Erythrocytapheresis versus phlebotomy for hereditary haemochromatosis

Abolaban, Heba; Fares, Maan; Haydour, Qusay; Ibrahim, Nazir; Rayess, Dona; Diab, Maria; Moujahed, Ahmad M Al

doi:10.1002/14651858.cd008855

Cited by 2 publications

(1 citation statement)

References 32 publications

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“…Currently, therapeutic phlebotomy is the primary treatment and standard approach recommended for individuals requiring treatment for HFE ‐HH (i.e., iron overload or symptoms) (Abolaban et al., ; Bacon et al., ; EASL, ). Erythrocytapheresis has also been as an alternative management of care for select individuals with the disorder to achieve iron depletion particularly among those with severe iron overload or other problems associated with the disorder not manageable by current therapeutic phlebotomy (Adams & Barton, ; Poullin & Levevre, ; Rombout‐Sestrienkova et al., ).…”

Section: Genetics/pathophysiology Of Hfe‐associated Hhmentioning

confidence: 99%

HFE -associated hereditary hemochromatosis: Overview of genetics and clinical implications for nurse practitioners in primary care settings

Emanuele

Tuason

Edwards

2014

Journal of the American Association of Nurse Practitioners

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Purpose HFE‐hemochromatosis is one of the most common genetic disorders in the United States among Caucasians of Northern European ancestry. The purpose of this article is to discuss HFE‐associated hereditary hemochromatosis (HH), including the genetics, pathophysiology, phenotype and genotype, diagnostics, and management utilizing a case‐based format as an exemplar. Data sources Online genetic resources; professional guidelines; review; and scientific articles. Conclusion HFE‐HH is an autosomal recessive disorder and two major genes C282Y and H63D are associated with HH (iron overload) susceptibility particularly C282Y/C282Y mutations. It has a variable penetrance and expression. Individuals who develop iron overload may develop broad symptoms, including joint discomfort, fatigue, decreased libido, and abdominal pain; and if left untreated, HFE‐HH has the potential of developing end‐organ disease including liver fibrosis, cirrhosis, and cancer; cardiac arrhythmias or heart failure; and diabetes. Suspicion of the disorder begins with personal and family history, transferrin saturation, and ferritin levels, and if high, genotyping to confirm the disorder. Management consists of correcting iron overload to prevent/delay end‐organ damage often consisting of intermittent phlebotomy. Implications for practice Knowledge of HFE‐HH is essential so that nurse practitioners can identify individuals at risk and to provide appropriate management of care and referral.

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Section: Genetics/pathophysiology Of Hfe‐associated Hhmentioning

confidence: 99%