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Hutchinson-Gilford progeria syndrome

1st described in 1886. Epidemiology: - rare, 100 cases reported worldwide [3] - 1 in 4,000.000 births [6] Pathology: 1) accelerated atherosclerosis 2) premature aging 3) alopecia 4) atrophy of subcutaneous fat 5) skeletal hypoplasia a) stiff joints b) hip dislocations 6) progerin (protein protein product of mutant LMNA gene) disrupts nuclear membrane, alters transcription Genetics: 1) point mutations in the LMNA gene a) mutations not found in parents, this NOT inherited b) point mutation C->T in exon 11 of the LMNA gene in 25 patients 1] results in a silent Gly-Gly change at codon 608 2] apparently occurs at cryptic splice site 3] results in protein with deleted C-terminus (50 amino acid residues) 4] C-terminus contains endoproteolytic cleavage site for normal synthesis of lamin A 5] result is abnormalities in nuclear membrane c) other point mutations in exon 11 the LMNA gene have been reported 2) 3 patients described without LMNA gene mutations Clinical manifestations: 1) normal development during the 1st year of life 2) growth retardation beginning in the 2nd year of life 3) mean age of diagnosis is 19 months 4) senile appearance a) dry, wrinkled, sclerotic skin b) alopecia c) bird-like facies d) joint contractures e) decreased body fat 5) farsightedness 6) low-frequency conductive hearing loss 7) speech deficits 8) dental abnormalities Laboratory: - prolonged prothrombin time [4] - thrombocytosis - increased serum phosphorus Special laboratory: - echocardiography may be useful in clinical trials [3] Complications: 1) atherosclerosis a) myocardial infarction b) TIA, stroke 2) LV diastolic dysfunction most common cardiac abnormality [3] - prevalence increases with age - LV systolic dysfunction & valvular heart disease less common 3) seizures Management: - lonafarnib may delay mortality [6] - pravastatin adds no cardiovascular benefit [7] - zoledronate may improve bone mineral density - prognosis - most patients die by the age of 13

General

progeroid syndrome

Database Correlations

OMIM 176670

References

  1. Harrison's Principles of Internal Medicine, 13th ed. Isselbacher et al (eds), McGraw-Hill Inc. NY, 1994, pg 1038
  2. Stedman's Medical Dictionary 26th ed, Williams & Wilkins, Baltimore, 1995
  3. Novelli G & D'Apice MR, Trends in Mol Med 9(9):370, 2003
  4. Merideth MA et al, Phenotype and course of Hutchinson-Gilford progeria syndrome. N Engl J Med 2008, 358:592 PMID: 18256394
  5. Prakash A, Gordon LB, Kleinman ME et al Cardiac Abnormalities in Patients With Hutchinson-Gilford Progeria Syndrome. JAMA Cardiol. Published online February 21, 2018 PMID: 29466530 https://jamanetwork.com/journals/jamacardiology/article-abstract/2672949
  6. Gordon LB, Shappell H, Massaro J et al Association of Lonafarnib Treatment vs No Treatment With Mortality Rate in Patients With Hutchinson-Gilford Progeria Syndrome. JAMA. 2018;319(16):1687-1695 PMID: 29710166 https://jamanetwork.com/journals/jama/fullarticle/2679278? - Hisama FM, Oshima J. Precision Medicine and Progress in the Treatment of Hutchinson-Gilford Progeria Syndrome. JAMA. 2018;319(16):1663-1664. PMID: 29710145 https://jamanetwork.com/journals/jama/fullarticle/2679255
  7. Gordon LB, Kleinman ME, Massaro J et al Clinical Trial of the Protein Farnesylation Inhibitors Lonafarnib, Pravastatin, and Zoledronic Acid in Children With Hutchinson-Gilford Progeria Syndrome. Circulation. 2016 Jul 12;134(2):114-25. PMID: 27400896 Free PMC Article