Glucose 6 phosphate dehydrogenase causes symptoms diagnosis treatment. Clinical pharmacology and pharmacotherapy

All symptoms of glucose-6-phosphate dehydrogenase deficiency are combined into 5 syndromes (a stable set of symptoms united by a single development).

Anemic (i.e. from the blood system):

• weakness, decreased performance;
• dizziness;
• fainting states;
• tinnitus, flashing "flies" before the eyes;
• shortness of breath (rapid breathing) and palpitations with little physical exertion;
• stitching pains in the chest.

• change in the color of urine (it becomes red, brown, black);
• pain in the lumbar region;
• edema (mainly of the face).

• Pain:
  • in the bones;
  • at the fingertips;
  • at the tips of the ears and nose.

• The formation of ulcers (deep defects) of the anterior surface of the legs.

• increase in body temperature;
• severe pain in the lumbar region;
• dark urine (it becomes darker than usual).

• tower (that is, elongated in height) skull;
• protruding zygomatic arches;
• narrow eye sockets;
• thickening of sections of the ribs at the point of their attachment to the sternum (the central bone of the anterior surface chest);
• shortening of fingers;
• curvature of the legs, etc.

Forms

According to the severity, depending on the content of hemoglobin (a special substance of erythrocytes (red blood cells) that carries oxygen) in the blood, there are:

• mild anemia (hemoglobin from 90 to 110 g / l, that is, grams of hemoglobin per 1 liter of blood);
• anemia moderate (hemoglobin from 90 to 70 g/l);
• severe anemia (hemoglobin less than 70 g/l).

Normally, in men, the hemoglobin content in the blood is 130/160 g / l. Situations in which blood hemoglobin ranges from 110 to 130 g / l are intermediate between the norm and anemia.

The reasons

Cause deficiency of glucose-6-phosphate dehydrogenase - a hereditary violation in the structure of genes (carriers of hereditary information). Defective genes can be inherited from one or both parents - in this case, the disease will be more severe.

Risk factors for hemolytic crises (a sharp increase in the destruction of erythrocytes - red blood cells).

• Physical:
  • prolonged exposure to sunlight;
  • hypothermia;
  • overheating.

• Chemical:
  • production (products of oil and gas processing, varnishes, paints, gasoline, etc.) - inhalation of vapors of these substances, their contact with the skin, penetration into the body with food and water can become dangerous;
  • drugs (painkillers, antimicrobials, vitamin K (necessary for the synthesis of coagulation factors by the liver), etc. Drugs are risk factors only for some people who have structural features of the body (which ones are not yet known), including when taking medications unreasonably .

• Biological - negative emotions, infections, injuries, surgeries, eating fava beans.

Diagnostics

• Analysis of the anamnesis of the disease and complaints (when (how long ago) did general weakness, pain in the bones and fingers, loss of appetite, shortness of breath, etc. appear, with which the patient associates the occurrence of these symptoms).
• Life history analysis. Does the patient have any chronic diseases, are there hereditary (passed from parents to children) diseases, does the patient have bad habits whether he took any drugs, whether he was in contact with toxic (poisonous) substances, whether the patient was in direct sunlight for a long time, hypothermia or overheating, etc.
• Physical examination. The color of the skin is determined (pallor is characteristic of anemia), the anterior surface of the legs is examined (possible presence of ulcers - deep defects), the pulse may be rapid, arterial pressure- reduced.
• Blood analysis. With the development of anemia (a decrease in the level of blood hemoglobin - a special substance of erythrocytes - red blood cells - carrying oxygen), a decrease in the number of erythrocytes and reticulocytes (erythrocyte precursor cells) is determined with an increase in their size, a decrease in hemoglobin levels, a decrease in the number of platelets (platelets). The shape and size of the blood cells remain normal. The color indicator (the ratio of the hemoglobin level multiplied by 3 to the first three digits of the number of red blood cells) does not change: normally, this indicator is 0.86-1.05.
• Analysis of urine. In the urine, mainly during a hemolytic crisis (a sharp increase in the destruction of red blood cells), free hemoglobin (that is, outside the red blood cells) and hemosiderin (a breakdown product of hemoglobin) are determined, which should not normally be.
• Blood chemistry. The level of cholesterol (fat-like substance), glucose (simple carbohydrate), creatinine (protein breakdown product), uric acid (decay product of substances from the cell nucleus) is determined to detect concomitant organ damage, electrolytes (potassium, sodium, calcium).
• Determination of glucose-6-phosphate dehydrosenase activity is an accurate method for making a diagnosis.
• Examination of bone marrow obtained by puncture (piercing with extraction of internal contents) of a bone, most often the sternum (the central bone of the anterior surface of the chest, to which the ribs are attached). In the bone marrow, with a deficiency of glucose-6-phosphate dehydrogenase, an increased formation of red blood cells of normal size and shape is determined.
• Electrocardiography (ECG). An increase in heart rate, malnutrition of the heart muscle, less often - heart rhythm disturbances are determined.
• Genetic examination (study of the hereditary properties of the organism) of the relatives of a patient with a deficiency of glucose-6-phosphate dehydrogenase, as well as the determination of the activity of this enzyme in them, makes it possible to identify people with a decrease in the activity of this enzyme and give them recommendations for the prevention of hemolytic crises (a sharp increase in the destruction of red blood cells) .
• Consultation is also possible.

