Spontaneous Nocturnal Leptin Secretion in Children with Myelomeningocele and Growth Hormone Deficiency

Trollmann, Regina; Dörr, H. G.; Gröschl, Michael; Blum, Werner; Rascher, Wolfgang; Dötsch, Jörg

doi:10.1159/000063580

Cited by 26 publications

(4 citation statements)

References 25 publications

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“…In contrast, in the Van Speybroeck et al [62] study, leptin was only measured once after fasting ( eight hours). Furthermore, the CA of patients in the Trollmann et al [66] study was 6.21 ± 0.52 years, which is close to the age when adiposity hypothetically begins to emerge in MMC [60,61], in contrast to the Van Speybroeck et al [62] study with a mean age of 10.0 ± 2.1 years, when adiposity is already established [60,61].…”

Section: Metabolic Bone Markersmentioning

confidence: 58%

“…Thus, early morning leptin ratios in the MMC group were higher than those in the control group. Since all the groups were matched for BMI values, the authors suggest that the pattern of leptin secretion in MMC patients may reflect hypothalamic dysregulation due to complex CNS anomalies [66]. The two studies are not directly comparable.…”

Section: Metabolic Bone Markersmentioning

confidence: 97%

“…Furthermore, the link between leptin signalling in the hypothalamus and the sympathetic regulation of bone turnover is recognized [65]. However, the impact of hypothalamic dysregulation due to complex CNS anomalies in MMC [66] can interfere with the pattern of leptin secretion in MMC.…”

Section: Nervous Systemmentioning

confidence: 99%

“…The two studies are not directly comparable. In the Trollmann study, in addition to including only GH-deficient MMC patients, nocturnal blood samples were collected every 20 min (from 08.00 p.m. to 06.00 a.m.) and GH and leptin concentrations were measured [66]. In contrast, in the Van Speybroeck et al [62] study, leptin was only measured once after fasting ( eight hours).…”

Section: Metabolic Bone Markersmentioning

confidence: 99%

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Update on bone fragility in spina bifida

Marreiros¹

2018

PRM

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BACKGROUND CONTEXT: Patients with spina bifida (SB) are at risk for pathological fractures and low bone mineral density (BMD). PURPOSE AND METHODS: This article reviews the literature and provides a comprehensive overview of how the characteristics of SB and its associated comorbidities intersect with bone fragility to identify possible pathophysiological mechanisms of fractures and low BMD. RESULTS: Bone fragility occurs early in the life of patients with SB as a result of a disturbance that determines changes in bone shape, quantity, and quality, as poor mineralization reduces bone stiffness. Bone fragility in SB occurs due to local and systemic factors and may be considered a state of impaired bone quality of multifactorial aetiology, with complex interacting influences of neurological, metabolic, and endocrinological origins and the presence of smaller bones. Bone fragility should be evaluated globally according to skeletal age and Tanner staging. The phases of the evolution of Charcot joints seem to intercept the evolution of epiphyseal fractures. Charcot arthropathy in SB may be initiated by the occurrence of repetitive trauma and fractures in epiphyseal and subepiphyseal regions, where there is a deficit of bone mineralization and greater bone mass deficits. CONCLUSION: Bone fragility in MMC potentially has a multifactorial neuro-endocrinological-metabolic-renal dimension, with smaller bones, lower bone mass, and mineralization deficits affecting bone strength.

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Section: Metabolic Bone Markersmentioning

confidence: 58%

Section: Metabolic Bone Markersmentioning

confidence: 97%

Section: Nervous Systemmentioning

confidence: 99%

Section: Metabolic Bone Markersmentioning

confidence: 99%

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Update on bone fragility in spina bifida

Marreiros¹

2018

PRM

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Peripheral Neuropathy Associated With Nucleoside Reverse Transcriptase Inhibitor Therapy

Cohen¹,

Bartt²

Infectious Disease

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Leukocyte-Derived Opioid Peptides and Inhibition of Pain

Machelska

Stein

2006

Jrnl NeuroImmune Pharm

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In peripheral inflamed tissue interactions between leukocyte-derived opioid peptides and opioid receptors on sensory neurons lead to potent, clinically relevant inhibition of pain. Opioid receptors are present on peripheral terminals of sensory neurons and are upregulated in inflammation. Their endogenous ligands, opioid peptides, are synthesized in circulating immune cells, which migrate to injured tissues directed by chemokines and adhesion molecules. Under stressful stimuli or in response to releasing agents (e.g., corticotropin-releasing factor, cytokines, catecholamines) leukocytes can secrete opioids. These peptides activate peripheral opioid receptors and produce analgesia by inhibiting the excitability of sensory nerves and/or the release of excitatory neuropeptides. These effects occur without central opioid side effects such as depression of breathing, clouding of consciousness, or addiction. Future research should elucidate the selective targeting of opioid peptide-containing immune cells to sites of painful tissue injury and the augmentation of opioid peptide and receptor synthesis.

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Spontaneous Nocturnal Leptin Secretion in Children with Myelomeningocele and Growth Hormone Deficiency

Cited by 26 publications

References 25 publications

Update on bone fragility in spina bifida

Update on bone fragility in spina bifida

Peripheral Neuropathy Associated With Nucleoside Reverse Transcriptase Inhibitor Therapy

Leukocyte-Derived Opioid Peptides and Inhibition of Pain

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