Concentrated mononuclear stem cell therapy associated with Nanopharmacology in a patient with Premature Aging (non-classical Progeria)

Main Article Content

Andrés Felipe Torres Obando
Juan Manuel Velasco Quijano
Juan Manuel Paez Ospina

Abstract

The following article presents the clinical case of a patient diagnosed with early aging (progeroid syndrome). Disease of incidence worldwide (1/8 000 000 live births), with few and failed therapeutic schemes, which do not allow evolution or control of the clinical picture, which presents a high mortality at early ages. For this reason it is important to report the clinical case of this patient, who entered our institution at the age of 9 years due to clinical failure of the secondary gait to decrease his muscular strength, associated with signs and symptoms of heart failure, deficit of his bone mass densitometry and progressive loss of hair, valued in a medical meeting by (medical director of cellular regeneration medicine, pediatrician (extra-institutional), anesthesiologist and epidemiologist) where it is approved the performance of treatment with cell regeneration medicine (nanopharmacology and stem cell therapy) for a a one-year period, therapy that allowed him, not only a brake of his initial symptomatology, but reversion of the illness. This article leaves open the possibility for the accomplishment of later studies that they involve the medicine of cellular regeneration like part of the treatment of the patients with this pathology.


 Note: in the medical board did not participate geneticist, the genetic diagnosis was never documented, due to the economic limitation of the family for the taking of the exams, reason for which the patient was managed from early stages as an early ailment syndrome (progeria not classic) without being able to pigeonhole the progeroid syndrome more quickly, despite the fact that phenotypically and clinically the patient presented a compatible picture.


 The patient is referred by an extra-institutional pediatrician (kenndy hospital) who knew the clinical case and the therapeutic processes that were carried out in cell regeneration medicine.

Downloads

Download data is not yet available.

Article Details

How to Cite
Torres Obando, A. F., Velasco Quijano, J. M., & Paez Ospina, J. M. (2019). Concentrated mononuclear stem cell therapy associated with Nanopharmacology in a patient with Premature Aging (non-classical Progeria). Pediatría, 52(2). https://doi.org/10.14295/p.v52i2.117
Section
Case report

References

Weinert BT, Timiras PS. Physiology of Aging Invited Review: Theories of aging. J Appl Physiol (1985). 2003 oct.;95(4):1706-16.

Kudlow BA, Kennedy BK, Monnat RJ Jr. Werner and Hutchinson-Gilford progeria syndromes: mechanistic basis of human progeroid diseases. Nat Rev Mol Cell Biol. 2007 my.;8(5):394-404.

Hayflick L. Theories of biological aging. Exp Gerontol. 1985;20(3-4):145-59.

Subramanian VV, Bickel SE. Aging predisposes oocytes to meiotic nondisjunction when the cohesin subunit SMC1 is reduced. PLoS Genet. 2008 nov.;4(11):1-12.

Xi H, Li C, Ren F, Zhang H, Zhang L. Telomere, aging and age-related diseases. Aging Clin Exp Res. 2013 my.;25(2):139-46.

Csoka AB, Cao H, Sammak PJ, Constantinescu D, Schatten GP, Hegele RA. Novel lamin A/C gene (LMNA) mutations in atypical progeroid syndromes. J Med Genet. 2004 abr.;41(4):304-8.

De Sandre-Giovannoli A, Bernard R, Cau P, Navarro C, Amiel J, Boccaccio I, et al. Lamin a truncation in Hutchinson-Gilford progeria. Science. 2003 jun. 27;300(5628):2055.

Hofer AC, Tran RT, Aziz OZ, Wright W, Novelli G, Shay J, et al. Shared phenotypes among segmental progeroid syndromes suggest underlying pathways of aging. J Gerontol A Biol Sci Med Sci. 2005 en.;60(1):10-20.

González Morán MG. Síndrome de Progeria de Hutchinson-Gilford. Causas, investigación y tratamientos farmacológicos. Educación química. 2014;25(4):432-9.

Viégas J, Souza PL, Salzano FM. Progeria in twins. J Med Genet. 1974 dic.;11(4):384-6.

O'Brien ME, Jensen S, Weiss AS. Hutchinson-Gilford progeria: faithful DNA maintenance, inheritance and allelic transcription of beta(1-4) galactosyltransferase. Mech Ageing Dev. 1998 mzo. 16;101(1-2):43-56.

Goldstein,S. Decrease sensitivity of and progeric human fibroblast to preparation of factors with insulinelike activity. New Engl J. 2001;202: 1305-09.

Ogihara T, Hata T, Tanaka K, Fukuchi K, Tabuchi Y, Kumahara Y. Hutchinson-Gilford progeria syndrome in a 45-year-old man. Am J Med. 1986 jul.;81(1):135-8.

Gabr M, Hashem N, Hashem M, Fahmi A, Safouh M. Progeria, a pathologic study.J Pediatr. 1960 jul.;57:70-7.

Reichel W, Garcia-Bunuel R. Pathologic findings in progeria: myocardial fibrosis and lipofuscin pigment. Am J Clin Pathol. 1970 febr.;53(2):243-53.

Similar Articles

<< < 20 21 22 23 24 25 

You may also start an advanced similarity search for this article.