Treatment of glucose-6-phosphate dehydrogenase deficiency

• Impact on the cause deficiency of glucose-6-phosphate dehydrogenase - currently not possible. Genetic studies are being carried out (that is, studies of genes - carriers of hereditary information) with the aim of introducing genes into the patient's body that provide normal level glucose-6-phosphate dehydrogenase.
• Bone marrow transplant performed in cases of severe deficiency of glucose-6-phosphate dehydrogenase activity. Bone marrow transplantation can partially replace Bone marrow of a patient with a disturbed cell structure to a healthy donor bone marrow. The appearance of full-fledged erythrocytes in the bloodstream significantly reduces the risk of hemolytic crises.
• Rapid replenishment of red blood cells (red blood cells) - transfusion of erythrocyte mass (erythrocytes isolated from donor blood) or (preferably) washed erythrocytes (donor erythrocytes devoid of potentially dangerous donor proteins on their surface) for health reasons (that is, when the patient's life is threatened). There are two conditions that threaten the life of a patient with anemia:
  • anemic coma (loss of consciousness with no response to external stimuli due to insufficient oxygen supply to the brain as a result of a significant or rapidly developed decrease in the number of red blood cells);
  • severe degree of anemia (that is, the blood hemoglobin level is below 70 g / l).

Complications and consequences

Complications of glucose-6-phosphate dehydrogenase deficiency.

• Anemia (a decrease in the level of hemoglobin - a special substance of erythrocytes - red blood cells - carrying oxygen) is the main complication of glucose-6-phosphate dehydrogenase deficiency. Some patients may never develop.
• Anemic coma - loss of consciousness with no response to external stimuli due to insufficient oxygen supply to the brain as a result of a significant or rapidly developed decrease in the number of red blood cells.
• Chronic renal failure (impairment of all kidney functions) develops when the kidneys are damaged by the breakdown products of red blood cells.
• Deterioration internal organs, especially in the presence of chronic diseases (for example, heart, kidney, etc.).

Prevention of glucose-6-phosphate dehydrogenase deficiency

• Prevention of glucose-6-phosphate dehydrogenase deficiency consists in determining the activity of this enzyme in potential parents. It is proposed to abandon the onset of pregnancy in cases of high risk of having a child with a pronounced deficiency in the activity of glucose-6-phosphate dehydrogenase.
• Prevention of hemolytic crises consists in the exclusion of provoking factors (for example, taking certain medications, eating fava beans, excessive psycho-emotional stress, etc.).

Additionally

• Glucose-6-phosphate dehydrogenase deficiency is the most common variant of hemolytic (that is, associated with increased destruction of red blood cells) anemia.
• According to the World Health Organization (WHO), more than 100 million people in the world suffer from this disease, mainly in countries with a hot climate.
• In Russia, a decrease in the activity of the enzyme glucose-6-phosphate dehydrogenase is determined in approximately every fiftieth person. Each of them can develop anemia.
• In the period between hemolytic crises (a sharp increase in the destruction of red blood cells), the patient may not experience discomfort, and in general analysis blood is determined by the normal level of erythrocytes and hemoglobin.
• Men get sick more often than women.

The most common fermentopathy is deficiency of glucose-6-phosphate dehydrogenase - found in approximately 300 million people; in second place is a deficiency in pyruvate kinase activity, found in several thousand patients in the population; other types of enzymatic defects in erythrocytes are rare.

