Literature DB >> 35776147

Proposing a clinical algorithm for better diagnosis of hypophosphatasia in resource-limiting situations.

Sreyanko Sadhukhan1,2, Poonam Mehta1,2, Singh Rajender1,2, Sushil Kumar Gupta3, Naibedya Chattopadhyay4,5.   

Abstract

Early diagnosis of hypophosphatasia (HPP) is challenging. Here, we propose to broaden the diagnostic criteria of HPP by reviewing published data on BMD and fractures in HPP patients. Non-osteoporotic fractures and higher than normal lumbar BMD were recurrent in HPP patients and could be included as diagnostic criteria. HPP is a genetic disorder caused by autosomal recessive or dominant loss-of-function mutations in the ALPL gene that encodes for tissue-nonspecific alkaline phosphatase (TNSALP). Expressive genetic heterogeneity and varying severity of TNSALP deficiency lead to a wide-ranging presentation of skeletal diseases at different ages that coupled with HPP's rarity and limitation of biochemical and mutational studies present serious hurdles to early diagnosis and management of HPP. To widen the scope of HPP diagnosis, we assessed the possibility of areal bone mineral density (BMD) as an additional clinical feature of this disease. PubMed, Web of Science, and ScienceDirect were searched with the following keywords: ("Hypophosphatasia OR HPP") AND ("Bone Mineral Density OR BMD") AND "Human". Studies and case reports of subjects with age ≥ 18 years and having BMD data were included. We pooled data from 25 publications comprising 356 subjects (90 males, 266 females). Only four studies had a control group. Biochemical hallmarks, pyridoxal 5'-phosphate (PLP) and phosphoethanolamine (PEA), were reported in fifteen and six studies, respectively. Twenty studies reported genetic data, nineteen studies reported non-vertebral fractures, all studies reported lumbar spine (LS) BMD, and nineteen reported non-vertebral BMD. Higher than normal and normal BMD at LS were reported in three and two studies, respectively. There was marked heterogeneity in BMD at the non-vertebral sites. Higher than normal or normal LS BMD in an adult with minimal or insufficient fractures, pseudofractures, non-healing fractures, fragility fractures, and stress fractures may be included in the diagnostic protocol of HPP. However, genetic testing is recommended for a definitive diagnosis.
© 2022. International Osteoporosis Foundation and Bone Health and Osteoporosis Foundation.

Entities:  

Keywords:  Bone mineral density; Diagnosis; Fracture; Hypophosphatasia

Year:  2022        PMID: 35776147     DOI: 10.1007/s00198-022-06480-1

Source DB:  PubMed          Journal:  Osteoporos Int        ISSN: 0937-941X            Impact factor:   4.507


  42 in total

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Authors:  H Clarke Anderson
Journal:  Curr Rheumatol Rep       Date:  2003-06       Impact factor: 4.592

Review 2.  Impact of blood collection devices on clinical chemistry assays.

Authors:  Raffick A R Bowen; Glen L Hortin; Gyorgy Csako; Oscar H Otañez; Alan T Remaley
Journal:  Clin Biochem       Date:  2009-10-12       Impact factor: 3.281

3.  Hypophosphatasia: validation and expansion of the clinical nosology for children from 25 years experience with 173 pediatric patients.

Authors:  Michael P Whyte; Fan Zhang; Deborah Wenkert; William H McAlister; Karen E Mack; Marci C Benigno; Stephen P Coburn; Susan Wagy; Donna M Griffin; Karen L Ericson; Steven Mumm
Journal:  Bone       Date:  2015-02-27       Impact factor: 4.398

Review 4.  Hypophosphatasia: nonlethal disease despite skeletal presentation in utero (17 new cases and literature review).

Authors:  Deborah Wenkert; William H McAlister; Stephen P Coburn; Janice A Zerega; Lawrence M Ryan; Karen L Ericson; Joseph H Hersh; Steven Mumm; Michael P Whyte
Journal:  J Bone Miner Res       Date:  2011-10       Impact factor: 6.741

5.  Pyrophosphate inhibits mineralization of osteoblast cultures by binding to mineral, up-regulating osteopontin, and inhibiting alkaline phosphatase activity.

Authors:  William N Addison; Fereshteh Azari; Esben S Sørensen; Mari T Kaartinen; Marc D McKee
Journal:  J Biol Chem       Date:  2007-03-23       Impact factor: 5.157

6.  Alkaline phosphatase: placental and tissue-nonspecific isoenzymes hydrolyze phosphoethanolamine, inorganic pyrophosphate, and pyridoxal 5'-phosphate. Substrate accumulation in carriers of hypophosphatasia corrects during pregnancy.

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Journal:  J Clin Invest       Date:  1995-04       Impact factor: 14.808

7.  A missense mutation in the human liver/bone/kidney alkaline phosphatase gene causing a lethal form of hypophosphatasia.

Authors:  M J Weiss; D E Cole; K Ray; M P Whyte; M A Lafferty; R A Mulivor; H Harris
Journal:  Proc Natl Acad Sci U S A       Date:  1988-10       Impact factor: 11.205

8.  Concerted regulation of inorganic pyrophosphate and osteopontin by akp2, enpp1, and ank: an integrated model of the pathogenesis of mineralization disorders.

Authors:  Dympna Harmey; Lovisa Hessle; Sonoko Narisawa; Kristen A Johnson; Robert Terkeltaub; José Luis Millán
Journal:  Am J Pathol       Date:  2004-04       Impact factor: 4.307

9.  Hypophosphatasia: a genetic-based nosology and new insights in genotype-phenotype correlation.

Authors:  Etienne Mornet; Agnès Taillandier; Christelle Domingues; Annika Dufour; Emmanuelle Benaloun; Nicole Lavaud; Fabienne Wallon; Nathalie Rousseau; Carole Charle; Mihelaiti Guberto; Christine Muti; Brigitte Simon-Bouy
Journal:  Eur J Hum Genet       Date:  2020-09-24       Impact factor: 4.246

Review 10.  Tissue Non-Specific Alkaline Phosphatase and Vascular Calcification: A Potential Therapeutic Target.

Authors:  Daniel Azpiazu; Sergio Gonzalo; Ricardo Villa-Bellosta
Journal:  Curr Cardiol Rev       Date:  2019
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