Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vitro studies on the effects of dexamethasone on human synovial cells have shown that with high concentrations of the steroid in the culture medium cellular activity was completely blocked whereas with low concentrations (10(-6)M), cellular density decreased but there was an increase in the synthesis of RNA, DNA, protein and hyaluronic acid. These data, coupled with clinical experience of using intra-articular hyaluronic acid to treat patients with osteoarthritis of the knee, prompted the investigators to carry out an open, randomized study of the use of very small doses of dexamethasone in association with hyaluronic acid in 40 osteoarthritic patients. Twenty patients received a weekly intra-articular injection of 20 mg sodium hyaluronate in 2 ml phosphate buffer for 5 weeks; the other 20 patients followed a similar treatment regimen, the only difference being the addition of 0.4 mg dexamethasone phosphate to the first injection. Clinical examination of the knee was made before each injection, 7 days after the fifth injection and 60 days after the start of the trial. Rating scale assessments were made at each visit of spontaneous pain, pain during the day, at night, weight bearing and whilst walking. The results showed that whilst a progressive decrease in all pain parameters was evident and persisted after the end of treatment in both patient groups, pain intensity decreased more rapidly and to lower levels in all but weight-bearing pain, as did improvement in joint mobility, in the combined treatment group. Local tolerance was good with both treatment regimens, with no untoward signs or symptoms at any time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic synergism between hyaluronic acid and dexamethasone in the intra-articular treatment of osteoarthritis of the knee: a preliminary open study. 146 45

Using 31P nuclear magnetic resonance, the following parameters were determined in the resting musculus erector spinae of five patients suffering from chronic low back pain, five patients with fibromyalgia, and five healthy controls: Inorganic phosphate (Pi), phosphocreatine (PCr), ATP gamma, ATP alpha, ATP beta. The intracellular pH was derived from the chemical shift of Pi referenced to the PCr resonance. In addition, the Pi-Index was calculated according to the formula: Pi/(Pi + PCr). We discovered a tendency towards a shift of the Pi resonance in the alcalic direction, which was the larger, the stronger muscle spasm was found on palpation. The pH showed the most reliable relationship to the clinical status of muscle spasm. The surprising finding that there is no acidification within the spasmed muscle indicates that generalized hypoxia does not exist in this tissue. This has already been shown with PO2 measurements. An intracellular acidification is only recorded during maximal isometric contraction. Thus, ischemia cannot be responsible for pain experienced during muscle spasm.
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PMID:[Recording muscle spasm in the musculus erector spinae using in vivo 31P magnetic resonance spectroscopy in patients with chronic lumbalgia and generalized tendomyopathies]. 147 7

In a randomised, double-blind, double-dummy, multiple dose, crossover study in 30 patients we compared an ibuprofen/codeine combination (400 mg ibuprofen/25.6 mg codeine phosphate) with a paracetamol/codeine/caffeine combination (1 g paracetamol/16 mg codeine phosphate/60 mg caffeine) for pain relief over 6 days after two-stage bilateral lower third molar removal. The ibuprofen combination produced significantly greater analgesia than the paracetamol combination, both on single-dose analysis of the first and second days and on multiple-dose measures for days 1, 2, 3 and 4. The mean incidence of adverse effects over the 6 days was 20% for both combinations. This trial design (crossover with multiple dosing in outpatients) is a sensitive way of testing for analgesia, and is potentially more predictive of adverse effect problems than single-dose studies. It confirms that multiple dosing may show increased efficacy.
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PMID:A multiple dose comparison of combinations of ibuprofen and codeine and paracetamol, codeine and caffeine after third molar surgery. 151 16