Prevalence

Glucose-6-phosphate dehydrogenase deficiency is unevenly distributed throughout the population different countries: most often found in residents of European countries located on the Mediterranean coast (Italy, Greece), among Sephardi Jews, as well as in Africa and Latin America. The lack of glucose-6-phosphate dehydrogenase is widely recorded in the former malarial regions of Central Asia and Transcaucasia, especially in Azerbaijan. It is known that tropical malaria patients with glucose-6-phosphate dehydrogenase deficiency died less often, since erythrocytes with enzyme deficiency contained less malarial plasmodia than normal erythrocytes. Among the Russian population, deficiency of glucose-6-phosphate dehydrogenase activity occurs in approximately 2% of people.

Although deficiencies in this enzyme are ubiquitous, the severity of the deficiency varies among ethnic groups. The following variants of enzyme deficiency in erythrocytes have been established: A + , A ", B + , B" and the Canton variant.

• The variant of glucose-6-phosphate dehydrogenase B + is normal (100% G-b-PD activity), most common among Europeans.
• The variant of glucose-6-phosphate dehydrogenase B "is Mediterranean; the activity of red blood cells containing this enzyme is extremely low, often less than 1% of the norm.
• Variant of glucose-6-phosphate dehydrogenase A + - enzyme activity in erythrocytes is almost normal (90% of the activity of variant B +)
• The variant of glucose-6-phosphate dehydrogenase D A "is African, the activity of the enzyme in erythrocytes is 10-15% of the norm.
• Variant of glucose-6-phosphate dehydrogenase Canton - in the inhabitants of Southeast Asia; enzyme activity in erythrocytes is significantly reduced.

It is interesting to note that the "pathological" enzyme of variant A" in terms of electrophoretic mobility and some kinetic properties is very close to the normal variants of glucose-6-phosphate dehydrogenase B + and A +. The differences between them lie in stability. It turned out that in young erythrocytes the activity of the variant enzyme A almost does not differ from that of variant B. However, in mature erythrocytes, the picture changes dramatically.This is due to the fact that the half-life in erythrocytes of the enzyme variant A is approximately 5 times (13 days) less than the enzymes of variant B (62 days). there is insufficient activity of glucose-6-phosphate dehydrogenase variant A" is the result of a much faster than normal denaturation of the enzyme in erythrocytes.

Frequency different types deficiency of glucose-6-phosphate dehydrogenase varies in different countries. Therefore, the frequency of people who “respond” with hemolysis to the action of provoking factors varies from 0 to 15%, and in some areas reaches 30 %.

Deficiency of glucose-6-phosphate dehydrogenase is inherited recessively, linked to the X chromosome. Women can be either homozygous (enzyme activity in erythrocytes is absent) or heterozygous (enzyme activity is 50%) carriers of the defect. In men, the activity of the enzyme is usually below 10 / o, which causes pronounced clinical manifestations illness.

Pathogenesis of glucose-6-phosphate dehydrogenase

Glucose-6-phosphate dehydrogenase is the first enzyme of pentose phosphate glycolysis. The main function of the enzyme is to reduce NADP to NADPH, which is necessary for the conversion of oxidized glutathione (GSSG) to the reduced form. Reduced glutathione (GSH) is required to bind reactive oxygen species (peroxides). Pentose phosphate glycolysis provides the cell with energy.

Lack of enzyme activity reduces the energy reserves of the cell and leads to the development of hemolysis, the severity of which depends on the amount and variant of glucose-6-phosphate dehydrogenase. Depending on the severity of the deficiency, 3 classes of G-6-PD variants are distinguished. Deficiency of glucose-6-phosphate dehydrogenase is linked to the X chromosome and is inherited recessively. Male patients are always hemizygous, while female patients are homozygous.

The most important function of the pentose cycle is to ensure sufficient production of reduced nicotinamide adenine dinucleotide phosphate (NADP) to convert the oxidized form of glutamine to the reduced form. This process is necessary for the physiological deactivation of oxidant compounds such as hydrogen peroxide that accumulate in the erythrocyte. With a decrease in the level of reduced glutathione or the activity of glucose-6-phosphate dehydrogenase, which is necessary to maintain it in a reduced form, under the influence of hydrogen peroxide, oxidative denaturation of hemoglobin and membrane proteins occurs. Denatured and precipitated hemoglobin is found in the erythrocyte in the form of inclusions - Heinz-Ehrlich bodies. Erythrocytes with inclusions are quickly removed from the circulating blood either by intravascular hemolysis, or Heinz bodies with part of the membrane and hemoglobin are phagocytosed by cells of the reticuloendothelial system and the erythrocyte takes the form of a "bitten" (degmacyte).

