Delayed somatic growth and pubertal development in human immunodeficiency virus-infected hemophiliac boys: Hemophilia Growth and Development Study

Gertner, Joseph M.; Kaufman, Francine; Donfield, Sharyne; Sleeper, Lynn A.; Shapiro, Amy D.; Howard, Craig D.; Gomperts, Edward D.; Hilgartner, Margaret W.

doi:10.1016/s0022-3476(05)83177-4

Cited by 54 publications

(37 citation statements)

References 16 publications

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“…On the contrary, BA and PAH seem to be unreliable predictors when compared to normal subjects, in which BA estimation is a useful tool to assess skeletal maturity, to predict final height and to monitor treatment regimens. This finding confirms the data of Gertner et al [30] in HIV-infected boys with hemophilia and is partially similar to that of other chronic disorders, such as inflammatory bowel diseases, rheumatoid arthritis, and cystic fibrosis. These diseases, in fact, show potentially profound effects upon growth, skeletal maturation and sexual development [34].…”

Section: Discussionsupporting

confidence: 92%

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Final Height in Patients Perinatally Infected with the Human Immunodeficiency Virus

et al. 2010

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Introduction: Data concerning final height are completely lacking in human immunodeficiency virus (HIV)-infected children. Design: Retrospective evaluation of auxological data up to final height in a cohort of patients with perinatal HIV infection. Patients and Methods: In 95 Caucasian patients (57 females and 38 males, median age 17.5 years) the following data were evaluated as standard deviation (SD) score: prepubertal height (PrH), height velocity (HV), final height (FH), target height (TH), FH minus PrH, predicted adult height (PAH), FH minus PAH, and FH minus TH. Results: Patients showed a significantly reduced PrH and FH compared to their TH (p < 0.001), even if no difference was evidenced between PrH and FH. Age at puberty onset displayed a negative significant correlation with PrH (p = 0.002) and CD4+ cell percentage (p < 0.01). Finally, HV displayed a significant correlation with viremia (p = 0.001), but not with CD4+ cell percentage. Conclusions: HIV perinatally infected patients show a FH significantly reduced and not in accordance with TH. Our data seem to suggest that the losses in stature accumulated throughout the total period of childhood and adolescence may contribute to their reduced FH.

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Section: Discussionsupporting

confidence: 92%

“…Gertner et al [30] reported reduced age-adjusted height and weight in HIV-infected boys with hemophilia in comparison to uninfected boys with hemophilia. Others found that perinatally HIV-infected boys and girls also had reduced height and weight growth compared with their uninfected peers [18,31,32,33].…”

Section: Discussionmentioning

confidence: 99%

Final Height in Patients Perinatally Infected with the Human Immunodeficiency Virus

et al. 2010

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“…[5][6][7][8] In the current investigation, our attention was focused primarily on the HIV Ϫ participants (n ϭ 126) in order to allow more specific delineation of the effects of inhibitors on maturation. Further, findings in this group are more clinically relevant to the adolescents with hemophilia currently under care.…”

Section: Introductionmentioning

confidence: 99%

Delays in maturation among adolescents with hemophilia and a history of inhibitors

Donfield

Lynn

Lail

et al. 2007

Blood

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Inhibitory antibodies to factors VIII or IX have the potential to affect a broad range of outcomes among people with hemophilia; however, their possible effect on growth and maturation has not been explored. We evaluated skeletal maturation (bone age), pubertal progression, serum testosterone levels, height velocity, and stature in the multicenter Hemophilia Growth and Development Study. A total of 333 children and adolescents (mean age, 12.4 years) were enrolled from 1989 to 1990 and followed for 7 years. Of these, 18% (n ‫؍‬ 60) had a history of inhibitors. Bone age among HIV ؊ adolescents with a history of inhibitors lagged 9 or more months behind those without inhibitors at every age from 12 to 15 years. Those with a history of inhibitors were older at every Tanner stage transition, attained a lower maximum growth velocity, and their serum testosterone levels were significantly lower compared with those without inhibitors. Delays were greater among HIV ؉ patients with a history of inhibitors compared with those without inhibitors; however, the differences were generally small and not statistically significant

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“…In children with HIV infection, they result from cytokine-mediated decrease in gonadotropin secretion, and are associated with delayed pubertal development and a significant reduction in skeletal maturation [21]. Primary decreases in gonadal function have also been reported in adults, where men with AIDS were found to have significant reductions in testosterone secretion [22].…”

Section: Chronic Illness and Bone Turnovermentioning

confidence: 99%

Mechanisms Influencing Bone Metabolism in Chronic Illness

Daci¹,

Cromphaut²,

Bouillon³

2002

Horm Res Paediatr

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Bone is permanently renewed by the coordinated actions of bone-resorbing osteoclasts and bone-forming osteoblasts, which model and remodel bone structure during growth and adult life. The origin of osteoblastic cells (osteoblasts, osteocytes and bone-lining cells) differs from that of osteoclasts, but both cell groups communicate with each other using cytokines and cell-cell contact as to optimally maintain bone homeostasis. This communication in many ways uses the same players as the communication between cells in the immune system. During acute life-threatening illness massive bone resorption is the rule, while bone formation is suppressed. During chronic illness, the balance between bone formation and bone resorption also shifts, frequently resulting in decreased bone mass and density. Several factors may contribute to the osteopenia that accompanies chronic illness, the most important being undernutrition and low body weight, inflammatory cytokines, disorders of the neuroendocrine axis (growth hormone/IGF-1 disturbances, thyroid and gonadal deficiency), immobilization, and the long-term use of glucocorticoids. Their combined effects not only influence the generation and activity of all bone cells involved, but probably also regulate their life span by apoptotic mechanisms. Osteopenia or even osteoporosis and bone fragility, and before puberty also decreased linear growth and lower peak bone mass are therefore frequent consequences of chronic illnesses.

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Delayed somatic growth and pubertal development in human immunodeficiency virus-infected hemophiliac boys: Hemophilia Growth and Development Study

Cited by 54 publications

References 16 publications

Final Height in Patients Perinatally Infected with the Human Immunodeficiency Virus

Final Height in Patients Perinatally Infected with the Human Immunodeficiency Virus

Delays in maturation among adolescents with hemophilia and a history of inhibitors

Mechanisms Influencing Bone Metabolism in Chronic Illness

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