G6PD Deficiency
nThe LeedsTeaching HospitalsNHS TrustG6PD deficiencyInformation for patients & families
IntroductionG6PD (glucose-6-phosphate dehydrogenase) deficiencydescribes a shortage of an enzyme (chemical) found in thered blood cells. It is very common in certain racial groups,and scientists think there are about 400 million people in theworld with G6PD deficiency.G6PD deficiency does not go away and is a lifelong condition.It is an inherited disease (i.e. passed on from previousgenerations). You cannot catch it by being in contact withsomeone else.It is more common in males and is usually passed on to malechildren from their mother, even though she has had nosymptoms herself. The mother is described as being a carrierof the condition. Your doctor can explain the way in whichit is inherited and the tests that can be done to check for thecondition.Most people with G6PD deficiency have a completely normallife as long as they avoid certain foods and drugs. Somepeople with the condition will get anaemia. Anaemia canmake children look pale and have less energy. This mayhappen after taking one of the drugs or eating the foodslisted below, or during an illness such as an infection. Somebabies with G6PD deficiency may have jaundice for longerthan usual in the first month of life. Jaundice makes the skinlook yellow because of the breakdown of red blood cells.2
Signs and symptomsIf your child has G6PD deficiency, they should be checked by adoctor whenever any of the following symptoms develop: pale skin (pallor) persistent and/or severe tiredness dark coloured urine (wee) jaundice (yellow skin or eyes).If you are worried or concerned please contact:Children’s Haematology and Oncology Day UnitMonday - Friday 8.30am - 6pmTel: 0113 392 7379Ward L316pm - 8:30am Weekends and bank holidaysTel: 0113 392 74313
Care at homeYou should always check with your doctor or pharmacistbefore giving any medication to your child.In particular your child should avoid the foods, drugs andchemicals on this list:Antibiotics Sulphonamides (check with your doctor) Co-trimoxazole (Bactrim, Septrin) Dapsone Chloramphenicol Nitrofurantoin Nalidixic acid AntimalarialsAlways discuss with your doctor before you take anyantimalarial medication such as: Chloroquine Hydroxychloroquine Primaquine Quinine MepacrineChemicals Moth balls (naphthalene) Methylene blue4
Foods Fava beans - also called broad beans(If you are not sure, identify the bean before using. Thehospital can help.)Other drugs Sulphasalazine Methyldopa Large doses of vitamin C Hydralazine Procainamide Quinidine Some anti-cancer drugsAlways check the labels of any medications you buy without aprescription.Be careful about using herbal, naturopathic or otheralternative / complementary therapies.5
Key points to remember G6PD is an inherited condition and cannot be spread fromone person to another. Most people with G6PD deficiency have a completelynormal life as long as they avoid certain foods and drugs. Some people with the condition will get anaemia orjaundice, especially after taking medicine or eating foodthey should avoid, or after an infection. Give copies of this factsheet to other people who care foryour child (e.g. school, nursery, crèche, babysitters) and takeit with you when you visit your GP.6
Useful contactsG6PD Deficiency Associationwww.g6pd.orgChildren’s Haematology and Oncology Day UnitLevel C, Clarendon wing, Leeds Children’s Hospital at LeedsGeneral InfirmaryReception: 0113 392 7179 (To re-arrange, cancel or checkappointments)Nurses: 0113 392 7379 (For medical advice)Unit Manager: Julie White, 0113 392 8806Ward L31Level A, Clarendon Wing, LGITel: 0113 392 74317
The Leeds Teaching Hospitals NHS Trust 1st edition (Ver 1)Developed by: Mike Richards, Consultant Paediatric Haematologist andBen Sykes, Clinical Nurse Specialist Paediatric HaematologyProduced by: Medical Illustration Services MID code: 20180316 009/BPLN004304Publication date09/2018Review date09/2021
6 Key points to remember G6PD is an inherited condition and cannot be spread from one person to another. Most people with G6PD deficiency have a completely normal life as long as they avoid certain foods and drugs. Some people with the condition will get anaemia or jaundice, especially after taking medicine or eating food
G6PD deficient according to WHO reports (6). G6PD deficiency screening studies carried out in Aegean region indicates that the frequency of severe G6PD deficiency in population conforms to the screening criteria of WHO G6PD Deficiency Working Committee. If severe G6PD deficient people consume certain oxidative foods such as fava beans
chromosomes (XX). The gene coding for G6PD enzyme is located on the X chromosome. As males have only one X chromosome and thus one copy of G6PD gene, they would have G6PD deficiency if the G6PD gene carries a mutation. The G6PD activity in the blood will be reduced. A female who has a mutant G6PD gene on one of her X
It is a lifelong condition, however G6PD deficient can have a completely normal life as long as they avoid triggers such as drugs and chemical exposures that can cause oxidant stress.[6] Prevalence of G6PD in Malaysia: Figure 2: An overview of G6PD deficiency prevalence in Malaysia [2]
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. As result males who inherit a G6PD mutation are hemizygous for the defect all their RBCs are affected. Females who inherit a heterozygous G6PD mutation
in an enzyme called G6PD, which helps defend red blood cells against stresses. Primaquine damages these cells so that they burst, leading to anaemia. This is a major problem because G6PD deficiency is common in regions where malaria is present: in some areas up
the disease. Normal G6PD is designated as type B. There are many types of variants of the mutated G6PD gene; among them, two types are commonly found as the cause of favism: type A- that is found in African populations and the Mediterranean variant that is most common in Caucasians, [3, 5]. G6PD deficiency is mainly expressed in male (XY)
G6PD Mahi-dol is the best-characterized Asian variant and is con-sidered predominant across Myanmar and Thailand [40,41]. Enzyme activity in G6PD Mahidol individuals is reduced to 5-32% of normal levels [42], and its prima-quine sensitivity phenotype lies between that of the G6PD A- and Mediterranean variants [43,44]. As for the
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