Drugs to Avoid in G6PD Deficiency Background: Glucose 6-phosphate dehydrogenase (G6PD) deficiency is a genetic blood disorder where an acute attack of a haemolytic anaemia occurs. It is highly common in certain ethnic groups such as: Asians, Africans and Mediterranean and more prevalent in males more than females (1,2) Safe to take But only in normal therapeutic doses [!!!] (Quoted from Ernest Beutler, M.D., Glucose-6-Phosphate Dehydro-genase Deficiency, in Erythrocyte disorders: Anemias due to increased destruction of erythrocytes with enzyme deficiencies, p. 598.) Acetaminophen (paracetamol, Tylenol, Tralgon, hydroxyac Medications that can probably be given safely Dehydrogenase (G6PD) Deficiency in therapeutic dosages to G6PD-deficient patients, including all compounds that were mentioned See table II for overview. by any author or source as causing haemolysis in G6PD-deficient patients, but where after careful 2.1 Methylthioninium Chloride (Methylene review.
93. Bupivacaine. C 18 H 28 N 2 O. High. All. Miscellaneous elements besides drugs that should be avoided: Fava Beans. (Some, but only some, prefer also to avoid red wine, henna (see below), all legumes, blueberries [also yogurts containing these], soya products, tonic water: whether you should avoid any of these would depend on your enzyme. . Some of these drugs may appear also in the list of Unsafe Drugs (marked as Low Risk)
G6PD Deficiency What Is G6PD Deficiency; Symptoms; Brochure; Neonates; Frequent Questions; Safe & Unsafe; lists of drugs and foodstuff to avoid and drugs that are safe to take. answers to frequent questions. It is brought here in a PDF format, viewable (and printable) using the Acrobat Reader plug-in Chapter 24. G6PD Deficiency. X-linked recessive deficiency in glucose-6-phosphate dehydrogenase enzyme leading to RBC hemolysis: More frequent in patients with African, southern European, Middle Eastern, southeast Asian, or central and southern Pacific Island descent The main anaesthetic concern in the treatment of patients with G6PD deficiency is the choice of drugs using for anaesthetic management, and postoperative pain therapy since exposure to oxidative drugs can lead to haemolytic crisis in these patients. Pathogenesis The G6PD is a key enzyme in glucose metabolism [6,10,15]. G6PD converts glucose-6 Risks for people with G6PD deficiency People with G6PD deficiency occasionally have a problem if they: eat broad beans get an infection come into contact with mothballs, or take certain medicines, such as Aspirin or Disprin, and some common antibiotics. Always check with your doctor whether certain medicines are safe to take
. Fortunately, most people with G6PD deficiency do not have problems on a daily basis. However, there are certain medications or foods that increase the rate of red blood cell breakdown break, resulting in haemolysis. G6PD deficiency is a metabolic disorder arising from genetic defects in the G6PD gene. The deficiency results in a breakdown of red blood cells (haemolysis) when the individual is exposed to particular medications eg. primaquine, pathogens or foods. Upon exposure to an oxidative substance Drug Search. Search our database for drug names and trade names in all countries. Enter a drug name or trade name to view risk level. Not finding any results does not necessarily mean the drug is safe to take. Our database includes the most commonly used drugs that might pose a risk to G6PD deficient subjects
Individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency may be more prone to methemoglobinemia and hemolysis [see Warnings and Precautions (5.1)]. ACZONE Gel, 5% and vehicle were evaluated in a randomized, double-blind, cross-over design clinical study of 64 subjects with G6PD deficiency and acne vulgaris G6PD Deficiency. G6PD, which stands for Glucose-6-Phosphate Dehydrogenase is an enzyme in the red blood cells. It acts to protect the red blood cells from hemolysis (breakage of the red blood cells) when exposed to certain medications, food or infections. G6PD deficiency occurs when there is reduced activity of the enzyme in the red blood cells G6PD deficiency is genetically heterogeneous; susceptibility to the hemolytic risk from drugs varies; thus, a drug found to be safe in some G6PD-deficient individuals may not be equally safe in others; Manufacturers do not routinely test drugs for their effects in G6PD-deficient individuals; the risk and severity of hemolysis is almost always.
