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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Progeria natural history, complications and prognosis

Introduction

Overview

Overview

The symptoms of Hutchinson-Gilford progeria syndrome (HGPS) usually develop in the first decade of life, complications of Hutchinson-Gilford progeria syndrome (HGPS) include progressive atherosclerosis and myocardial infarction. Prognosis is generally poor, in patients with Hutchinson-Gilford progeria syndrome (HGPS).

Natural History, Complications, and Prognosis

Natural History, Complications, and Prognosis

Natural History

  • The symptoms of Hutchinson-Gilford progeria syndrome (HGPS) usually develop in the first decade of life, and start with symptoms as follows:[1][2]
    • Failure to thrive
    • Loss of subcutaneous fat
    • Poor weight gain
      • Weight increase of only 0.44 kg/year
    • Short stature
      • Decreased linear weight gain
    • Alopecia

Complications

  • Common complications of Hutchinson-Gilford progeria syndrome (HGPS) include:[3][4][5]
    • Progressive atherosclerosis
    • Myocardial infarction
    • Transient ischemic attack (TIA)
    • Stroke
    • Exposure keratopathy
    • Conductive hearing loss

Prognosis

  • Prognosis is generally poor, in patients with Hutchinson-Gilford progeria syndrome (HGPS).[6]
  • The presence of progressive atherosclerosis is associated with a particularly poor prognosis among patients with Hutchinson-Gilford progeria syndrome (HGPS).
  • The average lifespan of patients with Hutchinson-Gilford progeria syndrome (HGPS) is about 15 years.[7][8]
References

References

  1. ↑ Gordon LB, McCarten KM, Giobbie-Hurder A, Machan JT, Campbell SE, Berns SD; et al. (2007). “Disease progression in Hutchinson-Gilford progeria syndrome: impact on growth and development”. Pediatrics. 120 (4): 824–33. doi:10.1542/peds.2007-1357. PMID 17908770.
  2. ↑ Merideth MA, Gordon LB, Clauss S, Sachdev V, Smith AC, Perry MB; et al. (2008). “Phenotype and course of Hutchinson-Gilford progeria syndrome”. N Engl J Med. 358 (6): 592–604. doi:10.1056/NEJMoa0706898. PMC 2940940. PMID 18256394.
  3. ↑ Ahmed MS, Ikram S, Bibi N, Mir A (2018). “Hutchinson-Gilford Progeria Syndrome: A Premature Aging Disease”. Mol Neurobiol. 55 (5): 4417–4427. doi:10.1007/s12035-017-0610-7. PMID 28660486.
  4. ↑ Ullrich NJ, Gordon LB (2015). “Hutchinson-Gilford progeria syndrome”. Handb Clin Neurol. 132: 249–64. doi:10.1016/B978-0-444-62702-5.00018-4. PMID 26564085.
  5. ↑ Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Stephens K; et al. (1993). “GeneReviews®”. PMID 20301300.
  6. ↑ Gordon LB, Massaro J, D’Agostino RB, Campbell SE, Brazier J, Brown WT; et al. (2014). “Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome”. Circulation. 130 (1): 27–34. doi:10.1161/CIRCULATIONAHA.113.008285. PMC 4082404. PMID 24795390.
  7. ↑ Gordon LB, Massaro J, D’Agostino RB, Campbell SE, Brazier J, Brown WT; et al. (2014). “Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome”. Circulation. 130 (1): 27–34. doi:10.1161/CIRCULATIONAHA.113.008285. PMC 4082404. PMID 24795390.
  8. ↑ Ahmed MS, Ikram S, Bibi N, Mir A (2018). “Hutchinson-Gilford Progeria Syndrome: A Premature Aging Disease”. Mol Neurobiol. 55 (5): 4417–4427. doi:10.1007/s12035-017-0610-7. PMID 28660486.

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