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

Cancer pain remains a major cause of suffering. Improvements in its management have made unrelieved cancer pain unacceptable. While pharmacotherapy is the mainstay of cancer pain treatment, other options such as radiotherapy, nerve blocks, etc., have to be considered as well. A comprehensive approach must also address psychosocial issues. A successful pharmacotherapy programme for cancer pain requires careful assessment of the origin and cause of the pain. The selection of analgesics has to be rationalised using a sequential approach such as the WHO stepladder. Oral application by the block in an individually titrated dosage is recommended. Although morphine remains the most useful opioid, it should be used in combination with nonopioids. Co-analgesics, which contribute to analgesia without being classical analgesics, should be used to treat pain of specific origin. Here membrane-stabilizers, antidepressants and steroids play an often underestimated role in the treatment of neurogenic pain. Anxiolytics and major tranquillisers should be avoided because they cause sedation without improving quality of analgesia. Calcitonin, diphosphonates and spasmolytics are of minor importance in this regard. Finally, concomitant medication to treat side effects of the therapy may be necessary in formulating a comprehensive treatment plan.
 ...
PMID:Pharmacological management of cancer pain. 137 59

Animal experiments demonstrate that the intracerebro-ventricular administration of calcitonin induces analgesia. During the treatment of such diseases as osteitis deformans Paget and acute pancreatitis with calcitonin no spectacular pain-relieving effect was evident, but the application of calcitonin in hypercalcemic patients with bone tumors led to considerable pain relief. Recent double-blind studies document the analgesic effectiveness of calcitonin in malignant diseases, but also against postoperative pains in nontumor patients. Calcitonin as an analgesic drug deserves further investigation.
 ...
PMID:Calcitonin: analgesic effects. 636 72

Calcitonin is a peptide hormone secreted by the C-cells of the thyroid gland. This hormone mainly acts in preventing bone resorption. Furthermore, calcitonin is involved in other biological actions, and in particular it is able to relieve pain independently of its peripheral effects on bone. Here, we examine the possible mechanisms of calcitonin-induced analgesia, with particular regard to the opioid system involvement. Several studies in animals and in humans demonstrate that calcitonin increases plasma beta-endorphin levels, acting at the hypothalamic and/or at the pituitary level, either directly or indirectly, through monoaminergic neurotransmitters. However, this calcitonin-induced beta-endorphin release has not always been observed. These different results are discussed, and a possible implication of sex and/or calcitonin dose employed has been examined. We conclude that the analgesic effects of calcitonin are multifactorial, and beta-endorphin plays its own specific role.
 ...
PMID:Calcitonin and beta-endorphin secretion. 806 Dec 53

Calcitonin (CT) produces long-lasting analgesia in patients suffering from painful diseases following repeated systemic injections, but there have been only a few contradictory reports on the antinociceptive action of systemic injections of CTs in animal experiments. This study was conducted to elucidate an antinociceptive action of systemic CT in rats. An injection of dilute formalin induced hyperalgesia for about 2 h. Single topical injections of 0.12 and 1.2 U, but not 0.012 U, of [Asu1.7] eel CT (eCT) into the same site of formalin injection inhibited the hyperalgesia. Repeated systemic injections of eCT (4 and 40, but not 0.4, U kg-1 day-1) for 7 days inhibited the hyperalgesia, while the single injection was without effects at doses tested. Although the highest dose of eCT (40 U kg-1 day-1) inhibited an increase in body weight following repeated injections, lower doses (0.4 and 4 U kg-1 day-1) were without effects. The suppression of hyperalgesia following repeated systemic injections of eCT (4 U kg-1 day-1) lasted for at least 24 h, and subsided by 3 days following the last eCT injection. These results indicate that the repeated systemic injections of eCT produce a long-lasting inhibition of formalin-induced hyperalgesia in rats. This inhibitory effect is similar to CT analgesia in human subjects in terms of a necessity for repeated administration, effective dose and long-lasting effects.
 ...
PMID:Antinociceptive effects of repeated systemic injections of calcitonin in formalin-induced hyperalgesic rats. 887 51

Calcitonin is one of three most important factors involved in the regulation of systemic calcium homeostasis. Since its discovery in 1961 the structure of calcitonin from different species including human was established, synthetized and developed for use in human clinic. Up to now calcitonin is utilized in treatment of hypercalcemia, Paget disease, algodystrophy, primary and secondary osteoporosis and analgesia. Beside comparative studies aiming on selection of the most effective protocol of treatment and utilization, lately calcitonin is extensively studies for its antifracture potency in osteoporosis. One of the substantial therapeutical progress also appeared the utilization of intransal preparation of calcitonin.
 ...
PMID:[Calcitonin -- 1998]. 1010 52

Trigeminal neuralgia (TN) has been recognized as one of the most common neurovascular syndromes caused by the vascular contact of the trigeminal nerve in its root entry zone (REZ) with a branch of the superior or anterior inferior cerebellar arteries, leading to a demyelinization of trigeminal sensory fibers within either the nerve root or, less commonly, the brainstem. There is a lack of certainty regarding the aetiology and pathophysiology of TN, therefore the treatment of trigeminal neuropathic pain disorders continues to be a major therapeutic challenge. The identification of novel therapeutic agents for the treatment of these disorders is important. Calcitonin (especially intranasal) provides an interesting analgesic effect in a series of painful conditions including reflex sympathetic dystrophy syndrome, adhesive capsulitis, ankylosing spondylitis, rheumatoid arthritis, vertebral crush fractures and metastasis, phantom limb pain, etc. Exogenous calcitonin is thought to cross the blood-brain barrier and to accumulate slowly in the brain, inducing analgesia once sufficient receptors are occupied. We hypothesize that calcitonin may has anti - trigeminal neuralgia properties. From the clinical point of use, the analgesic effect of calcitonin will be beneficial throughout the whole period of medical treatment of trigeminal neuralgia patients.
 ...
PMID:Could calcitonin be a useful therapeutic agent for trigeminal neuralgia? 1834 43