(G6PD) deficiency risk having severe adverse reactions if exposed to these drugs at certain doses. G6PD deficiency is the most common human enzyme defect, affecting approximately 400 million people worldwide. Scaling up radical cure regimens will require testing for G6PD deficiency, at two levels: 1) the individual level to ensur 7. La Verde N, Bramati A, Girelli S, et al: Safe chemotherapy and hormone therapy for treating early breast cancer in a glucose 6-phosphate dehydrogenase-deficient patient: Case report. Anticancer Drugs 23:758-60, 2012 8. Sonbol MB, Yadav H, Vaidya R, et al: Methemoglobinemia and hemolysis in a patient with G6PD deficiency treated with rasburicase G6PD deficiency Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked inherited disorder caused by a genetic defect in the red blood cell enzyme G6PD, which serves to protect red blood cells from oxidative injury. It can cause jaundice in newborns as well as acute hemolytic anemia in patients exposed t Effects of G6PD deficiency and CDA on post-treatment haemolysis risk In assessing the effect of G6PD deficiency and CDA treatment on a Hb ≥2 g/dl drop, all plausible interactions were considered but only the interaction CDA*G6PD de-ficiency was retained because, even if non-significant, effects were modified when the interaction was deleted
reviews have largely focused on drugs to be avoided in G6PD deﬁciency [4, 5]. Similarly, several reviews have suggested included glucose-6-phosphate deficiency, adverse events, side effects, haemolysis, herbal medicine, dietary supplements and Adverse effects of herbal or dietary supplements in G6PD deficiency: a systematic review. However in patients with G6PD deficiency, 8-aminoquinoline drugs stress the red blood cells to the extent that they can trigger acute hemolytic anemia, which is potentially lethal. For the safe use of 8-aminoquinoline drugs, there is an essential unmet need for a reliable test for G6PD deficiency as a point-of-care diagnostic. Technology solutio Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency in the world and renders those affected susceptible to potentially severe oxidative hemolysis. Although the resulting hemolysis is most often associated with drug exposure, it has also been reported after consumption of certain foods
Glucose-6-phosphate dehydrogenase (G6PD) deficiency represents one of the most common erythrocyte enzymopathy. In the era of drug-eluting stents (DESs), the use of prolonged dual antiplatelet therapy (DAPT) with aspirin (ASA) and thienopyridine (clopidogrel or ticlopidine) has become mandatory in the treatment of patients with acute coronary syndromes (ACS) and/or after percutaneous coronary. human pathology due to G6PD deficiency is preventable by population screening and avoidance ofprecipitants, haemolytic anaemia related to drugs, infection or ingestion of fava beans. The critical role of The genetic heterogeneity of G6PD deficiency means that a drug found to be safe in some deficient subjectsis notnecessarilysafeinall Mandi G, Witte S, Meissner P, et al. Safety of the combination of chloroquine and methylene blue in healthy adult men with G6PD deficiency from rural Burkina Faso. Trop Med Int Health. 2005;10(1):32-38. [PubMed 15655011] Sarkar S, Prakash D, Marwaha RK, et al. Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficiency
G6PD deficiency is usually seen in infants and children. It is one of the rare types of G6PD deficiency.4 Triggering factors There are several triggering factors for haemolytic anaemia in G6PD deficient patients, these include-Ø Medications and other chemical substances Several drugs have the potential to cause hemolysis in G6PD deficient. G6PD is the most common enzymatic deficiency in humans, 1,2 affecting approximately 5% of the world's population. 3 Currently, there are more than 180 reported genetic variants of G6PD and its expression can vary from a mild (class V) to a severe deficiency of the enzyme (class I). 3 G6PD deficient erythrocytes have difficulties in handling oxidative stress and, subsequently, are more.
