Transient hyperphosphatasemia in children revisited

Objective:  Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical characteristics of children diagnosed with TH compared to older studies in order to expand our knowledge and understanding of this...

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Published inPediatrics international Vol. 52; no. 6; pp. 866 - 871
Main Authors Dori, Neta, Levi, Lily, Stam, Tamar, Sukhotnik, Igor, Shaoul, Ron
Format Journal Article
LanguageEnglish
Published Melbourne, Australia Blackwell Publishing Asia 01.12.2010
Blackwell Publishing Ltd
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Online AccessGet full text
ISSN1328-8067
1442-200X
1442-200X
DOI10.1111/j.1442-200X.2010.03265.x

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Abstract Objective:  Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical characteristics of children diagnosed with TH compared to older studies in order to expand our knowledge and understanding of this condition and to try and find a subgroup of children who are more prone to develop TH. Methods:  We retrospectively studied 60 children diagnosed at Maccabi Health Services and Bnai Zion Medical Center, Haifa, Israel with TH between the years 2003–08. One hundred and twenty‐two children matched by age, gender and presenting symptoms served as the control group. The patients were divided into four subgroups by their presenting symptoms: infectious disease 33%, failure to thrive 28%, diarrhea 15% and other 23%. The Hydragel 7 ISO‐PAL® and Hydragel 15 ISO‐PAL® kits were used for the identification and quantification of ALP isoenzymes in human serum. Results:  The ALP levels of the study group were 805–8619 U\L (mean 2311 U\L), without differences between the subgroups. The mean duration of TH was 12 weeks. ALP isoenzymes levels were measured in one‐third of the patients, and showed that the bone isoenzyme was elevated in most. Forty‐three (71%) subjects were diagnosed in the second half of the calendar year. Conclusions:  We could not establish an etiological explanation for TH. We presume that it is a complex mechanism in which different stimuli led to upregulation of the enzyme.
AbstractList Objective:  Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical characteristics of children diagnosed with TH compared to older studies in order to expand our knowledge and understanding of this condition and to try and find a subgroup of children who are more prone to develop TH. Methods:  We retrospectively studied 60 children diagnosed at Maccabi Health Services and Bnai Zion Medical Center, Haifa, Israel with TH between the years 2003–08. One hundred and twenty‐two children matched by age, gender and presenting symptoms served as the control group. The patients were divided into four subgroups by their presenting symptoms: infectious disease 33%, failure to thrive 28%, diarrhea 15% and other 23%. The Hydragel 7 ISO‐PAL® and Hydragel 15 ISO‐PAL® kits were used for the identification and quantification of ALP isoenzymes in human serum. Results:  The ALP levels of the study group were 805–8619 U\L (mean 2311 U\L), without differences between the subgroups. The mean duration of TH was 12 weeks. ALP isoenzymes levels were measured in one‐third of the patients, and showed that the bone isoenzyme was elevated in most. Forty‐three (71%) subjects were diagnosed in the second half of the calendar year. Conclusions:  We could not establish an etiological explanation for TH. We presume that it is a complex mechanism in which different stimuli led to upregulation of the enzyme.
Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical characteristics of children diagnosed with TH compared to older studies in order to expand our knowledge and understanding of this condition and to try and find a subgroup of children who are more prone to develop TH.OBJECTIVEAlthough transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical characteristics of children diagnosed with TH compared to older studies in order to expand our knowledge and understanding of this condition and to try and find a subgroup of children who are more prone to develop TH.We retrospectively studied 60 children diagnosed at Maccabi Health Services and Bnai Zion Medical Center, Haifa, Israel with TH between the years 2003-08. One hundred and twenty-two children matched by age, gender and presenting symptoms served as the control group. The patients were divided into four subgroups by their presenting symptoms: infectious disease 33%, failure to thrive 28%, diarrhea 15% and other 23%. The Hydragel 7 ISO-PAL and Hydragel 15 ISO-PAL kits were used for the identification and quantification of ALP isoenzymes in human serum.METHODSWe retrospectively studied 60 children diagnosed at Maccabi Health Services and Bnai Zion Medical Center, Haifa, Israel with TH between the years 2003-08. One hundred and twenty-two children matched by age, gender and presenting symptoms served as the control group. The patients were divided into four subgroups by their presenting symptoms: infectious disease 33%, failure to thrive 28%, diarrhea 15% and other 23%. The Hydragel 7 ISO-PAL and Hydragel 15 ISO-PAL kits were used for the identification and quantification of ALP isoenzymes in human serum.The ALP levels of the study group were 805-8619 U\L (mean 2311 U\L), without differences between the subgroups. The mean duration of TH was 12 weeks. ALP isoenzymes levels were measured in one-third of the patients, and showed that the bone isoenzyme was elevated in most. Forty-three (71%) subjects were diagnosed in the second half of the calendar year.RESULTSThe ALP levels of the study group were 805-8619 U\L (mean 2311 U\L), without differences between the subgroups. The mean duration of TH was 12 weeks. ALP isoenzymes levels were measured in one-third of the patients, and showed that the bone isoenzyme was elevated in most. Forty-three (71%) subjects were diagnosed in the second half of the calendar year.We could not establish an etiological explanation for TH. We presume that it is a complex mechanism in which different stimuli led to upregulation of the enzyme.CONCLUSIONSWe could not establish an etiological explanation for TH. We presume that it is a complex mechanism in which different stimuli led to upregulation of the enzyme.
Objective: Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical characteristics of children diagnosed with TH compared to older studies in order to expand our knowledge and understanding of this condition and to try and find a subgroup of children who are more prone to develop TH. Methods: We retrospectively studied 60 children diagnosed at Maccabi Health Services and Bnai Zion Medical Center, Haifa, Israel with TH between the years 2003-08. One hundred and twenty-two children matched by age, gender and presenting symptoms served as the control group. The patients were divided into four subgroups by their presenting symptoms: infectious disease 33%, failure to thrive 28%, diarrhea 15% and other 23%. The Hydragel 7 ISO-PAL® and Hydragel 15 ISO-PAL® kits were used for the identification and quantification of ALP isoenzymes in human serum. Results: The ALP levels of the study group were 805-8619U\L (mean 2311U\L), without differences between the subgroups. The mean duration of TH was 12 weeks. ALP isoenzymes levels were measured in one-third of the patients, and showed that the bone isoenzyme was elevated in most. Forty-three (71%) subjects were diagnosed in the second half of the calendar year. Conclusions: We could not establish an etiological explanation for TH. We presume that it is a complex mechanism in which different stimuli led to upregulation of the enzyme. [PUBLICATION ABSTRACT]
Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical characteristics of children diagnosed with TH compared to older studies in order to expand our knowledge and understanding of this condition and to try and find a subgroup of children who are more prone to develop TH. We retrospectively studied 60 children diagnosed at Maccabi Health Services and Bnai Zion Medical Center, Haifa, Israel with TH between the years 2003-08. One hundred and twenty-two children matched by age, gender and presenting symptoms served as the control group. The patients were divided into four subgroups by their presenting symptoms: infectious disease 33%, failure to thrive 28%, diarrhea 15% and other 23%. The Hydragel 7 ISO-PAL and Hydragel 15 ISO-PAL kits were used for the identification and quantification of ALP isoenzymes in human serum. The ALP levels of the study group were 805-8619 U\L (mean 2311 U\L), without differences between the subgroups. The mean duration of TH was 12 weeks. ALP isoenzymes levels were measured in one-third of the patients, and showed that the bone isoenzyme was elevated in most. Forty-three (71%) subjects were diagnosed in the second half of the calendar year. We could not establish an etiological explanation for TH. We presume that it is a complex mechanism in which different stimuli led to upregulation of the enzyme.
Author Levi, Lily
Sukhotnik, Igor
Dori, Neta
Stam, Tamar
Shaoul, Ron
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Kerem E, Urbach J, Reifen RM, Ish-Horowicz M, Abrahamov A, Branski D. Transient hyperphosphatasemia of infancy. Isr. J. Med. Sci. 1987; 23: 890-2.
Rosalki SB, Foo AY. More on transient hyperphosphatasemia of infancy. Clin. Chem. 1983; 29: 723.
Garty B, Stayer D, Harell D, Cornblut B, Nitzan M. Transient hyperphosphatasemia of infancy. Harefuah 1992; 123: 519-21.
