Glucose-6-phosphate dehydrogenase deficiency medical therapy: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(6 intermediate revisions by 2 users not shown)
Line 2: Line 2:
__NOTOC__
__NOTOC__
{{Glucose-6-phosphate dehydrogenase deficiency}}
{{Glucose-6-phosphate dehydrogenase deficiency}}
{{CMG}}; {{AE}}{{MA}} [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu] [mailto:malihash@bidmc.harvard.edu]
{{CMG}}; {{AE}}{{MA}}  


==Overview==
==Overview==
There is no treatment for [disease name]; the mainstay of therapy is supportive care.
The mainstay of treatment for G6PD deficiency is avoidance of the foods such as [[Fava bean|fava beans]] and drugs that cause [[hemolysis]]. Pharmacologic medical therapy is recommended among patients with chronic [[hemolysis]]. [[Blood transfusion]] can be considered in the acute phase of [[hemolysis]].  
 
OR
 
Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].
 
OR
 
The majority of cases of [disease name] are self-limited and require only supportive care.
 
OR
 
[Disease name] is a medical emergency and requires prompt treatment.
 
OR
 
The mainstay of treatment for [disease name] is [therapy].
 
OR
 
The optimal therapy for [malignancy name] depends on the stage at diagnosis.
 
OR
 
[Therapy] is recommended among all patients who develop [disease name].
 
OR
 
Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
 
OR
 
Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
 
OR
 
Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
 
OR
 
Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].


==Medical Therapy==
==Medical Therapy==
* The mainstay of treatment for is avoidance of the foods such as fava beans and drugs that cause hemolysis.<ref name="pmid7949118">{{cite journal |vauthors=Beutler E |title=G6PD deficiency |journal=Blood |volume=84 |issue=11 |pages=3613–36 |date=December 1994 |pmid=7949118 |doi= |url=}}</ref>
* The mainstay of treatment for G6PD deficiency is avoidance of the foods such as [[Fava bean|fava beans]] and drugs that cause hemolysis.<ref name="pmid7949118">{{cite journal |vauthors=Beutler E |title=G6PD deficiency |journal=Blood |volume=84 |issue=11 |pages=3613–36 |date=December 1994 |pmid=7949118 |doi= |url=}}</ref>
* Neonatal jundice:
* Neonatal [[jaundice]]:
** Mild: no treatment
** Mild: no treatment
** Intermediate: phototherapy  
** Intermediate: [[phototherapy]]
** Sever: Exchange
** Severe: [[exchange transfusions|exchange transfusion]]
* Blood transfusion in acute phase of hemolysis
* [[Blood transfusion]] in acute phase of [[hemolysis]]
* Dialysis in acute kidney failure
* [[Dialysis]] in [[Acute kidney injury|acute kidney failure]]
* Folic acid for patients with chronic hemolysis  
* [[Folic Acid|Folic acid]] for patients with chronic [[hemolysis]]<ref name="pmid27040960">{{cite journal |vauthors=Luzzatto L, Nannelli C, Notaro R |title=Glucose-6-Phosphate Dehydrogenase Deficiency |journal=Hematol. Oncol. Clin. North Am. |volume=30 |issue=2 |pages=373–93 |date=April 2016 |pmid=27040960 |doi=10.1016/j.hoc.2015.11.006 |url=}}</ref>
*  
*  
*  
*  
Line 62: Line 22:
===Disease Name===
===Disease Name===
* '''Adult'''
* '''Adult'''
** Folic acid: 1 mg daily.
** [[Folic Acid|Folic acid]]: 1 mg daily
 
* '''Pediatric'''
***
**** 1
 
*
**


==References==
==References==
Line 76: Line 29:
{{WH}}
{{WH}}
{{WS}}
{{WS}}
[[Category: (name of the system)]]
<nowiki>{Glucose-6-phosphate dehydrogenase deficiency}}</nowiki>
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com]
Please help WikiDoc by adding content here.  It's easy!  Click  [[Help:How to Edit a Page|here]]  to learn about editing.
==Overview==
'''Glucose-6-phosphate dehydrogenase (G6PD) deficiency''' is an [[Sex-linked|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 [[Vicia faba|broad bean]]s, with a name derived from the [[Italian language|Italian]] name of the broad bean (''fava''). Sometimes the name, [[favism]], is alternatively used to refer to the enzyme
deficiency as a whole.
==Treatment==
* In the acute phase of hemolysis, [[blood transfusion]]s might be necessary. Blood transfusion is an important symptomatic measure, as the transfused red cells are generally not G6PD deficient.
* [[Dialysis]] in [[acute renal failure]]
* Some patients benefit from removal of the [[spleen]] ([[splenectomy]]), as this is an important site of [[red blood cell]] destruction. * [[Folic acid]] should be used in any disorder featuring a high [[red blood cell]] turnover.
* Although [[vitamin E]] and [[selenium]] have antioxidant properties, their use does not decrease the severity of [[G6PD deficiency]].
====Contraindicated medications====
{{MedCondContrAbs
|MedCond = Glucose-6-phosphate dehydrogenase (G6PD) deficiency  |Pegloticase}}
==References==
{{reflist|2}}
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}
[[Category:Disease]]
[[Category:Hematology]]
[[Category:Mature chapter]]
[[Need content]]

Latest revision as of 23:39, 19 December 2018


Glucose-6-phosphate dehydrogenase deficiency Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Glucose-6-phosphate dehydrogenase deficiency 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

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Glucose-6-phosphate dehydrogenase deficiency medical therapy On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Glucose-6-phosphate dehydrogenase deficiency medical therapy

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Glucose-6-phosphate dehydrogenase deficiency medical therapy

CDC on Glucose-6-phosphate dehydrogenase deficiency medical therapy

Glucose-6-phosphate dehydrogenase deficiency medical therapy in the news

Blogs on Glucose-6-phosphate dehydrogenase deficiency medical therapy

Directions to Hospitals Treating Glucose-6-phosphate dehydrogenase deficiency

Risk calculators and risk factors for Glucose-6-phosphate dehydrogenase deficiency medical therapy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahda Alihashemi M.D. [2]

Overview

The mainstay of treatment for G6PD deficiency is avoidance of the foods such as fava beans and drugs that cause hemolysis. Pharmacologic medical therapy is recommended among patients with chronic hemolysis. Blood transfusion can be considered in the acute phase of hemolysis.

Medical Therapy

Disease Name

References

  1. Beutler E (December 1994). "G6PD deficiency". Blood. 84 (11): 3613–36. PMID 7949118.
  2. Luzzatto L, Nannelli C, Notaro R (April 2016). "Glucose-6-Phosphate Dehydrogenase Deficiency". Hematol. Oncol. Clin. North Am. 30 (2): 373–93. doi:10.1016/j.hoc.2015.11.006. PMID 27040960.

Template:WH Template:WS