The study was aimed at developing a reference model for experimental pain and tenderness in the human temporal muscle by the local injection of hypertonic saline, potassium chloride and acidic phosphate buffer, using isotonic saline as control. The design was randomized and double-blind. Twenty healthy subjects had 0.2 ml test solution injected into one temporal muscle and saline into the other. Following each injection, pain was rated on a 10-point ordinal scale and pressure-pain thresholds were measured every minute for 10 min by a pressure algometer. Hypertonic saline (n = 11) and potassium chloride (n = 12) induced significantly more pain than isotonic saline (ANOVA, p less than 0.0001). Compared to control injections, hypertonic saline and potassium chloride induced a significant reduction in pressure-pain threshold (ANOVA, p less than 0.0001 and p less than 0.05). Forty-eight percent of the injections led to the referral of pain most often to the jaws. A positive correlation between the relative occurrence of referred pain and pain intensity was observed (p less than 0.001) as was a negative correlation between the decrease in pressure-pain threshold and pain intensity (p less than 0.05).
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PMID:Experimental pain in human temporal muscle induced by hypertonic saline, potassium and acidity. 157 38

The antinociceptive effect of subcortically administered nicotine was investigated in the rat using the hot-plate and tail-flick tests. Adult male Sprague-Dawley rats were implanted with guide cannulas aimed at 185 sites in the forebrain, midbrain and hindbrain. After 1 week, nicotine was injected in 0.5 microliter of 50 mM phosphate buffer, pH 7.4. The pedunculopontine tegmental nucleus (PPTg) of the mesopontine tegmentum and the nucleus raphe magnus (NRM) of the ventral medulla were the most sensitive sites of nicotine-induced antinociception. The median effective doses of nicotine to inhibit hot-plate or tail-flick nociception after PPTg or NRM administration ranged between 1.4 and 3 nmol. The lack of effect of s.c. injections of naloxone on the antinociception induced by nicotine in the PPTg or NRM ruled out endogenous opioid mechanisms. Coadministration of mecamylamine or pirenzepine with nicotine into the NRM competitively antagonized nicotine-induced antinociception. The administration of the muscurinic cholinergic type 2 receptor antagonist methoctramine into the NRM produced a strong antinociceptive response which was blocked by prior treatment of the NRM with hemicholinium-3. Hemicholinium-3 pretreatment of either the PPTg or the NRM antagonized the antinociception induced by nicotine at these sites. Hemicholinium-3 pretreatment of the NRM also antagonized the antinociception produced by s.c. administered nicotine. The antinociceptive effects of nicotine injected in the PPTg were blocked by procainamide injections in the NRM; however, the antinociceptive effects of nicotine injected in the NRM were not blocked by bilateral injections of procainamide in the PPTg. Both lesioning the PPTg with ibotenic acid and pretreating the NRM with hemicholinium-3 abolished completely the antinociception induced by nicotine or (+)-cis-dioxolane microinjections into the PPTg. However, neither ibotenic acid-induced nor electrolytic lesions of the PPTg alone altered CRL. The data support the existence of a tonically active cholinergic pathway which is under autoinhibitory control that originates in the PPTg, terminates in the NRM and modulates nociception by activating descending pain inhibitory systems relaying within the NRM.
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PMID:Characterization of the antinociception induced by nicotine in the pedunculopontine tegmental nucleus and the nucleus raphe magnus. 167 72

We compared the effect and toxicity of estramustine phosphate and weekly low-dose epirubicin in a prospective randomized trial in 41 patients with metastatic prostate cancer refractory to hormonal manipulation. No significant difference between treatment modalities was seen. Palliation was reached in over 60% of patients. The median survival was 15 months in both groups. Toxicity was mild. Further, we investigated the effect of epirubicin after the failure of preceding estramustine phosphate therapy in additional 20 patients. Pain relief was achieved in 50% of these patients. The median survival was 10 months. Toxicity was acceptable.
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PMID:Hormone-resistant metastatic prostate cancer. Comparisons between estramustine phosphate and low-dose epirubicin treatments. 170 66

