Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0596240 (cancer pain)
 3,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the analgesic effect of salmon calcitonin (sCT) on 14 patients with intractable cancer pain. The drug was administered by epidural infusion (4-8 bolus administrations in 48 h); the dosage was 100 IU/48 h in 5 patients and 400 IU/48 h in 9 patients. Significant, although limited, pain relief and nocturnal pain relief were obtained; the requirement for conventional analgesic drugs was substantially reduced. The treatment was well tolerated and no side effect was recorded. However, only in 3/14 patients did pain relief result in improvement of mobility, with two patients becoming able to ambulate; no patient experienced absence of pain. In general, the treatment produced only limited benefit and subsequent morphine treatment was required in all instances. Widespread use of epidural sCT in intractable cancer pain is not justified as a routine procedure and more substantial evidence is required to support the clinical utility of such an approach.
 ...
PMID:Analgesia with epidural calcitonin in cancer patients. 274 Dec 26

Although the pain-relieving activity of salmon calcitonin has been mainly demonstrated for painful bone metastases it has been postulated that the drug possesses a central analgesic activity which is independent of the opiate receptor system. Thus, 16 patients with neuropathic cancer pain due to radicular compression by extraskeletal metastases, and without the possibility of any specific anticancer treatment, entered the study. Of the 16, 11 were pretreated with opiate-type analgesics. Salmon calcitonin was applied once daily at a dose of 200 IU in 500 ml 0.9% NaCl infused over 1 h. The total duration of the treatment was 20 days. The pain-relieving effect was classified as very good, good, moderate and bad; in 10 patients it was described as bad, in 2 as moderate in 2 as good and in 2 as very good. The drug failed in 9/11 opiate-pretreated patients. It is suggested that salmon calcitonin pain-relieving activity might depend on the tumor type, previous pain-relieving drug intake and site of metastatic disease.
 ...
PMID:A pilot study to assess the efficacy of salmon calcitonin in the relief of neuropathic pain caused by extraskeletal metastases. 815 61

Certain types of cancer pain fail to respond well either to systemic drug therapy or to spinal opioids because of the occurrence of intolerable adverse effects. In addition to spinal opioids other drugs may produce an antinociceptive effect when administered by the spinal route, such as local anesthetics, NSAID, alpha 2-agonists, calcium-channel blockers, NMDA antagonists, cholinergic drugs, peptides such as somatostatin, octreotide or calcitonin, adenosine agonists, benzodiazepines, neurokinin and cholecystokinin antagonists, nitric oxide synthase inhibitors, corticosteroids, and enkephalinase inhibitors. All these drugs may be administered in combination between them, realising the so called balanced spinal analgesia. The aim of this study is to analyse: the available methods for the evaluation of pharmacological interactions, the types of interaction between different spinal antinociceptive drugs and the role of balanced spinal analgesia in the treatment of cancer pain. Analysis of the presented data shows that the spinal synergism between opioids-local anesthetics and opioids-alpha 2-agonists can be useful in the treatment of opioid refractory cancer pain. Furthermore, the use of cholinergic drugs combined with opioids and alpha 2-agonists may be promising. Finally, even if the synergism between NSAID or NMDA antagonists with opioids or alpha 2-agonists have been proved, at the moment their use in man by the spinal route is not advisable because of the absence of adequate studies on their neurotoxicity and adverse effects.
 ...
PMID:[Balanced spinal analgesia in the treatment of oncologic pain. Review of the literature]. 910 86

Although analgetic treatment, based on modifications of the three-step approach recommended by the WHO, remains the cornerstone of cancer pain control, other treatment options are also needed to improve pain relief in severe cases. The article consists in a discussion of such treatment alternatives, a guiding principle being that, where causal treatment is possible, symptomatic effects are likely to be more manifest and more enduring than if treatment is confined to symptom management. The tumour biological basis of the analgesic or anti-inflammatory potential of steroids, palliative radiotherapy, bisphosphonates, and even such modalities as hormonal manipulation in metastatic prostate cancer, or chemotherapy are also discussed, as are calcitonin and stabilising orthopaedic measures.
 ...
PMID:[Cancer-related pain requires targeted treatment. Analgesics are not the only therapeutic alternative]. 1002 19

