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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Incorrect treatment of chronic pain is common cause of patient's discontentment and suffering. The problem is mostly occurring because of inappropriate pain treatment. The WHO guidelines recommends declining of prejudices and using of strong opioids in therapy after the unsatisfactory treatment with weaker analgesics. Strong opioid analgesic fentanyl in transdermal system (Durogesic TTS) is introduced. In rheumatology, it is recommended for all conditions characterised by chronic pain with intensity 4 and more on the VAS scale (0-10). It is mostly used in rheumatoid arthritis, osteoarthritis, low back pain and neuropathic pain. Durogesic TTS provides continuous pain relief for 72 hours, with constant serum concentrations. It has to be gradually titrated and starting dose is 25 micrograms/h. Possible adverse events (nausea, vomiting, constipation, sedation, itching) are short termed, transitory and easily managed. Results of some clinical trials and personal experiences that are proving its efficacy and safety are presented.
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PMID:[Treatment of chronic pain--use of transdermal fentanyl (Durogesic TTS)]. 1247 59

Dihydroetorphine (DHE) is one of the strongest analgesic opioid alkaloids known; it is 1000 to 12000 times more potent than morphine. Several in vitro and in vivo studies have shown that DHE is a selective mu-opioid receptor (OP(3)) agonist that also binds and activates all human recombinant mu-, delta-, and kappa-opioid receptors (OP(3), OP(1), and OP(2)). The onset of the analgesic effect of DHE in rodents is rapid, 5 to 15 min after parenteral administration; the duration of action is short, the analgesic effect disappears within 120 min after administration. By oral administration much higher doses of DHE are required to produce analgesic effects. These characteristics are accounted for by the pharmacokinetic properties of DHE in the rat, namely, by rapid distribution of DHE from the injection site to the brain and rapid metabolism by glucuronidation in the gut and liver followed by elimination into the bile. Continuous infusion and repeated administration of DHE lead to the development of tolerance to analgesia, physical dependence, and a rewarding effect in normal rats but not in animals with formalin-induced inflammation. Although formalin-induced inflammation is only one type of pain stimulus, these findings suggest that DHE addiction would be observed only in the case of pain-free conditions. Clinical reports in China show that sublingual doses of DHE, 20 to 180 microg, produce a potent analgesic effect with only mild side effects, including dizziness, somnolence, nausea, vomiting, constipation, and shortness of breath. To improve the short-lasting effect following sublingual administration, transdermal delivery of DHE via a patch has been investigated. The patch formulation of DHE produces continuous analgesic effect with minimal physical dependence and rewarding effect in rats suffering from chronic pain. This patch formulation, which is very suitable for DHE, may be viable for the treatment of severe pain and is likely to improve patients' quality of life.
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PMID:Dihydroetorphine: a potent analgesic: pharmacology, toxicology, pharmacokinetics, and clinical effects. 1248 Nov 94

(1) First-line treatment for both acute and chronic pain is paracetamol or, if necessary, ibuprofen, a nonsteroidal antiinflammatory drug. If relief is inadequate, the best option is a combination of paracetamol with codeine (a weak opiate). (2) A fixed-dose combination of paracetamol (325 mg) and tramadol (37.5 mg), a weak opiate, arrived on the French market in May 2003. (3) In the acute setting, three trials in a total of 1197 patients showed that a single dose of the paracetamol 650 mg + tramadol 75 mg combination after dental surgery was no more effective than ibuprofen 400 mg. Compared with each drug used alone, the paracetamol + tramadol combination prolongs the analgesic effect but does not increase its intensity. (4) A trial after gynaecological surgery and another trial after orthopaedic surgery showed that a single dose of paracetamol 975 mg + tramadol 112.5 mg had similar efficacy to tramadol alone at 112.5 mg. (5) In the chronic setting, we found no trials comparing the paracetamol + tramadol combination with each drug used alone. A comparative double-blind trial in 462 patients with low back pain or osteoarthritic pain showed no difference in efficacy between paracetamol 325 mg + tramadol 37.5 mg and paracetamol 300 mg + codeine 30 mg. (6) The main adverse effects of the paracetamol + tramadol combination are the same as other weak opiates: nausea, vomiting, dizziness, headache, drowsiness and constipation. Tramadol carries a higher risk of drug interactions than codeine. (7) In practice, the paracetamol + tramadol combination offers patients no advantages relative to standard analgesics.
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PMID:Paracetamol + tramadol: new preparation. No advance. 1498 89

