Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042963 (vomiting)
31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Opiates, such as morphine, are typically employed to alleviate acute or chronic pain states. However, there are a myriad of side effects including constipation, nausea, respiratory depression, cough suppression, vomiting, sedation, addiction and tolerance. It has also been reported experimentally and clinically that exposure to opiate can elicit paradoxical pain (opiate-induced tactile hyperalgesia; OIH) in regions of the body unrelated to the initial pain complaint. Several mechanisms have been suggested to be responsible for OIH such as sensitization of peripheral nociceptors, enhanced production/release of glutamate and neuropeptides in the spinal cord, protein kinase C gamma-induced signaling, and/or enhanced descending facilitation of nociceptive pathways from the rostral ventromedial medulla; however signaling pathways known to lead to directly to OIH remain undiscovered. Recent publications from our laboratory and others have discovered a potentially important link to OIH that involves the chemokine (chemotactic cytokine), stromal-derived factor 1 (SDF1 also known as CXCL12) and its cognate receptor CXCR4.
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PMID:Opiate-induced hypernociception and chemokine receptors. 1960 47

Filgrastim, a recombinant G-CSF, is the standard drug used to mobilise haematopoietic stem cells for collection prior to autologous transplantation in patients with lymphoma and myeloma. Plerixafor, a CXCR4 receptor antagonist, is now authorised in the European Union for use in combination with G-CSF when stem cell mobilisation with G-CSF alone is unsuccessful. Clinical evaluation is based on two comparative trials with similar designs. In a trial in 302 myeloma patients, the G-CSF-plerixafor combination was associated with a statistically significantly higher rate of successful mobilisation, defined as collection of at least 6 x 10(6) CD34+ cells after one or two apheresis sessions, than a combination of G-CSF and placebo (71.6% versus 34.4%). The same effect was observed in a trial involving 298 lymphoma patients, in which the CD34+ cell target number was at least 5 x 10(6) after a maximum of 4 apheresis sessions (59% versus 20%). In these trials, the addition of plerixafor to G-CSF increased the frequency of injection site reactions (55% versus 36%) and was associated with twice as many gastrointestinal disorders (diarrhoea and nausea or vomiting). There was no difference between the combined treatments in terms of disease-related mortality at one year (about 8%). However, longer follow-up is needed to ensure that plerixafor does not lead to disease aggravation by mobilising malignant cells. Given the long-term uncertainties, plerixafor should be reserved for patients in whom G-CSF alone fails to yield a sufficient number of stem cells required for transplantation.
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PMID:Plerixafor. Only for certain patients when G-CSF stem cell mobilisation fails. 2093 42