Symptoms of glucose-6-phosphate dehydrogenase

The disease can be found in a child of any age. Reveal five clinical forms manifestations of deficiency of glucose-6-phosphate dehydrogenase in erythrocytes.

1. Hemolytic disease of the newborn, not associated with serological conflict (group or Rh incompatibility).

Associated with variants of glucose-6-phosphate dehydrogenase B (Mediterranean) and Canton.

Most common in newborn Italians, Greeks, Jews, Chinese, Tajiks, Uzbeks. Possible provoking factors of the disease are the intake of vitamin K by the mother and child; the use of antiseptics or dyes in the treatment of the umbilical wound; use of diapers treated with naphthalene.

Newborns with glucose-6-phosphate dehydrogenase deficiency in erythrocytes have hyperbilirubinemia with signs of hemolytic anemia, but evidence of serological conflict between mother and child is usually absent. The severity of gierbilirubinemia may be different, the development of bilirubin encephalopathy is possible.

1. Chronic non-spherocytic hemolytic anemia

It is found mainly in northern Europeans.

Seen in older children PI adults; increased hemolysis is noted under the influence of intercurrent infections and after taking medications. Clinically, there is constant moderate pallor of the skin, mild icterus, and slight splenomegaly.

1. Acute intravascular hemolysis.

Occurs in apparently healthy children after taking medications, less often in connection with vaccination, viral infection, diabetic acidosis.

Currently, 59 potential hemolytics have been identified in glucose-6-phosphate dehydrogenase deficiency. To the group medicines that necessarily cause hemolysis include: antimalarial drugs, sulfa drugs, nitrofurans.

Acute intravascular hemolysis develops, as a rule, 48-96 hours after the patient has taken a drug that has oxidizing properties.

Drugs that cause hemolysis in individuals with insufficient activity of glucose-6-phosphate dehydrogenase in erythrocytes

The severity of hemolysis varies depending on the degree of enzyme deficiency and the dose of the drug taken.

Clinically during an acute hemolytic crisis general state the child is severe, severe headache, febrile fever are noted. Skin and sclera pale icteric. The liver is most often enlarged and painful; the spleen is not enlarged. Repeated vomiting with an admixture of bile, intensely colored stools are observed. A typical symptom of acute intravascular hemolysis is the appearance of urine the color of black beer or a strong solution of potassium permanganate. With very intense hemolysis, acute renal failure and DIC may develop, which can lead to death. After the withdrawal of drugs that cause a crisis, hemolysis gradually stops.

1. Favism.

Associated with ingestion of fava beans (Vicia fava) or inhalation flower pollen some beans. Favism may occur upon first contact with the beans, or may be observed in individuals who have previously consumed these beans, but had no manifestations of the disease. Boys predominate among the patients. Favism most often affects children aged 1 to 5 years, in children early age the process is particularly difficult. Relapses of the disease are possible at any age. The time interval between the consumption of fava beans and the development of a hemolytic crisis ranges from several hours to several days. The development of a crisis may be preceded by prodromal signs: weakness, chills, headache, drowsiness, back pain, abdominal pain, nausea, vomiting. Acute hemolytic crisis is characterized by pallor, jaundice, hemoglobinuria, which persists for up to several days.

1. Asymptomatic form.

Laboratory data

In the hemogram of patients with glucose-6-phosphate dehydrogenase deficiency, normochromic hyperregenerative anemia of varying severity is detected. Reticulocytosis can be significant, in some cases reaching 600-800%, normocytes appear. Anisopoikilocytosis, basophilic puncture of erythrocytes, polychromasia are noted, fragments of erythrocytes (schizocytes) can sometimes be seen. At the very beginning of the hemolytic crisis, as well as in the period of hemolysis compensation after a special blood smear staining, Heinz-Ehrlich bodies can be found in erythrocytes. During the crisis, in addition, there is leukocytosis with a shift leukocyte formula to the left.

Biochemically, there is an increase in the concentration of bilirubin due to indirect, sharp increase plasma free hemoglobin levels, hypohaptoglobinemia.

In the bone marrow punctate, a sharp hyperplasia of the erythroid germ is revealed, the number of erythroid cells can reach 50-75% of the total number of myelokaryocytes, and erythrophagocytosis is detected.

