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)

The effect of dexamethasone on exercise-induced adrenocorticotropin (ACTH) secretion and dental analgesia was studied in healthy human subjects. Different levels of exercise (100-200 W) were produced by a cycle ergometer. Dental pain thresholds were tested with a constant current stimulator. Dental pain thresholds were elevated with increasing work loads, and the elevation was still significant 30 min after the end of the exercise. Dexamethasone produced a significant reversal of exercise-induced pain threshold elevations concomitantly with the suppression of exercise-induced ACTH release. The results suggest that the corticotropin releasing factor-ACTH axis is involved in the exercise-induced analgesia.
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PMID:Dexamethasone attenuates exercise-induced dental analgesia in man. 216 84

The effects of ip intra-PAG injection of ACTH on serotonin (5-HT), norepinephrine (NE) contents of hippocampus and hypothalamus and pain threshold were investigated. The results showed: (1) After ip ACTH, the pain threshold, the contents of 5-HT of the two brain regions and the NE content of hippocampus were markedly elevated. Prior destruction of periaqueductal gray (PAG), the elevation of pain threshold and the increase of the 5-HT contents of two brain regions due to ip ACTH were completely abolished, while the effect of ACTH in elevating NE content of hippocampus still persisted. (2) After intra-PAG injection of ACTH, the pain threshold and the 5-HT contents in hippocampus and hypothalamus were significantly increased, however, the NE levels in hippocampus and hypothalamus showed no significant changes. The analgesic effect of the intra-PAG injection of ACTH was prevented by icv LSD, but not by naloxone, atropine, hexamethonium and phentolamine. (3) After icv ACTH, the pain threshold did not change. These results suggest that the serotoninergic system may be activated by PAG for mediation of ACTH-induced analgesia.
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PMID:[Serotonin of hippocampus and hypothalamus taking part in the analgesic effect of adrenocorticotropic hormone in rats]. 216 93

Steroid-secreting tumors of the testis have generally been considered to be of Leydig cell origin. Testicular tumors in patients with congenital adrenal hyperplasia have been thought to be adrenal rests, but no conclusive evidence supporting the hypothesis has been presented. We report a morphological and biochemical analysis of a patient with 21-hydroxylase deficiency who developed bilateral nodular hyperplasia of steroid-secreting tissue within the testis, despite suppression therapy with both exogenous glucocorticoids and testosterone. The tissue was formed of confluent nodules of homogenous cells. Electron microscopy showed the cells to have abundant smooth endoplasmic reticulum, well developed Golgi apparatus, and mitochondria with predominantly tubular cristae, features characteristic of steroid-secreting cells of adrenocortical origin. Crystals of Reinke were not observed. Functional studies in vivo showed a marked response to ACTH infusion, with 17-hydroxyprogesterone rising from 56 to 13,500 ng/mL, cortisol from less than 2 to 19 micrograms/dL, and testosterone from 369 to 629 ng/dL, with an attendant increase in testicular size and pain over 48 h. Receptor studies in vitro revealed no gonadotropin receptors, but abundant angiotensin-II receptors. Enzyme activity analysis in vitro showed undetectable 21-hydroxylase activity and an enzyme profile consistent with adrenocortical cells rather than Leydig cells. Based on these morphological and biochemical findings, we conclude that the nodular steroidogenic tissue that replaced this patient's testes was of adrenal origin. The study documents for the first time the development of adrenocortical tumors from adrenal rest tissue within the testis.
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PMID:Steroidogenic enzyme activities, morphology, and receptor studies of a testicular adrenal rest in a patient with congenital adrenal hyperplasia. 233 78

Iatrogenic Cushing's syndrome has been reported after the use of nasal, aerosol, oral, and intramuscular steroid preparations. Presented is a case of Cushing's syndrome due to an epidural injection of methylprednisolone. A 24-year-old man had left arm pain after an occupational injury. Electromyography revealed C7 radioculopathy and cervical laminectomy was performed. Postoperatively, the patient noted improvement, however, he had recurrence of his symptoms within 1 month. Significant pain in the left arm, accompanied by swelling, persisted despite non-steroidal anti-inflammatory and anti-depressant medications. Repeat electromyography showed a resolving C7 with increased polyphasic potentials. Reflex sympathetic dystrophy was diagnosed and the patient received 3 stellate ganglion blocks with relief of the swelling, but only temporary relief of pain. He then underwent epidural injection of 60 mg of methylprednisolone. A cushingoid appearance was noted approximately 1 month later. Serum cortisol was undetectable, there was no adrenal response to synthetic ACTH, and urinary-free cortisol was below normal at 12. The patient eventually underwent a second surgical procedure for his pain and required steroid coverage. His pain subsequently showed slow improvement. Urinary-free cortisol normalized 4 months after onset; however, the patient's cushingoid appearance persisted for 12 months.
Pain 1990 Jan
PMID:Cushing's syndrome from epidural methylprednisolone. 233 20

