Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the influence of maternal serum B12 concentration on the inactivation of placental methionine synthase activity by nitrous oxide in an obstetric population. This group was known to include patients with a wide range of B12 values. Over 70% of patients were given nitrous oxide either for analgesia during labour or for delivery by Caesarean section, for periods ranging from a few minutes to 11 h. Patients undergoing normal delivery and Caesarean section under extradural anaesthesia served as controls. There was a highly significant relation between placental methionine synthase activity and duration of exposure to nitrous oxide. Inactivation was slower than that described for the liver, which may reflect the intermittent use. There was also a significant relation between maternal B12 and placental methionine synthase activity, but there was a wide scatter of results and the data were not thought to be predictive. There was evidence that inactivation by nitrous oxide was more rapid in patients with small concentrations of B12. We conclude that some patients with reduced serum concentrations of B12 may be at a disadvantage with nitrous oxide anaesthesia.
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PMID:Influence of vitamin B12 status on the inactivation of methionine synthase by nitrous oxide. 163 9

Recording of field potentials from different brain areas of freely behaving rats and subsequent spectral analysis of the signals has proved to be a most sensitive method in pharmacology. This new model is used to measure the effect on the electrical activity of the brain of repeated daily injections of 1 ml/kg of a vitamin B mixture (Neurobion, 1 ml containing 33.3 mg B1, 33.3 mg B6, and 0.333 mg B12). Subacute application of the vitamin B combination for 1 week in a group of six rats resulted in changes in the power spectra, which became more prominent from day to day. Particularly increases in the power of the alpha 1 and beta range from the thalamus dominated the vitamin-induced changes. From the comparison with earlier results obtained with centrally acting serotonergic drugs, it is concluded that the pharmacodynamic action of the vitamin B mixture predominantly influences this transmitter system. The same group of animals, once challenged with a single dose of 0.2 mg/kg morphine before the repeated vitamin treatment, responded to the same challenge after the treatment in a more sensitive manner. Particularly power changes in the beta range were more pronounced. This higher sensitivity to a morphine challenge persisted for more than 1 week after the end of the vitamin treatment which points to a plastic change in serotonergic neurotransmitter control processes. The results obtained here may be linked to the antinociceptive properties of the vitamin B mixture and practical consequences may include a reduction of morphine dose for analgesia during repeated vitamin B treatment.
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PMID:Influence of repeated vitamin B administration on the frequency pattern analysed from rat brain electrical activity (Tele-Stereo-EEG). 215 86

To explore the role of vitamin B in neural mechanisms of analgesia, we investigated the effect of a compound of vitamins B1, B6 and B12 (Neurobion, E. Merck) on the nociceptive responses of single neurons in the spinal cord dorsal horn in anesthetized cats. Intrathecal superfusion of Neurobion, using a small pool placed on the spinal surface, produced a significant dose-dependent depression in the responses evoked by noxious skin heating (50 or 52 degrees C, 10 s) of hindfoot skin, but not of spontaneous activity in dorsal horn neurons. These results indicate that the therapeutic effect of vitamin B compounds in the clinical management of pain may involve a suppression of nociceptive transmission at the spinal level.
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PMID:B vitamins suppress spinal dorsal horn nociceptive neurons in the cat. 322 8

Additive analgesic effects of long-term application of a combination of the vitamins B1, B6, B12 (thiamine diphosphate 100 mg, pyridoxsine-HCl 200 mg, cyanocobalamin 20 micrograms, p.o.) on a single dose of the nonsteroidal anti-inflammatory drug (NSAID) diclofenac (diclofenac-Na, 50 mg, p.o.) were investigated with a noninflammatory experimental pain model in 38 healthy volunteers. B-vitamins were given with 3 dosages/day for 1 week. Then experimental sessions of 3 h followed to test the analgesic efficacy of the NSAID. In these sessions, phasic pain was induced by intracutaneously applied brief electrical pulses (20 ms). Measured were the pain ratings, the cerebral potentials and the EEG delta power in responses to the stimuli as target variables for the analgesic test. Unspecific effects upon the vigilance system were evaluated by spontaneous EEG, auditory-evoked potentials and reaction times. The investigation was performed as a placebo-controlled, double-blind cross-over study. Blood samples were taken to monitor the plasma concentrations of the active agents. Whereas in the first block of stimuli (40-60 min after diclofenac medication) no analgesic effects of diclofenac could be observed, either given alone or after pretreatment with the B-vitamins, in the second stimulus block (100-120 min after medication) significant effects appeared in all target variables describing analgesia. Pain ratings were decreased by about 5%, late cerebral potentials by about 9% and stimulus-induced delta power of the EEG by about 14%. These effects were significant (p < 0.05, p < 0.01) against those under placebo, but came out to be independent of the B-vitamin pretreatment. No B-vitamin effects of the B-vitamins could be detected, either additive analgesic effects on diclofenac analgesia or on the concomitant variables describing unspecific sedative effects. Clearly the B-vitamin pretreatment for 1 week enlarged the plasma levels for vitamin B6 by 700%, for vitamin B1 by 70% and for vitamin B12 by 50%. All B-vitamin concentrations were independent of each other.
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PMID:Do the B-vitamins exhibit antinociceptive efficacy in men? Results of a placebo-controlled repeated-measures double-blind study. 760 64