Acetaminophen (APAP) 1000 mg, APAP 2000 mg, the combination of APAP 1000 mg plus codeine phosphate 60 mg (APAPCOD), and placebo (PBO) were compared in a 6-hour, randomized, single-dose, double-blind, parallel-group analgesic trial. All active treatments were statistically superior (p less than 0.05) to placebo for 4 hours after medication with respect to pain intensity (PI) and pain intensity difference (PID), and up to 3 hours regarding pain relief (PAR). The combination scored better than all other treatments on the summary analgesic efficacy measures sum PI (SUMPI), sum PID (SPID), and total PAR (TOTPAR). The combination was statistically superior to APAP 1000 mg on SUMPI, TOTPAR and maximum PAR (MAXPAR). Acetaminophen 2000 mg showed marginal numerical superiority over 1000 mg for SUMPI, but was not statistically superior for any summary efficacy measure. The 2000-mg dose was numerically inferior to APAPCOD for every summary efficacy measure and statistically inferior regarding SPID and MAXPAR. We concluded that codeine 60 mg added to acetaminophen 1000 mg offers analgesic advantages, and acetaminophen reaches an analgesic ceiling effect at 1000 mg using the dental pain model.
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PMID:Analgesic efficacy of acetaminophen 1000 mg, acetaminophen 2000 mg, and the combination of acetaminophen 1000 mg and codeine phosphate 60 mg versus placebo in acute postoperative pain. 174 22

The polymorphic cytochrome P-450 DB1 (P-450 IID6) is responsible for the O-demethylation of codeine to morphine by human liver microsomes. The influence of P-450 DB1 variable activity on the bioactivation of codeine in vivo to morphine and on its analgesic effect was investigated in phenotyped healthy volunteers--7 extensive [EM] and 1 poor [PM] metabolizer of debrisoquine. After pretreatment with oral placebo or quinidine sulphate 50 mg, codeine phosphate 100 mg or placebo were administered orally according to a double-blind randomized crossover design. In EM subjects the plasma morphine Cmax was 17.9 nmol/l, whereas virtually no morphine was detectable after quinidine pretreatment (1.5 nmol/l), and in the PM subject (0.60 nmol/l). In EM codeine significantly increased subjective (VAS) and objective (R-III reflex) pain thresholds in response to selective transcutaneous nerve stimulation, whereas no significant analgesia was detected after placebo, or after codeine with quinidine pretreatment, or in the PM. In PM of genetic origin, or due to environmental alteration of the phenotypic expression (i.e. drug interaction), codeine is not activated into morphine and is an inefficient analgesic.
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PMID:Impact of environmental and genetic factors on codeine analgesia. 178 73

We describe a 62-year-old male with brain metastasis from prostatic carcinoma, which regressed with medical and surgical endocrine therapies. The patient's presenting complaints were left periocular and deep ocular pain and a defect of the left visual field. During treatment of the above symptoms, macrohematuria, dysuria and pollakiuria occurred. Pathological examination of a transrectal needle biopsy disclosed moderately differentiated adenocarcinoma of the prostate. Computerized tomographic scan (CT) and magnetic resonance imaging demonstrated a brain tumor at the frontal skull base and the region of the frontal lobe suspected to be a metastasis of the prostatic carcinoma. One week after a period of daily administration of estramustine phosphate sodium, the prostate was observed to be softened and slightly decreased in size. The visual field defect and disturbance of urination gradually improved. The prostate decreased to normal size and no tumor mass could be detected on the brain CT after 3 months of treatment.
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PMID:Effect of endocrine therapy on a brain metastatic lesion of prostatic carcinoma. 179 3

Blind ending bifid ureter is a rare anomaly in the urinary tract. This anomaly may result from failure of a premature branch of the ureteral bud to join with the metanephric blastema. A 21-year-old man was admitted with macroscopic hematuria and colic pain in the left flank region. Urinalysis demonstrated hematopyuria and excretory urography suggested bifid ending accessory ureter with a stone on the left side. Surgical exploration showed that the accessory ureter was bifurcated from the left ureter at about 5 mm from the bladder wall and ran parallel with the left ureter. Although dense adhesions to the surrounding tissue existed, the accessory ureter was resected at the site of the junction. It measured 3 cm in length and 1 cm in greatest diameter. The stone found at the tip of the accessory ureter was composed of calcium oxalate (24%) and calcium phosphate (76%). Histological examination revealed that the ureter had all layers of normal ureteral structure and no renal tissue was identified in the specimen resected. During a follow-up period of 22 months after the operation, he was free of urinary tract infection and abdominal pain. Of 77 cases with blind ending bifid ureter reported in the Japanese literature, a ureteral stone was found in the blind branch in only 5 cases.
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PMID:[Blind ending bifid ureter with stone in the blind branch: report of a case]. 185 88


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