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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this article is to review the causes, the clinical manifestations and the management of the more frequent drug-induced rheumatic disorders. These include: (i) articular and periarticular manifestations induced by fluoroquinolones, nonsteroidal anti-inflammatory drugs, injections of corticosteroids, and retinoids; (ii) multisystemic manifestations such as drug-induced lupus and arthritis induced by vaccination, Bacillus Calmette-Guerin therapy and cytokines; (iii) drug-induced disorders of bone metabolism (corticosteroid-induced osteoporosis, drug-induced osteomalacia and osteonecrosis); and (iv) iatrogenic complex regional pain syndromes. Disorders caused by nonpharmacological and rarely used treatments have been deliberately excluded. Knowledge of these drug-induced clinical symptoms or syndromes allows an earlier diagnosis and treatment, and earlier drug withdrawal if necessary. With the introduction of new medications such as the recombinant cytokines and antiretroviral treatments, the number of drug-induced rheumatic disorders is likely to increase.
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PMID:Drug-induced rheumatic disorders: incidence, prevention and management. 1105 Dec 16

Alosetron (Lotronex) is a potent, highly selective 5-HT(3) antagonist. Animal models have shown it to be active in anxiety, psychosis, cognitive impairment, emesis and drug withdrawal, though its application in humans has been almost entirely restricted to irritable bowel syndrome (IBS). Alosetron does not cause adverse pharmacodynamic effects, is absorbed rapidly after oral administration and is widely distributed throughout tissues after oral or iv. dosing in animals. Its metabolism is rapid and extensive with N-demethylation, hydroxylation and oxidation. The drug, or its two principal metabolites, is equally excreted through the biliary tract and kidneys. Alosetron has proved safe in a range of toxicity studies; at high repeated dosing, clinical signs were transient and repeated administration produced no significant adverse effects on fertility, reproductive performance or fetal development. In pharmacokinetic studies, bioavailability of alosetron in healthy volunteers is approximately 60% and the plasma half-life is about 1.5 h. There are some gender differences in the pharmacokinetic profile, with 30 - 50% higher alosetron concentrations in females. No consistent differences in alosetron serum concentrations between the young and elderly were observed. The pharmacokinetics of single, oral doses of alosetron are linear up to 8 mg. In human pharmacodynamic studies, alosetron increased basal jejunal water and electrolyte absorption, increased colonic transit time and, consequently, whole gut transit time. Alosetron has been evaluated in two large Phase II trials (randomised, double-blinded, placebo-controlled) and in Phase III trials which included a four-week observation period after cessation. Dose response studies suggested that the effective dosages could be between 1 and 2 mg, twice-daily. In Phase II trials, alosetron, 1 mg b.i.d., resulted in a greater proportion of non-constipated IBS patients reporting adequate relief of pain and discomfort, as well as improvement of bowel symptoms, frequency, urgency and stool consistency when compared with placebo. However, this beneficial effect was seen exclusively among females. Phase III studies evaluated exclusively females with non-constipated IBS and confirmed the results of the Phase II studies. Alosetron was well-tolerated in all studies, with the most frequently recorded adverse event being constipation. Thus, alosetron appears promising in the treatment of abdominal pain and discomfort and normalising of bowel function in patients with non-constipated IBS. It also improves quality of life, has a high degree of tolerability and has an excellent safety profile to date.
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PMID:Pharmacology and clinical experience with alosetron. 1106 Jun 67

The goals of osteoarthritis therapy are to decrease pain and to maintain or improve joint function. The pharmacologic treatment of this condition has included the use of aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs. More recently, numerous studies have investigated the potential role of chondroprotective agents in repairing articular cartilage and decelerating the degenerative process. The reports of limited clinical experience with two of these agents, glucosamine and chondroitin sulfate, as well as the accompanying publicity in the popular media, have generated controversy. Advocates of these alternative modalities cite reports of progressive and gradual decline of joint pain and tenderness, improved mobility, sustained improvement after drug withdrawal, and a lack of significant toxicity associated with short-term use of these agents. Critics point out that in the great majority of the relevant clinical trials, sample sizes were small and follow-up was short-term.
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PMID:Use of glucosamine and chondroitin sulfate in the management of osteoarthritis. 1159 24

The frequent use (> 15 times/month) of medication for the treatment of acute migraine attacks may cause medication overuse headache. This kind of headache can be caused by the intake of combination analgesics, opioids, ergot alkaloids, and triptans. The delay between first intake and daily headache is shortest for triptans (1 to 2 years), longer for ergots (3 years), and longest for analgesics (5 years). Treatment includes drug withdrawal followed by structured acute therapy and initiation of migraine prophylactic treatment.
Curr Pain Headache Rep 2001 Dec
PMID:Analgesic/abortive overuse and misuse in chronic daily headache. 1167 89

