Transient hyperphosphatasemia in a child with nephrolithiasis and severe prematurity

Kutı́lek, Štěpán; Formanova, Daniela; Senkerik, Marian; Langer, J; Marková, Daniela; Skálová, Sylva

doi:10.1016/j.nefroe.2017.06.007

Cited by 1 publication

(1 citation statement)

References 7 publications

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“…Other studies show that bone turnover processes are altered in the event of infections, chronic illness, and malnutrition (Aris et al, 2000; Josse et al, 2015; Marriott, 2013; Marriott et al, 2004; Shead et al, 2010; Van den Berghe et al, 2003). Interestingly, in children, a series of case studies have shown that respiratory illnesses are associated with transient hyperphosphatasemia (in other words, a short period of increased bone formation marker levels) (Eboriadou et al, 2006; Kim et al, 2000; Kutilek et al, 2014). A condition such as hyperphosphatasemia may have occurred for at least some of the children in the OMI sample.…”

Section: Discussionmentioning

confidence: 99%

A biological approach to adult sex differences in skeletal indicators of childhood stress

O’Donnell

Hill

Anderson

et al. 2021

American Journal of Biological Anthropology

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Objectives: In previous work examining the etiology of cribra orbitalia (CO) and porotic hyperostosis (PH) in a contemporary juvenile mortality sample, we noted that males had higher odds of having CO lesions than females. Here, we examine potential reasons for this pattern in greater detail. Four non-mutually exclusive mechanisms could explain the observed sex differences: (1) sex-biased mortality; (2) sexual dimorphism in immune responses; (3) sexual dimorphism in bone turnover; or (4) sexual dimorphism in marrow conversion. Subjects and methods:The sample consists of postmortem computed tomography scans and autopsy reports, field reports, and limited medical records of 488 individuals from New Mexico (203 females; 285 males) aged between 0.5 and 15 years. We used Kaplan-Meier survival analysis, predicted probabilities, and odds ratios to test each mechanism.Results: Males do not have lower survival probabilities than females, and we find no indications of sex differences in immune response. Overall, males have a higher probability of having CO or PH lesions than females. Conclusions:All results indicate that lesion formation in juveniles is influenced by some combination of sex differences in the pace of red-yellow conversion of the bone marrow and bone turnover. The preponderance of males with CO and PH likely speaks to the potential for heightened osteoblastic activity in males. We find no support for the hypotheses that sex biases in mortality or immune responses impacted lesion frequency in this sample. Sex differences in biological processes experienced by children may affect lesion formation and lesion expression in later life.

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