Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of cancer pain, the incidence of pain associated with specific types of malignant tumors, and the nature of acute and chronic pain are discussed, and alternative delivery systems for pain management are described. More than 80% of cancer patients with advanced metastatic disease suffer moderate to severe pain. Most cancer pain is caused by direct tumor infiltration; approximately 20% of cancer pain may be attributed to the effects of surgery, radio-therapy, or chemotherapy. The incidence of cancer pain is related to tumor type; 70% or more of patients with tumors of the bone, cervix, and ovaries suffer cancer-related pain, while only 5% of patients with leukemia have pain. Pain is defined by the organs involved. Somatic pain is usually dull and well localized; visceral pain is generalized and difficult to describe. Other types of pain, including deafferentation pain and referred pain, are particularly difficult to manage. Cancer pain may be acute or chronic. The latter may cause psychological reactions that make effective treatment more challenging. Opiate analgesic agents, administered by the epidural or intrathecal routes, block pain more selectively and produce fewer adverse reactions than systemic analgesic agents. The duration and onset of analgesia depend on the lipophilicity of the agent used. Because pain is the most common complaint of the patient with cancer, clinicians should be aware of the range of pharmacologic and nonpharmacologic analgesic modalities available to them. Familiarity with newer modalities and delivery routes, such as spinal administration of opiate analgesics, is recommended.
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PMID:Understanding cancer pain. 220 10

Pain treatment for 17 pediatric cancer patients in our institution was evaluated and disirable cancer pain management for children was discussed. Most of the patients (aged 1-17 years) suffering severe pain for about one month were in the advanced stage of the malignant diseases (e.g. leukemia). The pain etiology was mostly tumor-associated while therapy-related pain accounted for 23.5%. These pains were treated with NSAIDs or pentazocine before the consultation with inadequate relief. Oral morphine sulfate or continuous intravenous morphine chloride was administered to 16 patients with successful pain relief and side effects such as nausea (52.9%) and drowsiness (41.2%). It took 5.5 days on average until adequate pain control methods were determined. It is known that most NSAIDs frequently used for pediatric pain possibly cause adverse effects such as platelet dysfunction or mucous membrane injury with a suppository, which could lead to a fatal disorder in clinically ill pediatric cancer patients. Moreover sufficient doses for the pain relief are not necessarily given to the pediatric patients because of a limit to the dosage of NSAIDs. The period of pediatric cancer pain in which the patient require a methodical treatment and receive benefit from pain relief is relatively short in the advanced stage, not to mention the early stage in which chemotherapy is efficacious against cancer disease itself. Therefore, to obtain effective pain control within a short time, the authors propose the pain management for advanced pediatric cancer patients by the two-step analgesic ladder prescribing weak or strong opioid analgesics first, adapted from the three-step ladder of the WHO Cancer Pain Relief, 1986.
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PMID:[Pain management in advanced pediatric cancer patients--a proposal of the two-step analgesic ladder]. 754 19

Accepted wisdom contends that sympathetically maintained pain is rare in cancer pain syndromes. But this may be more of an artifact of how we diagnose this condition than a reflection of its true prevalence. One area in which one might suspect this to be true is in postsurgical states. While there are case reports of sympathetically maintained pain occurring after radical neck dissection, orbital and maxillary exenteration, it has not been reported in the more common areas of postsurgical pain. For instance, although one should suspect that the nerve damage that accompanies post-thoracotomy and postmastectomy pain syndromes would bring into being a certain incidence of sympathetically maintained pain, it is difficult to find collaborative reports. This may have more to do with the difficulty inherent in diagnosing sympathetically maintained pain than its actual contribution to these persistent cancer pain syndromes. The reason that it is more commonly reported in limb amputation is less comprehensible since blocking the sympathetic fibers that travel to an extremity is easier than those going to the thoracic cavity. In addition to surgically induced sympathetically maintained pain, medical patients with lymphoma and leukemia may have an element of sympathetically maintained pain when they develop postherpetic neuralgia. While the contribution of sympathetically maintained pain in these cases is not totally ignored, its involvement, as in the surgical patients mentioned above, is worthy of another analysis. This paper will discuss the topics introduced above and suggest diagnostic and therapeutic options available for this condition.
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PMID:A review of sympathetically maintained pain syndromes in the cancer pain population: the spectrum of ambiguous entities of RSD, CRPS, SMP and other pain states related to the sympathetic nervous system. 1714 72

Imatinib, a selective tyrosine kinase inhibitor, is the first line treatment against chronic myelogenous leukaemia (CML) and gastrointestinal stromal tumors (GIST). Several fatal cases have been associated with imatinib hepatotoxicity. Acetaminophen, an over-the-counter analgesic, anti-pyretic drug, which can cause hepatotoxicity, is commonly used in cancer pain management. We assessed renal and hepatic toxicity after imatinib and acetaminophen co-administration in a preclinical model. Four groups of male ICR mice (30-35 g) were fasted overnight and administered either saline solution orally (baseline control), imatinib 100 mg/kg orally (control), acetaminophen 700 mg/kg intraperitoneally (positive control) or co-administered imatinib 100 mg/kg orally and acetaminophen 700 mg/kg intraperitoneally (study group), and sacrificed at 15 min, 30 min, 1 h, 2 h, 4 h and 6 h post-administration (n = 4 per time point). The liver and kidneys were harvested for histopathology assessment. The liver showed reversible cell damage like feathery degeneration, microvesicular fatty change, sinusoidal congestion and pyknosis, when imatinib or acetaminophen were administered separately. The damage increased gradually with time, peaked at 2 h but resolved by 4 h. When both drugs were administered concurrently, the liver showed irreversible damage (cytolysis, karyolysis and karyorrhexis) which did not resolve by 6 h. Very minor renal changes were observed. Acetaminophen and imatinib co-administration increased hepatoxicity which become irreversible, probably due to shared P450 biotransformation pathways and transporters in the liver.
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PMID:Histopathological study of the hepatic and renal toxicity associated with the co-administration of imatinib and acetaminophen in a preclinical mouse model. 2061 20