To verify the insufficiency of glucose-6-phosphate dehydrogenase in erythrocytes, methods of direct determination of enzyme activity in erythrocytes are used. The study is carried out in the period of hemolysis compensation.

To confirm the hereditary nature of the disease, the activity of glucose-6-phosphate dehydrogenase must also be determined in the patient's relatives.

Differential Diagnosis

It is carried out with viral hepatitis, other fermentopathies, autoimmune hemolytic anemia.

Treatment of glucose-6-phosphate dehydrogenase

It is necessary to exclude the use of drugs that provoke hemolysis. Folic acid is recommended.

With a decrease in hemoglobin concentration less than 60 g / l, replacement therapy erythrocyte mass (quality requirements and calculation of the volume of erythrocyte mass are presented below).

G-6-FDG - carbohydrate metabolism enzyme, a large number of the enzyme is found in erythrocytes. In the absence of G-6-FDG in erythrocytes, hemoglobin malfunction occurs. Congenital deficiency of G-6-PDG of erythrocytes refers to common hereditary anomalies (enzymopathies) and manifests itself clinically as hemolytic anemia.
Back in 1926, it was found that when using an antimalarial drug (pamachin) in a number of patients, a massive destruction of red blood cells occurred within a few days after taking it, jaundice developed, a sharp drop in hemoglobin, and blackening of urine. The reason was discovered in 1956 and was associated with a deficiency of the enzyme of the pentose phosphate pathway - G-6-PDG, which synthesizes NADPH. One of the main roles of NADRN in erythrocytes is the reduction of glutathione. The lack of reduced glutathione and the action of drugs such as pamaquin cause changes in the surface of red blood cells, which increases their destruction. The lack of glutathione is simultaneously accompanied by an increase in the formation of toxic peroxides, which also negatively affects the state of the cell membrane. Thus, deficiency of glucose-6-phosphate dehydrogenase is the cause of drug-induced hemolytic anemia.

Hereditary deficiency of erythrocyte enzymes is most often manifested by the action of certain toxins and drugs on the body in the form of acute hemolysis, less often chronic hemolysis. Among them, G-6PD deficiency is the most common.

G-6PD is the first enzyme of anaerobic glycolysis or pentose shunt. It plays a large role in the elimination of toxic peroxides in red blood cells. G-6PD is a polymer consisting of 2-6 units; dimer of two chains - active form enzyme; its concentration in the cell depends on the concentration of NADP, which increases under the influence of oxidants, leading to an increase in the activity of G-6PD.

There are over 100 variants of the G-6FD. In persons of different races, different G-6PD isoenzymes are found in erythrocytes, which differ somewhat in their activity and stability. In most cases, enzyme deficiency remains asymptomatic under normal conditions and is manifested by hemolytic crises when taking oxidant medications. Sometimes, with a more pronounced deficiency of G-6PD, hemolysis occurs chronically. It is always carried out with the accumulation of peroxides in erythrocytes, which contribute to the oxidation of hemoglobin (the appearance of Heinz bodies) and lipids of the erythrocyte membrane.

The genetic transmission of G-6PD deficiency is sex-linked. The corresponding gene is located on the X chromosome at a locus close to the locus of color blindness and distant from the locus of hemophilia. Men - carriers of the altered gene always show clinical manifestations of this pathology. In heterozygous women, the manifestations are mild or absent, and vice versa, in rare homozygous women, there is a pronounced enzymopenia.

According to some reports, there are more than 100 million carriers of the pathological gene. G-6PD deficiency is especially prevalent among dark-skinned individuals, including 10% of black Americans and 10-30% of black Africans. This pathology is also common in the Mediterranean basin, in the Middle East, in Saudi Arabia. She also meets Far East in China, Southeast Asia. In some cases, there is a distinct, as it were, protective effect of this pathology against malaria.

Clinic. The severity of the disease is related to the intensity of the deficiency. A small deficiency (within 20% of the norm) can manifest itself as acute drug-induced hemolysis, more pronounced - jaundice of the newborn, chronic hemolysis.

Episodes of acute hemolysis occur almost always under the influence of an oxidant drug, which was first described in the treatment with primaquine. Later, the effect of other antimalarial drugs, sulfonamides, nitrofuran derivatives (furadonin), some analgesics (amidopyrine, aspirin) and other drugs (quinidine, amilgan, benemid, etc.) became known. Insufficiency of the liver and kidneys (with a violation of the release of drugs from the body) favors acute hemolysis due to G-6PD deficiency.