Delta-9-tetrahydrocannabinol (THC) is increasingly used for the long-term treatment of nausea, vomiting, cachexia, and chronic pain. Recent reports, however, have indicated an increased risk of myocardial infarction and thromboangiitis obliterans after THC intake. Blood platelets have an essential role in the pathogenesis of these two diseases, but it is unclear whether platelets are potential target cells for cannabinoids. We investigated the effects of THC on human platelets and the expression of cannabinoid receptors on their cell membranes in this in vitro study. The effects of THC (final concentrations 10(-7) to 10(-5) M) on the expression of activated platelet fibrinogen receptor (glycoprotein IIb-IIIa) and P selectin were characterized by flow cytometry. Western blotting was performed with platelet membrane preparations to determine the surface expression of cannabinoid receptors on human platelets. THC increased the expression of glycoprotein IIb-IIIa and P selectin on human platelets in a concentration-dependent manner. The two known cannabinoid receptors (CB(1) and CB(2)) were both detected on the cell membrane of human platelets. Our functional results may suggest a receptor-dependent pathway of THC-induced platelet activation. However, further in vivo studies are warranted to evaluate the role of cannabinoid receptors in mediating the demonstrated procoagulatory effect of THC.
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PMID:The procoagulatory effects of delta-9-tetrahydrocannabinol in human platelets. 1538 62

We report the case of an 81-year old woman with stupor, confusion, somnolence, vomiting, and reduced food intake for 5 days. Laboratory investigations revealed low serum concentrations of sodium and potassium with a serum osmolality of 225 mOsm/kg H (2)O in the face of an inappropriately concentrated urine with an osmolality in the normal range, suggesting the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in the absence of renal insufficiency, adrenal insufficiency, and hypothyroidism. Careful drug evaluation revealed amitriptyline and citalopram as possible inciters of antidiuretic hormone secretion. Subsequently, these drugs were withdrawn. Under continuous sodium substitution and fluid restriction serum sodium normalized and the patient's symptoms resolved. She was fully alert by day 15. We conclude that hyponatremia secondary to SIADH was the cause of the patient's neurologic symptoms. Clinicians should be aware of this possible side effect of central acting agents such as amitriptyline and citalopram, drugs that are often used to treat elderly patients suffering from depression or chronic pain.
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PMID:Citalopram therapy as a risk factor for symptomatic hyponatremia caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH): a case report. 1602 23