G6PD deficiency is the most common human enzyme deficiency, more prominent in descendants of African, Middle Eastern, Asian and Mediterranean regions . A study of 2.3 million active-duty service members tested for G6PD deficiency from 2004-2018 in United States, showed that 11.2% of male an Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an inherited disorder caused by a genetic defect in the red blood cell (RBC) enzyme G6PD, which generates NADPH and protects RBCs from oxidative injury. G6PD deficiency is the most common enzymatic disorder of RBCs. G6PD deficiency is an X-linked disorder Summary. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is most common in African, Middle Eastern, Asian and some Mediterranean populations
These antibiotics are also safe to use throughout the pregnancy: Erythromycin, Amoxicillin, Z-pack (Azithromycin), Keflex, Macrobid (unless you have a rare disorder called G6PD deficiency) The following medication/over-the-counter products are safe to use in the usual recommended dose AFTER YOUR FIRST TRIMESTER (AFTER 12 WEEKS OF PREGNANCY) Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect, which may present as acute hemolysis, neonatal jaundice, or chronic hemolysis. Ingestion of fava beans, as well as infection and certain drugs, are the most typical causes of acute hemolysis in people with G6PD deficiency. Aspirin, the cornerstone in current therapies for the prevention of. The following is a partial list of medications and chemicals that individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency should avoid: Acetanilid Furazolidone Isobutyl nitrite Nalidi. G6PD deficiency is the most common human enzyme defect, affecting approximately 400 million people worldwide.Scaling up radical cure regimens will require testing for G6PD deficiency, at two levels: 1) the individual level to ensure safe case management, and 2) the population level to understand the risk in the local population to guide.
• patients with G6PD deficiency or unknown G6PD status due to the risk of hemolytic anemia [see Warnings and Precautions (5.1)]. • breastfeeding by a lactating woman when the infant is found to be G6PD deficient or if the G6PD status of the infant is unknown [see Use in Specific Populations (8.2)] Group on G6PD deficiency in 1985. The meeting report in the Bulletin of the World Health Organization (3) described 310 G6PD variants according to a slightly modified version1 of the five classes in Table 1. Since 1986, when the full G6PD cDNA sequence was published, it has been possible to identify th G6PD deficiency is an inherited condition. It is when the body doesn't have enough of an enzyme called G6PD (glucose-6-phosphate dehydrogenase). This enzyme helps red blood cells work properly. A lack of this enzyme can cause hemolytic anemia. This is when the red blood cells break down faster than they are made severity of hemolytic anemia varies among individuals with G6PD deficiency. Education of patients and their parents regarding safe and unsafe medications and foods is crucial to prevent future episodes of hemolysis. In many cases all members of the patient's family should avoid such precipitating foods. G6PD deficiency is a sex-linked disorder
Safe And Unsafe Drugs Chemicals And Anaesthetic Agents In The Download Table . G6pd Pdf Mims Summary Table Drugs To Avoid In G6pd Deficiency Pharmacological Class Drugs Anthelmintics U2022 U00df Naphthol U2022 Niridazole U2022 Stibophen Course Hero Introduction. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an enzymopathy affecting human red blood cells. 1 It is an X-linked, hereditary genetic defect prevalent in more than 400 million people worldwide. 1 The G6PD is an enzyme necessary for the production of antioxidants that protect red blood cells from oxidative stressors. 1 In the case of G6PD deficiency, red blood cells can. G6PD deficiency is caused by inherited variations in the G6PD gene. Because this is a genetic condition, G6PD deficiency is a life-long condition. Testing for G6PD deficiency. There are two ways to test for G6PD deficiency: a blood test for enzyme activity and a pharmacogenetic test. You may have had one or both of these tests done
G6PD Lifestyle Guide. Oxidative Stress is known to compromise the health of the human body. Any stimuli (trigger) that cause oxidative stress could possibly bring on an attack of Acute Hemolytic Anemia to those who are G6PD deficient. We found established lists of drugs, chemicals, foods, & herbs that are known to cause oxidative stress However, G6PD deficiency is common among blacks and Asians. In a study of 63,302 US military personnel, 2.5% of males and 1.6% of females overall were deficient. Prevalence was higher among African American males (12.2%) and females (4.1%), as well as Asian males (4.3%). 8 G6PD deficiency may play a role in COVID-19 severity of illness and. Background. Deficiency of glucose-6-phosphate dehydrogenase (G6PD) is the most common human enzyme deficiency. It affects 400 million people worldwide.1 G6PD deficiency exhibits an X-linked mode of inheritance. Mutations of the G6PD gene result in different phenotypical variants with different levels of enzyme activity G6pd Pdf Mims Summary Table Drugs To Avoid In G6pd Deficiency Pharmacological Class Drugs Anthelmintics U2022 U00df Naphthol U2022 Niridazole U2022 Stibophen Course Hero . Safe And Unsafe Drugs Chemicals And Anaesthetic Agents In The Download Table
