe that taking insulin can turn Type 2 into Type 1. The cause of Type 1 is still unknown.

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Type one Type 1 is where the pancreas completely shuts down, whereas Type 2 just sees reduced efficiency. So Type 1 is worse. (also, in most cases, not all but most, weight loss would 'cure' the type 2 diabetes; the person would no longer suffer from it. essentially, type 2 is the pancreas simply not making enough insulin for the size of the body. clearly, if the body got smaller, the problem would no longer be a problem!! type 1 is permanent. there is no known way of 'curing' it

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You can type the numerator, a slash, and the denominator, for example, 1/2.You can type the numerator, a slash, and the denominator, for example, 1/2.You can type the numerator, a slash, and the denominator, for example, 1/2.You can type the numerator, a slash, and the denominator, for example, 1/2.

It depends if you have type 1 or type 2. Type 2's cannot take it. A type 1 however, would be able to take it. If the type 2 was actually in disguise as a type 1 they could take it

They both are a disease, but with type 1 you are insulin dependent, type 2 you moistly have to take pills.

Type 1 is more serious than type 2. In type 1, you have to inject insulin. In some cases you have to do that in type 2. In type 2, you can be cured by good eating habits and exercise. Type 1 is more chronic.

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There is not "stage 1" and "stage 2" herpes. There are two types of herpes -- type 1 and type 2. Type 2 is more likely to recur.


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