Alterations in cartilage metabolism by neurostimulant drugs

Kilgore, B S; Dickinson, Linda C.; Burnett, Charles R.; Lee, Jason; Schedewie, H; Elders, M. Joycelyn

doi:10.1016/s0022-3476(79)80007-4

Cited by 25 publications

(12 citation statements)

References 8 publications

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“…9,13 Growth retardation specifically targeting height in the MA-exposed children may also be due to interference with cartilage metabolism. 30 MA has an inhibitory effect on mineral uptake by cartilage in vitro as well as a marked reduction in the activity of enzymes involved in the biosynthetic pathway. 30 As such, direct inhibitory effects on cartilage growth may interfere with bone growth, ultimately leading to shorter stature in the exposed children.…”

Section: Discussionmentioning

confidence: 98%

“…30 MA has an inhibitory effect on mineral uptake by cartilage in vitro as well as a marked reduction in the activity of enzymes involved in the biosynthetic pathway. 30 As such, direct inhibitory effects on cartilage growth may interfere with bone growth, ultimately leading to shorter stature in the exposed children. Further, cocaine has been shown to impair placental transport of amino acids, which also may be a mechanism for growth impairment with MA.…”

Section: Discussionmentioning

confidence: 98%

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The Effects of Prenatal Methamphetamine Exposure on Childhood Growth Patterns from Birth to 3 Years of Age

et al. 2011

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We examined the effects of prenatal methamphetamine (MA) exposure on growth parameters from birth to age 3 years. The 412 subjects included (n = 204 exposed) were enrolled at birth in the Infant Development, Environment and Lifestyle study, a longitudinal study assessing the effects of prenatal MA exposure on childhood outcomes. Individual models were used to examine the effects of prenatal MA exposure on weight, head circumference, height, and weight-for-length growth trajectories. After adjusting for covariates, height trajectory was lower in the exposed versus the comparison children (p = 0.021) over the first 3 years of life. Both groups increased height on average by 2.27 cm per month by age 3 years. In term subjects, MA exposure was also associated with a lower height trajectory (p = 0.034), with both the exposed and comparison groups gaining 2.25 cm per month by age 3 years. There was no difference in weight, head circumference, or weight-for-length growth trajectories between the comparison and the exposed groups. Children exposed prenatally to MA have a modest decrease in height growth trajectory during the first 3 years of life with no observed difference in weight, head circumference, or weight-for-length trajectories.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

The Effects of Prenatal Methamphetamine Exposure on Childhood Growth Patterns from Birth to 3 Years of Age

et al. 2011

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“…Serum somatomedin C activity was reported to be normal in a previous study [32]. On the other hand, an in vitro study showed that methylphenidate and other psychostimulants inhibited IGF bioactivity in cartilage tissue [33]. A cross-sectional study undertaken in 6- to 16-year-old (mixed prepubertal and pubertal) children with ADHD found no difference in GH, GHBP and IGF-I levels between a methylphenidate-treated group and control group [34].…”

Section: Discussionmentioning

confidence: 99%

Height, Weight, IGF-I, IGFBP-3 and Thyroid Functions in Prepubertal Children with Attention Deficit Hyperactivity Disorder: Effect of Methylphenidate Treatment

Bereket¹,

Turan²,

Karaman³

et al. 2005

Horm Res Paediatr

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Objective: To investigate if there are any disease-related or methylphenidate-induced aberrations in growth parameters, growth hormone insulin-like growth factor (IGF)-I, IGFBP-3 axis and the thyroid function tests in children with attention deficit hyperactivity disorder (ADHD). Methods: Newly diagnosed and untreated prepubertal children with ADHD were longitudinally followed before and approximately every 4 months after methylphenidate treatment for up to 16 months. Height SDS, weight SDS, BMI SDS, serum GH, IGF-I, IGFBP-3, T₄, free T₄, T₃, and TSH were measured at each visit. Results: All of the examined parameters were within normal limits for age before treatment. Methylphenidate treatment did not significantly affect SDS of height, weight, BMI, IGF-I and IGFBP-3 in the long run. Serum T₄ and free T₄ levels showed modest reductions within normal limits in a time-dependent manner. Conclusions: Prepubertal children with ADHD had normal height, weight, BMI, serum IGF-I and IGFBP-3 and thyroid functions. Methylphenidate treatment had no sustained effects on growth parameters, IGF-I and IGFBP-3 during the follow-up period of this study. However, it caused a mild decrease in total and free T₄ which may warrant further monitoring.

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“…Furthermore, older results on the effect of stimulant medication on GH secretion appear to be somewhat contradictory. Indications from a number of laboratories are that stimulant usage can cause a decrease in GH secretory activity [37][38][39][40], as well as a decrease in IGF levels [2,41]. A case study by Barter and Krammer [38] showed that methylphenidate is associated with suppression of sleep-induced GH release, while a case study by Holtkamp et al [37] found a decrease in GH secretion in a child experiencing almost complete growth arrest following methylphenidate intake.…”

Section: Stimulants and Growth Hormonementioning

confidence: 99%

“…Furthermore, Aarskog et al [39] reported that methylphenidate results in a delayed GH response to L-3,4-dihydroxyphenylalanine (L-dopa), while Hunt et al [40] found that methylphenidate causes a decreased GH response to the adrenergic agonist clonidine. Kilgore et al [41], moreover, found that methylphenidate and related psychostimulants result in an inhibition of IGF bioactivity in cartilage tissue.…”

Section: Stimulants and Growth Hormonementioning

confidence: 99%

Stimulants and growth in children with attention-deficit/hyperactivity disorder

Negrao

Viljoen

2011

Medical Hypotheses

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a b s t r a c tInitial suggestions that suppression of growth may be an intrinsic characteristic of attention-deficit/ hyperactivity disorder (ADHD) have now largely been disproven. Although controversy persists regarding the possible negative effect of adrenergic stimulants on growth in children with ADHD, the consensus that appears to be reached in the scientific literature is that stimulant usage may cause a manageable attenuation of growth in these children. Since it is known that stimulants increase the amount of dopamine and noradrenaline in the synapse, this writing suggests that these increases in dopamine and noradrenaline are responsible for the growth attenuation in these children. It appears that increased amounts of dopamine and noradrenaline have the ability to inhibit the secretion of growth hormone and growth-related hormones such as prolactin, thyroid hormones, sex hormones and insulin. Therefore, it would be reasonable to suggest that the increases in dopamine and noradrenaline caused by stimulant usage can disrupt the homeostasis of both growth hormone and growth-related hormones, generating the potential for the suppression of growth.

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Alterations in cartilage metabolism by neurostimulant drugs

Cited by 25 publications

References 8 publications

The Effects of Prenatal Methamphetamine Exposure on Childhood Growth Patterns from Birth to 3 Years of Age

The Effects of Prenatal Methamphetamine Exposure on Childhood Growth Patterns from Birth to 3 Years of Age

Height, Weight, IGF-I, IGFBP-3 and Thyroid Functions in Prepubertal Children with Attention Deficit Hyperactivity Disorder: Effect of Methylphenidate Treatment

Stimulants and growth in children with attention-deficit/hyperactivity disorder

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