Calcitonin (CT) is a peptide hormone that is secreted by the parafollicular cells of the thyroid in response to elevated serum calcium levels. It acts to reduce serum calcium by inhibiting bone resorption and promoting renal calcium excretion. In addition to this hypocalcemie effect, calcitonin modulates the renal transport of water and several ions other than calcium and acts on the central nervous system to induce analgesia, anorexia, and gastric secretion. The CT receptor, a member of a newly described family of serpentine G protein-coupled receptors, has recently been shown to couple to multiple trimeric G proteins, thereby activating several signaling proteins, including protein kinase C, cAMP-dependent protein kinase and calcium/calmodulin-dependent protein kinase. In kidney proximal tubule cells (LLC-PK1), the CT-activated signaling mechanisms vary in a cell cycle-dependent manner, with the receptor coupling through a G(s) protein during G(2) phase and through a G(i) protein and possibly a G(q) protein during S phase. These signaling mechanisms differentially modulate the activities of Na(+)/K(+)-ATPase and the apical Na(+)/H(+) exchanger, effector molecules that play important roles in transepithelial Na(+) transport. Cloning of CT receptors has revealed the presence of alternatively spliced cassettes, resulting in the expression of different isoforms of the receptor. The availability of these recombinant CT receptors has allowed preliminary characterization of the effects of changes in the receptor's structure on its ligand binding and signal transduction properties. Thus, the cellular and molecular biology of CT is complex, with several structurally related peptide ligands and multiple isoforms of the CT receptor that can independently activate diverse signaling pathways. As the recent exciting results in this field are extended, we can expect rapid progress in understanding the molecular basis of the diverse effects of CT and, possibly, of the CT-related peptides CGRP and amylin.
 ...
PMID:Signal transduction by calcitonin Multiple ligands, receptors, and signaling pathways. 1840 35

Calcitonin is a polypeptide hormone that bone resorption-inhibitory and analgesic effects, and has been used over many decades as a drug for the treatment of osteoporosis in Japan and overseas. Reports of large-scale studies of this hormone therefore as yet are few, compared to recently introduced drugs. Calcitonin is prescribed in injectable form in Japan while nasal spray preparations are widely used in Europe and the Unites States. Its characteristic effect of analgesia is slow in onset as compared with anti-inflammatory analgesic agents. A mechanism of action involving its serotonin receptor expression-mediated effect on pain impulse transmission has been demonstrated. On account of this effect, calcitonin is recommended for use in the management of pain in patients with fresh vertebral fractures.
 ...
PMID:[Calcitonin]. 1883 43

Calcitonin operates predominantly to regulate acute hypercalcemic states. The response to calcium challenges is lowest in elderly women; however, the contribution of calcitonin to the etiology of osteoporosis is unclear. The calcitonin receptor is a member of a supergene family consisting of G-protein-linked receptors with seven domains spanning the cellular membrane. These receptors are distributed in calcium-responsive tissues, gut, and hypothalamus and mediate calcitonin's known clinical effects of hypocalcemia, enhanced gastric motility, and analgesia. Therapeutic use of calcitonin is indicated in both perimenopausal and postmenopausal women with contraindications or intolerance to estrogen replacement therapy, Paget's disease, painful vertebral compression fractures, and steroid-induced osteopenia.
 ...
PMID:Calcitonin. 1907 52

Behcet's disease (BD) is a chronic, multisystem inflammatory disorder characterized by relapsing oral aphthous and genital ulcers, ocular inflammation, erythemanodosum and folliculitis-like lesions of the skin, arthritis, and central nervous system involvement. Its pathogenesis has not been fully elucidated but the etiology is accepted to be multifactorial, therefore the treatment of Behcet's disease continues to be a major therapeutic challenge. The identification of novel therapeutic agents for the treatment of these disorders is important. Calcitonin (CT), a peptide hormone secreted in response to hypercalcemia, has the dual effect of inhibiting osteoclast recruitment as well as their resorptive activity. A number of reviews have concluded that salmon calcitonin is safe and effective in the treatment of osteoporosis. Calcitonin abrogated the stimulating effect of RANKL or prednisolone; similar results were obtained with OPG. Additionally, the analgesic activity of salmon calcitonin has been shown in several controlled prospective double-blind studies to improve pain. Exogenous calcitonin is thought to cross the blood-brain barrier and to accumulate slowly in the brain, inducing analgesia once sufficient receptors are occupied. Since CT could antagonize resorptive and analgesic activity by competitively binding to CTR and has been considered as a specific antagonist, we postulate that the CT could function as a novel agent to inhibit BD. In our opinion, if the hypothesis proved to be practical, CT could be widely used in clinical settings to treat BD.
 ...
PMID:Inhibition of Behcet's disease by calcitonin. 1929 90


1 2 Next >>