Opiates are the primary treatment for pain management in cancer patients reporting moderate to severe pain, and are being increasingly used for non-cancer chronic pain. However, prolonged administration of opiates is associated with significant problems including the development of antinociceptive tolerance, wherein higher doses of the drug are required over time to elicit the same amount of analgesia. High doses of opiates result in serious side effects such as constipation, nausea, vomiting, dizziness, somnolence, and impairment of mental alertness. In addition, sustained exposure to morphine has been shown to result in paradoxical pain in regions unaffected by the initial pain complaint, and which may also result in dose escalation, i.e. 'analgesic tolerance'. A concept that has been gaining considerable experimental validation is that prolonged use of opioids elicits paradoxical, abnormal pain. This enhanced pain state requires additional opioids to maintain a constant level of antinociception, and consequently may be interpreted as antinociceptive tolerance. Many substances have been shown to block or reverse antinociceptive tolerance. A non-inclusive list of examples of substances reported to block or reverse opioid antinociceptive tolerance include: substance P receptor (NK-1) antagonists, calcitonin gene-related peptide (CGRP) receptor antagonists, nitric oxide (NO) synthase inhibitors, calcium channel blockers, cyclooxygenase (COX) inhibitors, protein kinase C inhibitors, competitive and non-competitive antagonists of the NMDA (N-methyl-D-aspartate) receptor, AMPA (alpha-amino-3-hydroxy-5-methyl-4 isoxazolepropionic acid) antagonists, anti-dynorphin antiserum, and cholecystokinin (CCK) receptor antagonists. Without exception, these substances are also antagonists of pain-enhancing agents. Prolonged opiate administration indeed induces upregulation of substance P (SP) and calcitonin gene-related peptide (CGRP) within sensory fibers in vivo, and this is accompanied by an enhanced release of excitatory neurotransmitters and neuropeptides from primary afferent fibers upon stimulation. The enhanced evoked release of neuropeptides is correlated with the onset of abnormal pain states and opioid antinociceptive tolerance. Importantly, the descending pain modulatory pathway from the brainstem rostral ventromedial medulla (RVM) via the dorsolateral funiculus (DLF) is critical for maintaining the changes observed in the spinal cord, abnormal pain states and antinociceptive tolerance, because animals with lesion of the DLF did not show enhanced evoked neuropeptide release, or develop abnormal pain or antinociceptive tolerance upon sustained exposure to opiates. Microinjection of either lidocaine or a CCK antagonist into the RVM blocked both thermal and touch hypersensitivity as well as antinociceptive tolerance. Thus, prolonged opioid exposure enhances a descending pain facilitatory pathway from the RVM that is mediated at least in part by CCK activity and is essential for the maintenance of antinociceptive tolerance.
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PMID:Is paradoxical pain induced by sustained opioid exposure an underlying mechanism of opioid antinociceptive tolerance? 1621 2

The association between migraine and functional gastrointestinal disorders has been confirmed by many clinical observations and epidemiological studies. In most patients during the attacks of migraine, apart from various neurological and vascular symptoms, gastrointestinal disturbances occur including nausea, vomiting, abdominal pain or diarrhea. Functional gastrointestinal disorders, such as irritable bowel syndrome (IBS), are reported in migraine patients in periods between the attacks as well. On the other hand 23-53% of IBS patients have frequent headaches. Migraine and IBS often coexist with fibromyalgia and other chronic pain syndromes and functional disorders. Migraine and IBS affect approximately 10-20% of the general population, usually young adults. Both diseases are more prevalent in women, perhaps due to the role of estrogen in their pathogenesis. Looking for the common pathogenetic mechanisms of IBS and migraine the role of the brain-gut axis, neuroimmune and neuroendocrine interactions are being considered. The influence of stress on symptom occurrence and severity seems to be associated with hyperactivity of the hypothalamic-pituitary-adrenal axis. The enteric nervous system as a source of numerous neurotransmitters and visceral reflexes is a plausible common pathogenic link between IBS and migraine. In particular serotonin being the main neurotransmitter of the gastrointestinal tract plays a relevant role in the pathogenesis of IBS as well as migraine. Nowadays, agonists and antagonists of serotoninergic receptors are the most efficacious drugs for IBS and migraine therapy. Some side effects of triptans, 5-HT(1B/D) agonists, used in migraine treatment may be connected with the influence of triptans on the gastrointestinal functions. A better understanding of the relationship between migraine and IBS may result in more effective treatment of both diseases.
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PMID:[Migraine and irritable bowel syndrome]. 1641 71

