Glucose-6-phosphate dehydrogenase deficiency history and symptoms: Difference between revisions
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{{Glucose-6-phosphate dehydrogenase deficiency}} | {{Glucose-6-phosphate dehydrogenase deficiency}} | ||
'''For patient information, click [[Xyz (patient information)|here]]''' | |||
{{CMG}}; {{AE}}{{MA}} | |||
{{SK}} | |||
==[[Xyz overview|Overview]]== | |||
==[[Xyz historical perspective|Historical Perspective]]== | |||
==[[Xyz classification|Classification]]== | |||
==[[Xyz pathophysiology|Pathophysiology]]== | |||
==[[Xyz causes|Causes]]== | |||
==[[Xyz differential diagnosis|Differentiating Xyz from other Diseases]]== | |||
==[[Xyz epidemiology and demographics|Epidemiology and Demographics]]== | |||
==[[Xyz risk factors|Risk Factors]]== | |||
==[[Xyz screening|Screening]]== | |||
==[[Xyz natural history, complications and prognosis|Natural History, Complications and Prognosis]]== | |||
==Diagnosis== | |||
[[Xyz diagnostic study of choice|Diagnostic study of choice]] | [[Xyz history and symptoms|History and Symptoms]] | [[Xyz physical examination|Physical Examination]] | [[Xyz laboratory findings|Laboratory Findings]] | [[Xyz electrocardiogram|Electrocardiogram]] | [[Xyz x ray|X-Ray Findings]] | [[Xyz echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Xyz CT scan|CT-Scan Findings]] | [[Xyz MRI|MRI Findings]] | [[Xyz other imaging findings|Other Imaging Findings]] | [[Xyz other diagnostic studies|Other Diagnostic Studies]] | |||
==Treatment== | |||
[[Xyz medical therapy|Medical Therapy]] | [[Xyz interventions|Interventions]] | [[Xyz surgery|Surgery]] | [[Xyz primary prevention|Primary Prevention]] | [[Xyz secondary prevention|Secondary Prevention]] | [[Xyz cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]] | |||
==Case Studies== | |||
[[Xyz case study one|Case #1]] | |||
[[Category: (name of the system)]] | |||
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com] | {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com] | ||
Revision as of 19:30, 30 July 2018
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Glucose-6-phosphate dehydrogenase deficiency Microchapters |
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Differentiating Glucose-6-phosphate dehydrogenase deficiency from other Diseases |
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Diagnosis |
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For patient information, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]
Synonyms and keywords:
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Xyz from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
Case #1 Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.D. [4]
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Overview
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive hereditary disease featuring abnormally low levels of the G6PD enzyme, which plays an important role in red blood cell function. Individuals with the disease may exhibit non-immune hemolytic anemia in response to a number of causes. It is closely linked to favism, a disorder characterized by a hemolytic reaction to consumption of broad beans, with a name derived from the Italian name of the broad bean (fava). Sometimes the name, favism, is alternatively used to refer to the enzyme deficiency as a whole.
History and Symptoms
History
- Patients are almost exclusively male, due to the X-linked pattern of inheritance, but female carriers can be clinically affected due to lyonization where random inactivation of an X-chromosome in certain cells creates a population of G6PD deficient red cells coexisting with normal red cells.
- History of hemolytic crises occurs 2-4 days in response to:
- Certain drugs:
- Primaquine (an antimalarial)
- Sulphonamide antibiotics
- Sulphones (e.g. dapsone, used against leprosy)
- Other sulphur-containing drugs: glibenclamide (an anti-diabetic drug)
- Nitrofurantoin (an antibiotic often used for urinary tract infections)
- Vitamin K analogues
- Several others[1]
- Henna can cause a haemolytic crisis in G6PD deficient infants.[2]
- Certain foods, most notably broad beans
- Illness (severe infections)
- Diabetic ketoacidosis
- Certain drugs:
Symptoms
- Symptoms suggestive of anemia such as fatigue, palpitation
- Prolonged jaundice
- Hemolytic features like dark colored urine
- Abdominal or back pain
- Very severe crises can cause acute renal failure
References
- ↑ "The G6PD Deficiency Homepage -- Table 2". Retrieved 2007-10-28.
- ↑ Raupp P, Hassan JA, Varughese M, Kristiansson B (2001). "Henna causes life threatening haemolysis in glucose-6-phosphate dehydrogenase deficiency". Arch. Dis. Child. 85 (5): 411–2. PMID 11668106.