After taking medication, after 2-3 days, hemolysis develops with anemia, fever, jaundice, and in the case of massive hemolysis - hemoglobinuria. Anemia is usually moderate, normochromic, with an increase in the number of reticulocytes; Heinz bodies are found in erythrocytes. Anemia increases by the 10th day. Then, from the 10th to the 40th day (even if the medication is not stopped), repair occurs, anemia decreases, the number of red blood cells increases with high reticulocytosis (up to 25-30%), reflecting the intensity of bone marrow hematopoiesis. Finally, the so-called equilibrium phase occurs, during which there is no anemia, although hemolysis and active hematopoiesis are still ongoing. The subsequent recovery is due to the fact that the "old" erythrocytes sensitive to the drug are gradually destroyed, and the newly formed ones contain a larger amount of G-6PD and are resistant to hemolysis. However, this resistance is relative (taking large doses of the drug can cause hemolysis) or temporary. These manifestations with a rather favorable course are more characteristic of persons with dark skin. In persons with white and yellow skin manifestations of G-6PD deficiency may be more severe. Intensive hemolysis is accompanied by fever, shock, hemoglobinuria, anuria. The severity of manifestations does not decrease if the drug is not canceled. The disease is provoked by many different medicines, and above all those mentioned above, which are sometimes administered in small doses and for a short time. Some infections (flu, viral hepatitis) can also provoke acute hemolysis.

Chronic hemolytic anemia due to G-6PD deficiency occurs only in whites. Anemia is found in newborns and young children. It remains moderately pronounced, sometimes complicated by acute hemolysis or erythroblastopenia. growth disorders and serious complications characteristic of sickle cell disease and thalassemia are not observed.

As a diagnostic, a simple, indicative test is the detection of Heinz bodies. Spontaneously or after incubation in the presence of phenylhydrazine, inclusions, which are precipitates of hemoglobin derivatives, are found in a significant part of G-6PD-deficient erythrocytes. Heinz bodies are nonspecific and occur in patients with other erythrocyte enzymopathies, toxic anemia, and hemoglobin instability. A number of methods for the semi-qualitative determination of G-6PD deficiency make it possible to detect it before the development of hemolysis. Most of them are based on the use of the sensitivity of the colored indicator to the phenomenon of the conversion of NADP to NADH, which occurs under the action of G-6PD. Thus, the Motulski test is based on measuring the discoloration time of cresyl diamond. The Brewer test evaluates the rate of reduction of methemoglobin by methylene blue.

Enzyme activity is quantified using spectrophotometry and colorimetry. When evaluating the results of these tests at different stages of patient observation, there may be errors associated, in particular, with the fact that high reticulocytosis can mask G-6PD deficiency, since these cells contain a larger amount of the enzyme.

Treatment this pathology is symptomatic. In acute hemolysis with a large drop in hemoglobin, blood transfusions are performed. Insufficiently substantiated use of drugs that cause acute hemolysis in G-6PD deficiency should be avoided.

Included in the pentose phosphate pathway, a metabolic pathway that provides the formation of cellular NADP-H from NADP +. NADP-H is necessary to maintain the level of reduced glutathione in the cell, the synthesis of fatty acids and isoprenoids. The person has a hereditary disorder of G6PD activity, or glucose-6-phosphate dehydrogenase deficiency leads to hemolytic non-spherocytic anemia.

Reaction

Main catalyzed reaction:

D-glucose-6-phosphate + NADP + ↔ D-glucono-1,5-lactone-6-phosphate + NADPH

Structure

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See what "Glucose-6-phosphate dehydrogenase" is in other dictionaries:

glucose-6-phosphate dehydrogenase- An enzyme that catalyzes the oxidation of glucose 6 phosphate with the formation of reduced NADP; one of the most famous hereditary pathologies deficit G. 6 f.; G. 6 f. often used as a population genetic marker (G 6 PDH, G 6 ... ... Technical Translator's Handbook

Glucose 6 phosphate dehydrogenase, G6PD glucose 6 phosphate dehydrogenase [EC 1.1.1.49]. An enzyme that catalyzes the oxidation of glucose 6 phosphate to form reduced NADP; one of the most famous hereditary pathologies is the deficiency of G. 6 f. ... ... Molecular biology and genetics. Dictionary.

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