We report three cases of peripheral neuropathy in patients with sickle cell disease. All had a history of frequent painful crises and regular attendance at our Accident and Emergency department where nitrous oxide analgesia was administered for prolonged periods. All three patients (one male and two females) presented with difficulty in walking associated with paraesthesiae, and neurological examination revealed signs compatible with a peripheral sensorimotor neuropathy, later confirmed by nerve conduction studies. Serum vitamin B12 levels were mildly reduced in two patients and very low in one patient (< 10 ng/l). Haemoglobin levels in all the patients were unchanged compared with their steady-state levels but one had developed a macrocytosis (103 fl). Schilling tests were normal in two patients, and two patients had negative gastric parietal antibodies. All three patients were given intramuscular vitamin B12 in addition to avoiding further exposure to nitrous oxide, and their neurological symptoms improved completely. As nitrous oxide is known to cause a neuropathy similar to that seen in pernicious anaemia, we postulate that nitrous oxide analgesia combined with low B12 levels was the cause of the marked neuropathy in these patients. As a result of our observations and the probable association, we now do not use nitrous oxide analgesia in the management of patients with sickle cell disease.
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PMID:Sickle cell disease and nitrous oxide-induced neuropathy. 1067 96

Disregarding pain resulting from vitamin deficiency, an analgesic effect seems to be exerted only by vitamin B1 (thiamine), vitamin B6 (pyridoxines), and vitamin B12 (cobalamine), particularly when the three are given in combination. The analgesic effect is attributed to an increased availability and/or effectiveness of noradrenaline and 5-hydroxytryptamine acting as inhibitory transmitters in the nociceptive system. In animal experiments, high doses of these vitamins administered alone or in combination inhibited nociceptive behavior and depressed the nociceptive activity evoked in single neurons of the dorsal horn of the spinal cord and in the thalamus. Moreover, they were found to enhance the antinociceptive effect of non-opioid analgesic agents on withdrawal reflexes. Clinical data fail in most cases to meet current standards of evaluation (randomization, double-blindness). Still, it appears that high doses of the vitamins B1, B6, and B12 administered separately or in combination can alleviate acute pain and potentiate the analgesia caused by non-opioid analgesics such as the NSAIDs and metamizol (dipyrone). Therapeutic effects are observed in neuropathic pain and pain of musculoskeletal origin. Vitamin B6 is effective in the carpal tunnel syndrome which, however, is attributed at least in some cases to vitamin B6 deficiency. It is also worth noting that the B vitamins are shown to enhance the beneficial effect of diclofenac in acute low-back pain so that either the duration of treatment or the daily dose of diclofenac may be reduced. The use of high doses of vitamin B6 may be limited by a neurotoxic effect. The effectiveness of B vitamins in depressing chronic pain has not been established. It would be interesting to know if the B vitamins are of use as adjuvants in the treatment of tumor pain.
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PMID:[Analgesic and analgesia-potentiating action of B vitamins]. 1279 82

Medicines reconciliation is integral to patient safety, symptom control and reducing patient anxiety. During a 3-month period on the respiratory ward at St. Peter's Hospital, 54% of drug charts were not reconciled with pre-admission medicines at the point of discharge for admissions up to 17 days. Only 18% were reconciled within 24 hours of admission. 50% of drug charts were missing 0-2 pre-admission medicines and 50% were missing 3-5 pre-admission medicines. The most common medicines that were not reconciled included topical applications which included eye, ear, nasal and skin applications (14%); vitamins i.e. vitamin B12 and thiamine, analgesia, PRN inhalers (11% individually); antidepressants and lipid regulators (6% individually); amongst a range of other medications including antiplatelets, calcium channel blockers, ACE inhibitors and diuretics. Two interventions were carried out to improve the rate of medicines reconciliation onto hospital drug charts with pre-admission medicines. These were: 1) a green sticker placed in the medical notes by the pharmacist when drug charts were incomplete, which required a date and signature from the doctor when the drug chart had been reconciled 2) the placing of the loose medicines reconciliation record (a list of pre-admission medicines retrieved from a reliable source usually by the pharmacist) to the front of the drug chart. These measures were designed to alert the doctors that the drug chart was incomplete. After 2 PDSA cycles, the results showed positive outcomes. In 75% of the cases where the interventions were used, medicines reconciliation was complete at the point of discharge with 34% of drug charts reconciled within 24 hours of admission. Of the 25% of drug charts that were not reconciled despite the use of the interventions, 100% of them were missing 0-2 medicines however 0% were missing 3-5 medicines. This highlights that the interventions were effective in improving the rates of medicines reconciliation.
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PMID:Improving medicines reconciliation rates at Ashford and St. Peter's Hospitals NHS Foundation Trust. 2882 9

The first clinical application of nitrous oxide (N2O) was in 1844, by an American dentist named Horace Wells who used it to control pain during tooth extraction. Since then, N2O has shared a 170-year history with modern dental anesthesia. N2O, an odorless and colorless gas, is very appealing as a sedative owing to its anxiolytic, analgesic, and amnestic properties, rapid onset and recovery, and, in particular, needle-free application. Numerous studies have reported that N2O can be used safely and effectively as a procedural sedation and analgesia (PSA) agent. However, N2O can lead to the irreversible inactivation of vitamin B12, which is essential for humans; although rare, this can be fatal in some patients.
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PMID:Complications caused by nitrous oxide in dental sedation. 2974 81