Surgical hypophysectomy performed in 18 cases with hormone-dependent carcinoma resulted in tumour regression in 38.8% of the cases, and pain relief in 88%. Neuroadenolysis performed 170 times on 130 cases resulted in pain relief in 94% with hormone-dependent carcinoma, and 70% with non-dependent carcinoma. The clinical investigations, following performance of neuroadenolysis, indicate suppressed pituitary function, significant increase of ACTH, thyrotropin-releasing hormone and vasopressin in the cerebrospinal fluid (CSF), delay of long latencies in somatosensory evoked potential and increased pain threshold of C-fibres. Increase of beta-endorphin in CSF was very brief. Though the exact physiological activity in pain sensation of those peptides other than endorphins still remains obscure, increase of the peptides which are mainly synthesized in the hypothalamopituitary axis, along with suppressed pituitary function, is considered to exert a long-lasting suppressive effect on the mediation and perception of cancer pain through C-fibres and the central nervous system.
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PMID:The pituitary as a target of antalgic treatment of chronic cancer pain: a possible mechanism of pain relief through pituitary neuroadenolysis. 243 39

Peptides derived from pro-opiomelanocortin (POMC) influence neurodevelopmental processes. Earlier studies indicated that MSH/ACTH compounds improved behavioral efficiency in retarded individuals. Recent studies have shown that opiate blockers reduce treatment-resistant self-injurious behavior (SIB), an autistic-like, developmental disorder. Although the exact mechanisms are unknown, prenatal POMC disregulation, addiction to endogenous opiates and elevated pain threshold have been proposed to account for this behavior. In study one, four SIB patients were given 0, 25, 50 or 100 mg of naltrexone on separate weeks in a double blind, Latin square design. A specific dose dependent reduction in SIB was observed in three patients. In study two, plasma b-endorphin was measured in 40 patients with SIB, a related behavior, stereotypy (ST) or controls. SIB and ST patients had higher levels of endorphin than controls. These data added new support for the role of b-endorphin in a treatment-resistant patient group.
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PMID:Beta-endorphin disregulation in autistic and self-injurious behavior: a neurodevelopmental hypothesis. 246 89

Beta-endorphin release was studied in 40 patients after surgery for thyroid cancer or after femoral amputation due to malignant malformations in bones and soft tissues of the lower extremities. In thyroid surgery beta-endorphin release was more marked under neuroleptanalgesia than under combined electroanesthesia. A correlation between beta-endorphin and ACTH levels has been established. It indicates a stress nature of neuropeptide release. In patients with femoral amputation an increased beta-endorphin release was not observed. Possible mechanisms of beta-endorphin level elevation are discussed in terms of modern concepts of pain modulation.
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PMID:[Effect of electroanesthesia and neuroleptanalgesia on blood plasma beta-endorphin level during surgical intervention in cancer patients]. 252 96

The effect of acupuncture on sensory thresholds was studied in 6 healthy subjects. The modes of acupuncture studied were: 1. manual stimulation, 2. electrical stimulation at 2 Hz, 3. electrical stimulation at 80 Hz. Superfiscial-acupuncture was used as placebo. Insertions of needles or application of electrodes were bilateral, at St 7 (intrasegmental) or Li 4 (extrasegmental). The study showed that manual or electro-acupuncture were effective when used intrasegmentally, raising pain threshold values 1.1 to 1.4 times that prior to stimulation. The pain threshold elevation obtained was not significantly related to plasma levels of beta-endorphin, ACTH or prolactin. Other sensory thresholds, thermal, vibrotactile and electrotactile were unaffected by such conditioned stimulation. Superfiscial-acupuncture had no significant effect on the sensory thresholds tested.
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PMID:Acupuncture and sensory thresholds. 253 64

The aim of the work was to study the effect of glucocorticoids, opiates and stressful stimuli on dipeptidyl peptidase IV (DP IV, EC 3.4.14.5) activity of T lymphocytes prepared from the thymus of intact and adrenalectomized rats. Four week old male rats of Wistar strain were used. The in vivo administration of ACTH, dexamethasone and morphine treatment resulted in an increase of DP IV activity in the cell suspension. In adrenalectomized rats ACTH treatment failed to modify the enzyme activity, however, pain or emotional stress resulted in an elevated DP IV activity. Morphine and D-Met2-Pro5-enkephalinamide resulted in a dose dependent activation of DP IV in T cells, an effect which could be modified by naloxone pretreatment. Our findings show that DP IV mechanisms in T cells are highly sensitive to exogenous and endogenous steroids, opiates and biologically active substances released in response to stress in rats.
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PMID:Changes of dipeptidyl peptidase (DP IV) activity in the T lymphocytes of rats following administration of ACTH, dexamethasone and opiates. 254 37

In this study we have examined the results of salmon calcitonin treatment on migraine pain. The mechanism by which calcitonin induces analgesia is still not understood. We observed the effect of a 5-day treatment with salmon calcitonin (IM 100 IU/day) on circulating levels of beta-endorphin, ACTH, and cortisol in 20 patients with migraine during the headache-free period. All 3 hormones were increased after the calcitonin administration and the maximum increase was obtained in beta-endorphin levels. There were significant statistical correlations between beta-endorphin, ACTH, and cortisol levels determined before and after calcitonin treatment.
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PMID:Treatment of migraine with salmon calcitonin: effects on plasma beta-endorphin, ACTH and cortisol levels. 256 Apr 8


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