The aim of this investigation was to determine whether murine models of inflammatory, neuropathic and cancer pain are each characterized by a unique set of neurochemical changes in the spinal cord and sensory neurons. All models were generated in C3H/HeJ mice and hyperalgesia and allodynia behaviorally characterized. A variety of neurochemical markers that have been implicated in the generation and maintenance of chronic pain were then examined in spinal cord and primary afferent neurons.Three days after injection of complete Freund's adjuvant into the hindpaw (a model of persistent inflammatory pain) increases in substance P, calcitonin gene-related peptide, protein kinase C gamma, and substance P receptor were observed in the spinal cord. Following sciatic nerve transection or L5 spinal nerve ligation (a model of persistent neuropathic pain) significant decreases in substance P and calcitonin gene-related peptide and increases in galanin and neuropeptide Y were observed in both primary afferent neurons and the spinal cord. In contrast, in a model of cancer pain induced by injection of osteolytic sarcoma cells into the femur, there were no detectable changes in any of these markers in either primary afferent neurons or the spinal cord. However, in this cancer-pain model, changes including massive astrocyte hypertrophy without neuronal loss, increase in the neuronal expression of c-Fos, and increase in the number of dynorphin-immunoreactive neurons were observed in the spinal cord, ipsilateral to the limb with cancer. These results indicate that a unique set of neurochemical changes occur with inflammatory, neuropathic and cancer pain in C3H/HeJ mice and further suggest that cancer induces a unique persistent pain state. Determining whether these neurochemical changes are involved in the generation and maintenance of each type of persistent pain may provide insight into the mechanisms that underlie each of these pain states.
 ...
PMID:Murine models of inflammatory, neuropathic and cancer pain each generates a unique set of neurochemical changes in the spinal cord and sensory neurons. 1086 52

Adjuvant analgesics are defined as drugs with a primary indication other than pain that have analgesic properties in some painful conditions. The group includes numerous drugs in diverse classes. Although the widespread use of these drugs as first-line agents in chronic nonmalignant pain syndromes suggests that the term "adjuvant" is a misnomer, they usually are combined with a less-than-satisfactory opioid regimen when administered for cancer pain. Some adjuvant analgesics are useful in several painful conditions and are described as multipurpose adjuvant analgesics (antidepressants, corticosteroids, alpha(2)-adrenergic agonists, neuroleptics), whereas others are specific for neuropathic pain (anticonvulsants, local anesthetics, N-methyl-D-aspartate receptor antagonists), bone pain (calcitonin, bisphosphonates, radiopharmaceuticals), musculoskeletal pain (muscle relaxants), or pain from bowel obstruction (octreotide, anticholinergics). This article reviews the evidence supporting the use of each class of adjuvant analgesic for the treatment of pain in cancer patients and provides a comprehensive outline of dosing recommendations, side effects, and drug interactions.
 ...
PMID:Adjuvant analgesics in cancer pain management. 1547 43

We investigated some neurochemical changes that take place in the spinal cord dorsal horn in a mouse model of neuropathic cancer pain. The model was produced by inoculation of Meth-A sarcoma cells to the vicinity of the sciatic nerve, which resulted in growth of a tumor mass embedding the nerve. Hind paw-lifting, a behavioral sign of spontaneous pain, was at maximum on Day 18, but decreased thereafter. The decrease was likely caused by progression of motor paralysis. On Day 18, thermal and mechanical pain thresholds of the affected paw were significantly increased. Histologically, the sciatic nerve presented damages to both unmyelinated and myelinated fibers on Day 18, which were more pronounced on Day 25. In the spinal cord, c-Fos-positive cells were significantly increased in the superficial and deep layers on Day 18. The number of c-Fos-positive cells in the superficial layer correlated with the duration of paw-lifting. The increase in c-Fos-positive cells was still present on Day 25 despite decreased paw-lifting. Substance P and calcitonin gene-related peptide were up-regulated on Day 18 but down-regulated on Day 25. A marked up-regulation of dynorphin A (DynA) was present on Day 18 and persisted through Day 25. Our model caused progressive damage to the sciatic nerve and presented spontaneous pain-behavior while the paw became hyposensitive to mechanical and thermal stimuli. Since the up-regulation of DynA in the dorsal horn persisted and paralleled the increase in c-Fos-positive cells, the release of DynA may be associated with spontaneous pain in our model.
 ...
PMID:Change of dorsal horn neurochemistry in a mouse model of neuropathic cancer pain. 1573 48

Functional and anatomical relationships among primary afferent fibers, blood vessels, and cancers are poorly understood. However, recent evidence suggests that physical and biochemical interactions between these peripheral components are important to both tumor biology and cancer-associated pain. To determine the role of these peripheral components in a mouse model of cancer pain, we quantified the change in nerve and blood vessel density within a fibrosarcoma tumor mass using stereological analysis of serial confocal optical sections of immunostained hind paw. To this end we introduced the Discoma coral-derived red fluorescent protein (DsRed2) into the NCTC 2472 fibrosarcoma line using the Sleeping Beauty transposon methodology, thus providing a unique opportunity to visualize tumor-nerve-vessel associations in context with behavioral assessment of tumor-associated hyperalgesia. Tumors from hyperalgesic mice are more densely innervated with calcitonin gene related peptide (CGRP)-immunoreactive nerve fibers and less densely vascularized than tumors from non-hyperalgesic mice. As hyperalgesia increased from Day 5 to 12 post-implantation, the density of protein gene product 9.5 (PGP9.5)-immunoreactive nerves and CD31-immunoreactive blood vessels in tumors decreased, whereas CGRP-immunoreactive nerve density remained unchanged. Importantly, intra-tumor injection of a CGRP1 receptor antagonist (CGRP 8-37) partially blocked the tumor-associated mechanical hyperalgesia, indicating that local production of CGRP may contribute to tumor-induced nociception through a receptor-mediated process. The results describe for the first time the interaction among sensory nerves, blood vessels and tumor cells in otherwise healthy tissue, and our assessment supports the hypothesis that direct tumor cell-axon communication may underlie, at least in part, the occurrence of cancer pain.
 ...
PMID:Tumor-induced mechanical hyperalgesia involves CGRP receptors and altered innervation and vascularization of DsRed2 fluorescent hindpaw tumors. 1583 73