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Onica D, Torssander J, Waldenlind L. Recurrent transient hyperphosphatasemia of infancy in an adult. Clin. Chem. 1992; 38: 1913-15.
Wolf PL. The significance of transient hyperphosphatasemia of infancy and childhood to the clinician and clinical pathologist. Arch. Pathol. Lab. Med. 1995; 119: 774-5.
Kruse K, Bartels H, Gunther H. Serum alkaline phosphatase isoenzymes in epileptic children receving anticonvulsant drugs. Eur. J. Pediatr. 1977; 126: 237-42.
Bettica P, Moro L, Robins SP et al. Bone-resorption markers galactosyl hydroxylysine, pyridinium crosslinks, and hydroxyproline compared. Clin. Chem. 1992; 38: 2313-18.
Schonau E, Herzog KH, Bohles HJ. Transient hyperphosphatasaemia of infancy. Eur. J. Pediatr. 1988; 148: 264-6.
Suzuki M, Okazaki T, Nagai T, Toro K, Setonyi P. Viral infection of infants and children with benign transient hyperphosphatasemia. FEMS Immunol. Med. Microbiol. 2002; 33: 215-18.
Mahy BW, Rowson KE, Parr CW. Studies on the mechanism of action of Riley virus. IV. The reticuloendothelial system and impaired plasma enzyme clearance in infected mice. J. Exp. Med. 1967; 125: 277-88.
Kraut JR, Metrick M, Maxwell NR, Kaplan MM. Isoenzyme studies in transient hyperphosphatasemia of infancy. Ten new cases and a review of the literature. Am. J. Dis. Child. 1985; 139: 736-40.
Kruse K. Normal bone turnover in isolated hyperphosphatasemia. J. Pediatr. 1985; 106: 946-8.
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1992; 123
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2002; 33
1982; 100
1988; 34
2000; 93
2003; 39
1977; 126
1999; 41
1985; 106
1992; 38
1977; 23
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1982; 28
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1954; 74
1997; 35
1967; 125
2001; 37
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1983; 29
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References_xml – reference: Garty B, Stayer D, Harell D, Cornblut B, Nitzan M. Transient hyperphosphatasemia of infancy. Harefuah 1992; 123: 519-21.
– reference: Stein P, Rosalki SB, Foo AY, Hjelm M. Transient hyperphosphatasemia of infancy and early childhood: Clinical and biochemical features of 21 cases and literature review. Clin. Chem. 1987; 33(2 Pt 1): 313-18.
– reference: Kraut JR, Metrick M, Maxwell NR, Kaplan MM. Isoenzyme studies in transient hyperphosphatasemia of infancy. Ten new cases and a review of the literature. Am. J. Dis. Child. 1985; 139: 736-40.
– reference: Posen S, Lee C, Vines R, Kilham H, Latham S, Keefe JF. Transient hyperphosphatasemia of infancy - an insufficiently recognized syndrome. Clin. Chem. 1977; 23(2 Pt 1): 292-4.
– reference: Griffiths J, Vernocchi A, Simoni E. Transient hyperphosphatasemia of infancy and childhood. A study of serum alkaline phosphatase by electrofocusing techniques. Arch. Pathol. Lab. Med. 1995; 119: 784-9.
– reference: Nathan E. Transient hyperphosphatasemia of infancy. Acta Paediatr. Scand. 1980; 69: 235-8.
– reference: Stepan JJ, Kutilek S, Bayer M. Transient hyperphosphatasaemia in infancy associated with an increased urinary hydroxyproline excretion. Clin. Chim. Acta. 1995; 233: 115-18.
– reference: Onica D, Torssander J, Waldenlind L. Recurrent transient hyperphosphatasemia of infancy in an adult. Clin. Chem. 1992; 38: 1913-15.
– reference: Schonau E, Herzog KH, Bohles HJ. Transient hyperphosphatasaemia of infancy. Eur. J. Pediatr. 1988; 148: 264-6.
– reference: Bettica P, Moro L, Robins SP et al. Bone-resorption markers galactosyl hydroxylysine, pyridinium crosslinks, and hydroxyproline compared. Clin. Chem. 1992; 38: 2313-18.