Pharmacologic therapy is not used in glucose-6-phosphate dehydrogenase (G6PD) deficiency. Treatment of hyperbilirubinemia in G6PD-deficient neonates, when indicated, is with phototherapy and exchange transfusions.  Prophylactic oral phenobarbital does not decrease the need for phototherapy or exchange transfusions in G6PD-deficient neonates.  The heme analogue tin-mesoporphyrin (SnMP) has. The A-G6PD deficiency with acute intermittent hemolysis is the most common clinical presentation and is observed in Africans. The Mediterranean type of G6PD deficiency is more severe than the type A-G6PD deficiency. The G6PD deficiency affects about 10% of Afro-Americans and West Africans, 5-15% of Kurds, and 5-35% of Sardinians [240-242]
INTRODUCTION. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most prevalent enzyme deficiency in the world, affecting at least 330 million individuals worldwide. 1 This metabolic enzyme plays an important role in protecting erythrocytes against oxidative stress, thereby preventing hemolysis. Individuals with G6PD deficiency are susceptible to oxidants such as drugs (eg, some. caused by Plasmodium vivax, safe access to primaquine has been denied by the absence of capacity to diagnose glucose-6-phosphate dehydrogenase (G6PD) deficiency in the impoverished rural tropics. Therapy of acute P. vivax malaria requires two distinct classes of antimalarial drugs: blood schizontocidal an
. 1. Avoid Taking Certain Medications. The best way to avoid symptoms due to G6PD deficiency is to limit exposure to the triggers. It's very important for people with G6PD deficiency to avoid taking a number of high riskmedications, which can potentially cause severe reactions Aspirin is the first recommended antiplatelet agent to prevention secondary stroke, but its safety and efficacy in stroke patients with glucose-6-phosphate dehydrogenase deficiency remain unclear. We sought to evaluate its safety and efficacy in ischemic stroke patients with and without glucose-6-phosphate dehydrogenase deficiency G6PD deficiency is a genetic disorder that most often affects males. It happens when the body doesn't have enough of an enzyme called glucose-6-phosphate dehydrogenase (G6PD). G6PD helps red blood cells work. It also protects them from substances in the blood that could harm them. Most people with.
G6PD deficiency (Glucose 6-phosphate dehydrogenase) leads to a condition called hemolytic anemia. Causes of G6PD deficiency is an abnormal gene located in the X-chromosome, therefore, it is more common in males. Hemolytic anemia caused by G6PD deficiency generally occurs after exposure to malaria medications, antiitching drugs, and fava beans G6PD deficiency is a lifelong condition that can be very successfully managed forever. 700,000,000 have g6pd deficiency. It's easily manageable if you know all the trigger dangers . For a full list of medications to avoid , this list from G6PD.org is a good one available online
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an uncommon inherited enzyme deficiency characterized by hemolytic anemia, caused by the inability of erythrocytes to detoxify oxidizing agents such as drugs, infectious diseases, or fava bean ingestion. In this later case, the disorder is known as favism. The aim of the present report was to present a review of the literature in this. G6PD deficiency occurs most frequently in certain parts of Africa, Asia, the Mediterranean, and the Middle East. G6PD deficiency is caused by mutations in the G6PD gene. Treatment may involve medicines to treat infection, stopping drugs that are causing red blood cell destruction, and/or transfusions, in some cases 2) G6PD helps red blood cells work. It also protects them from substances in the blood that could harm them. In people with G6PD deficiency, either the red blood cells do not make enough G6PD or what they do make doesn't work as it should. Without enough G6PD to protect them, the red blood cells break apart. This is called hemolysis (hih-MOL-ih-sis) phosphate dehydrogenase (G6PD) deficiency are more prone to hemolysis with the use of certain drugs. G6PD deficiency is most prevalent in populations of African, South Asian, Middle Eastern, and Mediterranean ancestry. In clinical trials, there was no evidence of clinically relevant hemolysis or hemolytic anemia in subjects treate The use of a G6PD inhibitor as general anesthetic drugs may worsen health of the patients with G6PD deficiency and may lead to fatal outcome. In conclusion, we think that the results of this case report may be useful in choosing of anesthetic drugs for use in a patient with G6PD deficiency. CORRESPONDENCE T