There is no uniform etiology of cancer pain. It is essential to understand the pathogenesis of pain as far as possible before a therapeutic modality can be conceived. The anatomical relation of the painproducing lesion to the site of pain perception should be clear (local, projected and referred pain). The origin of cancer-induced pain is classified as follows: malignant, mostly metastatic bone lesions, compression and infiltration of peripheral nerval structures, expansion in limited spaces, distension of liver, obstruction of blood vessels, obstruction and distension of the intestine, other abdominal or thoracic processes that produce visceral pain, infiltration and ulceration of soft tissue in sensitive areas. There are also pain syndromes caused by cancer therapy: post-operative, post-radiation and post-chemotherapy pain. Attention is drawn to the difficulties of pain recording and pain measurement. Psychological and social aspects of cancer patients emphasize the importance of a sufficient pain therapy which is divided into non-drug therapy and drug therapy. Various specialities can contribute therapeutic modalities for the treatment of cancer pain. Surgery, orthopedics, neurosurgery, radiotherapy and others have their specific methods. Anesthesiological methods are mentioned in more detail. The celiac plexus block with alcohol as a simple, safe and efficious procedure should become available to any patient with upper abdominal visceral tumor pain. Attention is drawn to the hospice movement, which is more or less unknown in central Europe. Psychological aspects of cancer patient care are considered. Drug therapy is of greater importance than all other methods. That is the domain of the general practitioner. Commonly used analgesic antipyretics and NSAIDs are listed in Table 1. The principles of opioid therapy follow. Due consideration is given to neuroleptics and antidepressive drugs. Information about hormones (corticosteroids, calcitonin a. o.) in cancer pain therapy conclude this survey. Enormous differences of morphine use (Austria: 0.66 kg vs Denmark 16.59 kg per million people per year) indicate that there is a great demand for further professional education in this field.
 ...
PMID:[Cancer pain.]. 1841 90

Nociceptive stimuli are modulated at the dorsal horn of the spinal cord. This modulation is performed by various systems working independently complementarily, additively or supra-additively. Non-opioid analgesics relieve pain without a motor blockade. In contrast to spinal opioids a reduced risk of respiratory depression is expected. In the therapy of chronic pain non-opioid analgesics may be an alternative, given alone or in combination with an opioid. Clinically relevant dosages for antinociception mediated by the alphaadrenoceptoragonistclonidine are >/=150 mug epidurally. Clonidine is effective in reducing acute and chronic pain. In combination with opioids the action of the opioids is intensified. Clonidine intensifies and prolongs the action of local anesthetics. If opioid tolerance occurs, epidural clonidine alone or in combination with an opioid has good antinociceptive action.Midazolam, a water-soluble benzodiazepine, was injected spinally for the reduction of pain for various indications (postoperative, malignancy, chronic back pain, spinal spasticity). Spinal benzodiazepine should not be injected into the spine in patients until it has been proven that there are no neurotoxic effects. Intrathecally injectedbaclofen is a well-known means of reducing spinal spasticity. Used in this way, it may have a secondary analgesic effect. No significant direct analgesic effect has so far been demonstrated. Spinalcalcitonin often leads to insufficient pain relief when given alone. Combination with an opioid may reduce the dosage of the opioid. Nausea and vomiting are frequent side effects of spinal calcitonin. Intrathecalsomatostatin produces antinociception. However, in animal studies neurotoxic action has been observed. Administration in man has not yet been proved to be safe. Spinalketamine has procluted controversial results in clinical studies, and has not yet been excluded that the substance is not neurotoxic.Lysine acetylsalicylic acid (L-ASA) has been given intrathecally for the therapy of severe cancer pain and chronic back pain. In most patients good analgesia was observed up to 2 months after a single injection. If neurotoxity can be excluded, L-ASA may be an alternative in the therapy of cancer pain before neurodestructive therapy is done.
 ...
PMID:[Intrathecal and epidural administration of non-opioid analgesics in acute and chronic pain treatment.]. 1841 40


1 2 Next >>