– reference: Kruse K, Bartels H, Gunther H. Serum alkaline phosphatase isoenzymes in epileptic children receving anticonvulsant drugs. Eur. J. Pediatr. 1977; 126: 237-42.
– reference: Kutilek S, Bayer M. Transient hyperphosphatasemia - where do we stand? Turk. J. Pediatr. 1999; 41: 151-60.
– reference: Kruse K. Normal bone turnover in isolated hyperphosphatasemia. J. Pediatr. 1985; 106: 946-8.
– reference: Mahy BW, Rowson KE, Parr CW. Studies on the mechanism of action of Riley virus. IV. The reticuloendothelial system and impaired plasma enzyme clearance in infected mice. J. Exp. Med. 1967; 125: 277-88.
– reference: Moss DW. Alkaline phosphatase isoenzymes. Clin. Chem. 1982; 28: 2007-16.
– reference: DeVito GA Jr. Transient elevation of alkaline phosphatase possibly related to trimethoprim-sulfamethoxazole therapy. J. Pediatr. 1982; 100: 998-9.
– reference: Kruse K, Kracht U. [Isolated elevation of serum alkaline phosphatase]. Dtsch. Med. Wochenschr. 1985; 110: 669-74.
– reference: Suzuki M, Okazaki T, Nagai T, Toro K, Setonyi P. Viral infection of infants and children with benign transient hyperphosphatasemia. FEMS Immunol. Med. Microbiol. 2002; 33: 215-18.
– reference: Schambeck CM, Kopp A, Mora-Maza G, Keller F. Transient alkaline hyperphosphatasaemia in an adult: Biochemical peculiarities. Eur. J. Clin. Chem. Clin. Biochem. 1997; 35: 441-4.
– reference: Crofton PM. What is the cause of benign transient hyperphosphatasemia? A study of 35 cases. Clin. Chem. 1988; 34: 335-40.
– reference: Kerem E, Urbach J, Reifen RM, Ish-Horowicz M, Abrahamov A, Branski D. Transient hyperphosphatasemia of infancy. Isr. J. Med. Sci. 1987; 23: 890-2.
– reference: Kutilek S, Bayer M. Transient hyperphosphatasaemia of infancy and early childhood - clinical and laboratory data of 52 patients. J. Paediatr. Child Health. 2003; 39: 157.
– reference: Rosalki SB, Foo AY. More on transient hyperphosphatasemia of infancy. Clin. Chem. 1983; 29: 723.
– reference: Wolf PL. The significance of transient hyperphosphatasemia of infancy and childhood to the clinician and clinical pathologist. Arch. Pathol. Lab. Med. 1995; 119: 774-5.
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SSID ssj0008784
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Snippet Objective:  Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the...
Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the clinical...
Objective: Although transient hyperphosphatasemia (TH) has been well known for decades, its etiology and pathophysiology remain unclear. We aimed to study the...
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StartPage 866
SubjectTerms Age Factors
alkaline phosphatase
Alkaline Phosphatase - blood
Asthma - diagnosis
Asthma - enzymology
Bacterial Infections - diagnosis
Bacterial Infections - enzymology
child
Child, Preschool
Developmental Disabilities - diagnosis
Developmental Disabilities - enzymology
Diarrhea, Infantile - diagnosis
Diarrhea, Infantile - enzymology
Enzymes
Failure to Thrive - diagnosis
Failure to Thrive - enzymology
Feeding and Eating Disorders - diagnosis
Feeding and Eating Disorders - enzymology
Female
gamma-Glutamyltransferase - blood
Humans
Infant
isoenzyme
Isoenzymes - blood
Male
Medical diagnosis
Metabolic disorders
Pediatrics
Reagent Kits, Diagnostic
Reference Values
Retrospective Studies
Risk Factors
Seasons
Sex Factors
Virus Diseases - diagnosis
Virus Diseases - enzymology
Title Transient hyperphosphatasemia in children revisited
URI https://api.istex.fr/ark:/67375/WNG-FQPP6R9B-1/fulltext.pdf
https://cir.nii.ac.jp/crid/1573668925621141632
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1442-200X.2010.03265.x
https://www.ncbi.nlm.nih.gov/pubmed/21029252
https://www.proquest.com/docview/818683680
https://www.proquest.com/docview/820789989
Volume 52
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