Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of adjuvant arthritis (AA) on the endocrine circadian rhythms of plasma prolactin (PRL), growth hormone (GH), insulin-like growth factor-1 (IGF-1), luteinizing hormone (LH), testosterone, and melatonin and of pituitary PRL and GH mRNA in male Long Evans rats. Groups of control and AA rats (studied 23 days after AA induction) that were housed under a 12/12 h light/dark cycle (light on at 06:00 h) were killed at 4 h intervals starting at 14:00 h. Cosinor analysis revealed a significant 12 h rhythm in PRL and PRL mRNA (p < 0.001) in controls with peaks at 14:00 h and 02:00 h, respectively. The peak at 02:00 h was abolished in the AA group resulting in a significant 24 h rhythm in parallel with that of PRL (p < 0.05) and PRL mRNA (p < 0.0001). Growth hormone showed no rhythm, but a significant rhythm of GH mRNA was present in both groups (p < 0.0001). Insulin-like growth factor-1 showed a 24 h rhythm in control but not in AA rats. The mean values of GH, GH mRNA, and IGF-1 were significantly reduced in AA. Luteinizing hormone displayed a significant 24 h rhythm (p < 0.01) peaking in the dark period in the control but not AA group. Testosterone showed in phase temporal changes of LH levels with AA abolishing the 02:00 h peak. Melatonin exhibited a significant 24 h rhythm in control (p < 0.001) and AA (p < 0.01) rats with maximum levels during the dark phase; the mesor value was higher in the AA males. These results demonstrate that AA interferes with the rhythms of all the studied hormones except the non-24 h (arrhythmic) GH secretion pattern and the rhythm in melatonin. The persistence of a distinct melatonin rhythm in AA suggests the observed disturbances of hormonal rhythms in this condition do not occur at the level of the pineal gland.
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PMID:Daily profiles of plasma prolactin (PRL), growth hormone (GH), insulin-like growth factor-1 (IGF-1), luteinizing hormone (LH), testosterone, and melatonin, and of pituitary PRL mRNA and GH mRNA in male Long Evans rats in acute phase of adjuvant arthritis. 1453 56

Immunosuppressants, including methotrexate and more recently anti-TNF alpha, anti-IL1 and anti-IL6 receptor, have modified the prognosis of juvenile idiopathic arthritis. Growth hormone was shown to limit growth retardation due to general corticotherapy.
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PMID:[New treatments for idiopathic juvenile arthritis]. 1989 51

Growth hormone has been available for treatment of various conditions for over 50 years. There have been a number of chronic disease states in which it has been used, such as chronic kidney disease, which became a US Food and Drug Administration (FDA)-approved indication in 1993. For other chronic disease states there have been clinical studies supporting its use, but they have not yet been approved as a indications by the FDA. Examples of such diseases are cystic fibrosis, chronic arthritis, short bowel syndrome, burn trauma, and hypophosphatemic rickets.
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PMID:Growth and growth hormone treatment in children with chronic diseases. 2309 68

MicroRNAs are involved in multiple pathophysiological networks and in the pathogenesis of a broad spectrum of human disorders, including cancer and inflammatory diseases. Impaired linear growth is encountered in children with chronic inflammatory conditions such as cystic fibrosis, inflammatory bowel diseases, juvenile idiopathic arthritis, celiac disease and in subjects born intrauterine growth restricted/small for gestational age. Children with inflammatory conditions may also be at risk of developing insulin resistance as a result of the inflammatory process and concurrent therapy. Chronic inflammation may lead to a continuum of abnormalities in the Growth hormone/Insulin-like growth factor 1 (GH/IGF-I) axis, including relative GH insufficiency, GH/IGF-I resistance due to down regulation of GH and IGF-I receptors, changes in GH and IGF-I bioavailability due to modifications of binding proteins, and/or impaired GH/IGF-I signaling. The aim of this review is first to summarize the current knowledge concerning microRNAs involved in inflammation in the most relevant chronic inflammatory diseases in childhood, second to provide new insights into miRNA regulation of growth and insulin sensitivity mediated by the inflammatory processes. We evaluated single microRNAs involved in inflammation in the single conditions mentioned above and verified which had validated and predicted targets within the GH receptor, IGF-I type 1 receptor and insulin receptor interactomes. The findings show a new link among inflammation, growth and insulin sensitivity mediated by miRNAs that warrants further research in the future.
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PMID:MicroRNAs link chronic inflammation in childhood to growth impairment and insulin-resistance. 2939