Legend: This is a listing of drugs and compounds reviewed for safety in G6PD deficient patients by the Clinical Pharmacogenetics Implementation Consortium (CPIC) and the FDA. = A compound/drug for which all references with an available review are in agreement that there is a risk of hemolysis in G6PD deficient individuals or the FDA label for. or deficient) ranged from 0 percent (8)-30.5 percent (9). It is expected that G6PD-deficiency prevalence would be half as much in females as the male G6PD-deficiency prevalence rate, and G6PD-intermediate prevalence would be twice as much in females. • Three studies reported quantitative G6PD deficiency estimates by spectrophotometry for males A G6PD screen was performed during his stay, and this was negative for deficiency. As there was a strong suspicion of a G6PD deficiency due to the onset of hemolysis and symptoms after high-dose vitamin C infusion with resultant methemoglobinemia, we requested records from the physician who administered the high-dose vitamin C
Glucose-6-phosphate dehydrogenase (G6PD) de- ficiency is the most common enzyme deficiency producing disease in humans.' but there arc few reports 2,3 in the literature regarding anaesthcsia in patients with this disorder. Haemolysis of red cells in G6PD-deficient individuals may occur after the use of a long list of oxidant drugs . Usage in Pregnancy. Safe usage of this preparation in pregnancy has not been established. Primaquine is contraindicated in pregnant women. Even if a pregnant woman is G6PD normal, the fetus may not be (see CONTRAINDICATIONS). Lactatio other antimalarial drugs are available. Other considerations • ood for last-minute travelers who know G that they do not have G6PD deficiency . because the drug is started 1-2 days before traveling to an area where malaria transmission occurs. • verdose of antimalarial drugs, including O primaquine, can be fatal. Medication shoul Some vivax malaria-endemic countries where G6PD deficiency testing is generally unavailable have adopted the once-weekly radical cure regimen (0.75 mg/kg/week for 8 weeks), known to be safer in less severe G6PD deficiency variants. There is substantial room for improvement in radical cure policies and practices distribution of G6PD low-function alleles correlates with malaria endemic regions, and this originally prompted the notion that G6PD deficiency confers protection from malaria. Populations from Asia, Africa and the Middle East are associated with the highest prevalence of G6PD deficiency (Supplemental Table S3, S4 and S5)
Hemolytic anemia and G6PD deficiency. Due to the risk of hemolytic anemia in patients with G6PD deficiency, G6PD testing has to be performed before using primaquine. Due to the limitations of G6PD tests, physicians need to be aware of residual risk of hemolysis and adequate medical support and follow-up to manage hemolytic risk should be available In Italy, the enzymopenia G6PD is often incorrectly called favism, since the hemolytic crisis due to the ingestion of fava beans is the best-known clinical manifestation. People with G6PD deficiency are mostly asymptomatic and hemolysis is determined - with very few exceptions - by a triggering factor (3,4)
However, the greatest limitation in the use of this drug is the risk of haemolysis in patients with a significant enzymatic deficiency of G6PD . G6PD deficiency is an X-linked genetic disorder that affects more than 400 million people worldwide, and its average prevalence in countries with endemic malaria is 8% (3-30%) [8, 9] However, a significant obstacle to its use for the treatment of vivax malaria has been concern about its safety in populations with G6PD deficiency, in whom it may precipitate acute haemolytic anaemia. G6PD deficiency is relatively common in malaria-endemic countries, and its prevalence is highest in sub-Saharan Africa and the Arabian Peninsula All G6PD mutations known (Table 2), except G6PD A, are associated with more or less severe enzyme deficiency but never with complete loss of activity; there are no frameshift mutations in the database (such mutations presumably are lethal; dis- cussed previously and later), and the only nonsense mutation has been found in a het- erozygous woman. Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is the most common enzyme deficiency of human erythrocyte affecting more than 400 million people worldwide.In India, G6PD deficiency was first reported in 1963 and since then various investigations have been conducted across country. The objective of this work was to study the prevalence of G6PD deficiency in dif- ferent ethnic, caste and. INTRODUCTION. G6PD is the most common enzymatic deficiency in humans, 1,2 affecting approximately 5% of the world's population. 3 Currently, there are more than 180 reported genetic variants of G6PD and its expression can vary from a mild (class V) to a severe deficiency of the enzyme (class I). 3 G6PD deficient erythrocytes have difficulties in handling oxidative stress and, subsequently, are.