Drug challenge test (DCT) is performed to evaluate chronic pain pharmacologically and determine its medical treatment. One test drug is administered in one day for DCT and characterization of the test drug. Four patients developed side effects of the test drugs for DCT in whom other drug tests were postponed or canceled. A 58-year-old man with multiple arthritis of rheumatic arthritis and fibromyalgia had headache, nausea, and vomiting all day after ketamine test. A 76-year-old man with chronic general pain and failed back surgery syndrome had vomiting and abdominal discomfort two hours after morphine test and had redness and itching on his bilateral forearms the following day. A 78-year-old man with chronic lumbar and right lower limb pain due to L 4-5 lumbar disc herniation and postherpetic neuralgia felt dizzy, fell down and bruised on his lower back and left knee twelve hours after morphine test. A 32-year-old woman with chronic pelvic pain had skin eruption on her thigh the day after phentolamine test. Although the amount of the test drug in DCT is small and its half-life is short, long-term side effects might occur. We should decrease the amounts or frequencies of ketamine and morphine, and administer them taking long intervals before other tests.
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PMID:[Postponed or canceled drug challenge tests and side effects of the test drug--a report of four cases]. 1649 93

There is convincing evidence that acupuncture (AP) is effective for the treatment of postoperative and chemotherapy-induced nausea/vomiting, as well as postoperative dental pain. Less convincing data support AP's efficacy for chronic pain conditions, including headache, fibromyalgia and low back pain. There is no evidence that AP is effective in treating addiction, insomnia, obesity, asthma or stroke deficits. AP seems to be efficacious for alleviating experimental pain by increasing pain thresholds in human subjects and it appears to activate analgesic brain mechanisms through the release of neurohumoral factors, some of which can be inhibited by the opioid antagonist naloxone. In contrast to placebo analgesia, AP-related pain relief takes some time to develop and to resolve. Furthermore, repetitive use of AP analgesia can result in tolerance that demonstrates cross-tolerance with morphine. However, it appears that not all forms of AP are equally effective for providing analgesia. In particular, electro-AP seems to best deliver stimuli that activate powerful opioid and nonopioid analgesic mechanisms. Thus, future carefully controlled clinical trials using adequate electro-AP may be able to provide the necessary evidence for relevant analgesia in chronic pain conditions, such as headache, fibromyalgia, irritable bowel syndrome and low back pain.
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PMID:Mechanisms of acupuncture analgesia for clinical and experimental pain. 1673 14

Tramadol, a centrally acting analgesic, consists of two enantiomers, both of which contribute to analgesic activity via different mechanisms. (+) Tramadol and the metabolite (+) -O- desmethyl-tramadol (M1) are agonists of the mu opioid receptor. (+) Tramadol also stimulates presinaptic release of serotonin and inhibits serotonin reuptake whereas (-) tramadol inhibits norepinephrine reuptake. Thus tramadol enhances inhibitory effects on pain transmission both by opioid and monoaminergic mechanisms. The complementary and synergistic actions of the two enantiomers improve the analgesic efficacy and tolerability profile of the racemate. Following oral administration the bioavailability of tramadol is high and with new slow release preparations twice daily administration enables effective pain control. The recommended maximum daily dose of tramadol is 400 mg/day. Tramadol is characterised by low plasma protein binding and quite extensive tissue distribution. Elimination is primarily by the hepatic route (metabolism by CYP2D6) and partly by the renal route. It is effective in different types of moderate-to-severe acute and chronic pain, including neuropathic pain, low back pain, osteoarthritis pain and breakthrough pain. It also causes fewer opioid-type adverse effects, e.g. nausea, drowsiness, vomiting, dry mouth and constipation. Although trials in literature demonstrate immune-stimulating effects of tramadol, there are also trials suggesting immunesuppressive effects that are lesser than morphine. Owing to its pharmacological properties, tramadol is more appropriate than NSAIDs for patients suffering from gastrointestinal and renal problems. Besides its proven clinical efficacy tramadol is a safe drug as respiratory depression, cardiovascular side effects, drug abuse and dependence are of minor clinical relevance, unlike some other opioids.
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PMID:[An atypical opioid analgesic: tramadol]. 1678 63


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