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Nonopioid and Adjuvant Analgesic Agents
Published in Pamela E. Macintyre, Stephan A. Schug, Acute Pain Management, 2021
Pamela E. Macintyre, Stephan A. Schug
Renal toxicity, historically linked to phenacetin, rarely occurs with paracetamol despite its apparent COX-2 inhibitory effect (Graham et al, 2013). It is specifically recommended for use in patients with renal impairment. Paracetamol hypersensitivity and allergies are unlikely, and it can be used in patients with aspirin-exacerbated respiratory disease (AERD). Compared with NSAIDs, paracetamol causes little or no gastrointestinal (GI) toxicity, and it does not have a significant effect on platelet function, although it can enhance the effect of warfarin (Graham et al, 2013). It can lead to hemolysis if given to patients with the extremely rare glucose-6-phosphate dehydrogenase (G6PD) deficiency.
Blistering skin disorders
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
Skin lesions respond rapidly to the drug dapsone (50–200 mg per day) in most patients. However, dapsone has several potential toxic side effects, including haemolysis, methaemoglobinaemia, and sulfaemoglobinaemia, and may itself cause rashes such as fixed drug eruption. It should not be given to patients with glucose 6-phosphate dehydrogenase deficiency. A gluten-free diet will improve the gastrointestinal lesion and skin disorder in many patients after some months. Topical superpotent corticosteroids, though not useful alone, may help alleviate pruritus when given along with dapsone.
Genetics and metabolic disorders
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
3.33 Which of the following inborn errors of metabolism is X-linked in inheritance?Tay Sachs disease.Fabry disease.Glucose-6-phosphate dehydrogenase deficiency.Menkes disease.Lowe syndrome.
Glucose-6-phosphate dehydrogenase deficiency screening and gene analysis in blood donors of Guangdong province
Published in Hematology, 2022
Hong-Feng Liang, Fen Lin, Jin Lu, Zhi-Xiao Chen, Li-Ye Yang
Guangdong is a high incidence area of G6PD deficiency [8–10,12]. Up to date, blood products are still not required to be checked for G6PD deficiency in China. Generally, most patients with G6PD deficiency usually do not have any symptom, and some will volunteer to donate blood. There is no relative law and regulation for limiting these carriers to donate blood, but the impact of the donated blood on the recipients is not determined clearly yet. Theoretically, hemolysis could occur when the red blood cells with G6PD deficiency encounter oxidative agents or infection. It is clear that antimalarial drugs such as primaquine and quinoline, sulfonamides (sulfonamides isoxazolyl, sulfapyridine, etc.), antipyretics, and analgesics (acetanilide) could cause hemolysis in G6PD-deficient patients [14]. Some commonly used drugs such as acetaminophen, chloramphenicol, and streptomycin have been shown to induce hemolysis [14]. If the recipients received G6PD-deficient blood, and were administered these drugs mentioned above coincidently, the transfused blood could not take effect, and adversely, this act could produce transfusion reaction caused by intravascular hemolysis.
Prevalence of G6PD deficiency in Thai blood donors, the characteristics of G6PD deficient blood, and the efficacy of fluorescent spot test to screen for G6PD deficiency in a hospital blood bank setting
Published in Hematology, 2022
Phinyada Rojphoung, Thongbai Rungroung, Usanee Siriboonrit, Sasijit Vejbaesya, Parichart Permpikul, Janejira Kittivorapart
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked inherited disorder that is characterized by the insufficiency of an enzyme that is used in the pentose phosphate pathway to generate nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is a crucial oxidation reduction molecule that protects red blood cells (RBC) from reactive oxygen species (ROS). Patients with G6PD deficiency manifest varying degrees of acute hemolysis in response to oxidative stress precipitated by certain medications and foods. Transfusion of red cell products from G6PD enzyme deficient donors could cause a potentially unfavorable outcome, especially in newborns and those with hemoglobinopathies [1–3]. Current screening criteria of blood donors relative to red cell disorders in Thailand relies mostly on history taking and point-of-care hemoglobin (Hb) testing. The screening of G6PD deficiency is not performed in the donors at the moment. According to the World Health Organization (WHO) Blood Donor Selection guidelines, only donors with a previous history of hemolysis are to be permanently deferred [4]. However, countries with a high prevalence of G6PD deficiency should establish their own criteria for screening at-risk donors, and they should establish their own transfusion guidelines [5].
Concurrence of glucose-6-phosphate dehydrogenase deficiency in pregnancy
Published in Journal of Obstetrics and Gynaecology, 2022
Avir Sarkar, Minakshi Rohilla, Snigdha Kumari
Glucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency is an inherited monogenic X-linked inborn error of metabolism. G6PD deficiency is global in nature, it has a worldwide incidence of 7.9% and occurs most often in the tropical and subtropical zones of the Eastern Hemisphere (Africa, Europe and Asia). G6PD enzyme deficiency in India ranges from 1 to 10% which is population specific and much more in tribal population (WHO) (Lauden et al. 2019). Interestingly, the prevalence is strikingly low in north India and ranges between 1.2 and 4.4% (Kumar et al. 2016). G6PD is an enzyme essential for glycolysis in tissues including red blood cells. It catalyses nicotinamide adenine dinucleotide phosphate (NADP) to its reduced form, NADPH which in turn protects RBCs from oxidative damage and consequent haemolysis often triggered by stress, infection, drugs like sulfa products, nitro-compounds, nalidixic acid, chemicals like naphthalenes, aniline dyes and certain food products like fava beans, food colouring agents like 1-phenylazo-naphthol-6-sulphonic acid, etc. (Lee et al. 2017). Chronic persistent anaemia refractory to iron supplementation with or without jaundice may be a presenting feature of G6PD deficiency. Females generally escape clinically obvious manifestations of G6PD deficiency due to its X-linked inheritance; however, pregnancy may precipitate haemolysis leading to maternal anaemia (Perkins 1976; Kuliszkiewicz-Janus and Zimny 2003). Two cases of G6PD deficiency detected in pregnancy are reported along with review of relevant literature.