Glucose 6 phosphate dehydrogenase (G6PD) deficiency is a hereditary condition in which red blood cells break down when the body is exposed to certain foods, drugs, infections or stress.It occurs when a person is missing or has low levels of the enzyme glucose-6-phosphate dehydrogenase. This enzyme helps red blood cells work properly. Symptoms during a hemolytic episode may include dark urine. G6PD Deficiency . Background . X-linked disorder, the most common enzymatic disorder of RBCs. Hemolysis is the result of the inability of the RBC to protect itself from oxidative stress. Spectrum of disease: chronic hemolysis, intermittent hemolysis, hemolysis only with triggers, no hemolysi Partial List of Drugs and Chemicals in Glucose-6-Phosphate Dehydrogenase Deficiency* Unsafe for Class I, II, and III Variants. Safe for Class II and III Variants *Note: This is a partial list only. Source: Beutler E. G6PD deficiency. Blood. 1994 Dec 1; 84(11):3613-3636. Acetanilid. Acetaminophen. Dapsone. Aminopyrine. Furazolidon
Glucose-6-phosphate dehydrogenase deficiency. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a condition in which red blood cells break down when the body is exposed to certain drugs or the stress of infection. It is hereditary, which means it is passed down in families Glucose-6-phosphate dehydrogenase (G6PD) deficiency was originally recognized through its association with haemolysis related to eating fava beans (' favism ') and primaquine ingestion. 178 G6PD deficiency is the most common enzyme defect in humans and is present in about 400 million people worldwide (Figure 65.10). 179,180 It is an X. and deficient G6PD activity levels and as an aid in the identification of people with G6PD deficiency. Therefore, it is not approved to rule in or out G6PD deficiency or to be the sole basis for clinical decisions taken concerning administration of medicines known to induce acute hemolytic anemia in subjects with G6PD deficiency
This is a pretty good list. Drugs to Avoid List G6PD Deficiency Avoid List All legumes prohibited (chickpeas, lentils, peanuts, beans, beans, soybeans, soybean oil. Hemolytic reactions to this substance have been reported only in few, isolated cases and no written reference exists as of this time. Among the alternatives are Paracetamol, which is generally considered safe, and flurbiprophene. Probably safe in moderate doses. Use with caution and not in combination with other drugs In the recent review article published in Drug Safety by Youngster and colleagues, methylthioninium chloride (methylene blue) was identified as one of seven drugs that should be avoided in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency due to evidence of an association with haemolysis.However, this conclusion was based on case reports from the literature of only five.
G6PD deficiency is a genetic condition caused by a lack of the G6PD enzyme in the blood. Learn about G6PD deficiency symptoms, diagnosis, and treatment A G6PD deficiency is an inherited disorder. It's most common in men of African, Asian, or Mediterranean descent. It's the result of X-linked recessive transmission, which means it's much. Using G6PD tests to enable the safe treatment of Plasmodium vivax infections with primaquine on the Thailand-Myanmar border: A cost-effectiveness analysis. PLoS Negl Trop Dis . 2017 May. 11 (5.
Other G6PD variants including Kaiping (18%, 9/50), Viangchan (6%, 3/50), Mediterranean (4%, 2/50), Union (2%, 1/50) and Canton (2%, 1/50) were also observed. Results of this study suggest that more concern for proper and safe use of PQ as a radical cure of malaria in Myanmar is needed by combining G6PD deficiency test before PQ prescription [Hundreds of forbidden drugs] Parents whose child with glucose-6-phosphate dehydrogenase (G6PD) deficiency have this nightmare of guarding against drugs or medicines which may cause contraindications of hemolytic anemia (breakup of red blood cells) to their child. There are indeed many drugs or medicines which are forbidden to be used for children with this genetic disease Synonyms: G6PD/G-6-PD deficiency, non-spherocytic haemolytic anaemia The enzyme glucose-6-phosphate dehydrogenase (G6PD) is one of the enzymes of the pentose phosphate pathway. This pathway is involved in keeping an adequate amount of the coenzyme nicotinamide adenine dinucleotide phosphate (NADPH) in cells