This paper represents a review, by experts, of current opinion and information on intermittent claudication (IC) and the role that cilostazol plays in its treatment. IC is a common and debilitating condition that has a significant adverse impact on health-related quality of life (HR-QoL). It is currently under-recognised as a powerful marker of increased cardiovascular (CV) risk. The clinical priority is secondary prevention -- sometimes referred to as best medical therapy aimed at reducing CV risk. However, the priority for most patients (often overlooked by clinicians) is symptom relief: an increase in walking distance leading to an improvement in HR-QoL. The symptoms of IC may be improved by exercise, pharmacotherapy, and when these are unsuitable or unsuccessful, endovascular or surgical intervention. Cilostazol is indicated for the improvement of maximal and pain-free walking distance in patients with IC who do not have rest pain or tissue necrosis. In clinical trials, cilostazol improved symptoms both objectively and subjectively, and also improved HR-QoL. Cilostazol is usually well tolerated, with adverse events being generally mild to moderate in intensity, and transient or resolved after symptomatic treatment (e.g. non-prescription analgesics). Such events only infrequently require permanent drug withdrawal. There are no interactions with other drugs commonly prescribed in patients with IC, such as statins and anti-platelet agents. Cilostazol also has a range of potentially beneficial effects that may in the future be proven to decrease CV risk and modify the underlying process of atherosclerosis. Cilostazol represents the best evidence-based pharmacological therapy available for the symptoms of IC and should be the first-line treatment for symptom improvement in appropriate patients. Based on the available treatment strategies, the paper presents a suggested algorithm for the management of IC highlighting the role of cilostazol.
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PMID:The role of cilostazol in the treatment of intermittent claudication. 1546

Several 5-HT3 receptor antagonists are available (tropisetron, ondansetron, granisetron, dolasetron, and palonsetron), and further compounds are in clinical development. These substances show only minor differences in the activity profile regarding their affinity for particular receptors. 5-HT3 receptor antagonists are primarily used and found effective in the prevention and treatment of chemotherapy-induced nausea and emesis, and in postoperative nausea and vomiting (PONV). Antagonism of the 5-HT3 receptors in the peripheral and central nervous system is a probable mechanism of action. The substances are suitable as first-line therapy (combined with a corticosteroid) for the prevention of acute nausea and vomiting in patients treated with moderately to severely emetogenic chemotherapeutic agents. This combination is also moderately effective in the prevention of delayed nausea and vomiting. 5-HT3 receptor antagonists are an important constituent in the prevention and treatment of emesis and nausea caused by radiation therapy, especially in patients receiving whole body or upper abdominal treatment. Alosetron was found clinically effective in diarrhoea-predominant irritable bowel syndrome, whereas tropisetron in fibromyalgia and related pain disorders. Further indications for such treatment include anxiety disorders, alcohol dependence, drug withdrawal, and psychosis related to treatment of Parkinson's disease. 5-HT3 receptor antagonists are well tolerated with the most frequently reported adverse effects being headache, constipation, dizziness, tiredness, and gastrointestinal disturbances such as abdominal pain or constipation. Intravenous administration of serotonin induces the Bezold-Jarisch reflex and causes small reversible changes in electrocardiogram (ECG) parameters.
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PMID:Spectrum of use and tolerability of 5-HT3 receptor antagonists. 1551 6

Inappropriate use of headache medication (>15 times/month) for the treatment of headache episodes may contribute to the development of chronic headache which is refractory to most treatments. Physicians experienced in the treatment of migraine and other headaches are well aware that the daily intake of antipyretic or antiinflammatory analgesics, opioids, ergot alkaloids and "triptans" may result in chronic daily headache. Conversely, if a patient complains of chronic headache and takes pain medication every day, this headache is most likely to be caused and sustained by the medication and will vanish or improve with abstinence. Treatment includes drug withdrawal followed by structured acute therapy and initiation of migraine prophylactic treatment.
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PMID:Clinical features and therapy of medication overuse headache. 1568 4

Sulfamethoxazole-trimethoprim (cotrimoxazole) is an antibiotic combination widely used for infections treatment and prophylaxis. These and others sulfonamides have been implicated in a rare syndrome of choroidal effusion with transient myopia and angle-closure glaucoma. Previous cases reported in literature evolved to complete resolution after drug withdrawal. In contrast, we describe a rare case in which a patient developed the syndrome while taking cotrimoxazole, but did not recover visual acuity. A 49-year-old man started Pneumocystis carini prophylaxis with cotrimoxazole; four days later, the patient presented severe ocular pain, hyperemia and chemosis. Intraocular pressure reached more than 50 mmHg in both eyes a 360 degrees choroidal effusion occurred. Medication was removed soon after the diagnosis was suspected and intraocular pressure decreased in four days. Even so total cataract and phthisis bulbi occurred in both eyes two months later. This would be the first case in the literature in which the outcome was unfavorable despite early diagnosis and withdrawal of the drug.
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PMID:[Bilateral angle-closure glaucoma induced by trimetoprim and sulfamethoxazole combination: case report]. 1776 63

We investigated the effect of chronic administration of different pain medications on the activity of the serotonin transporter (SERT) in patients with medication overuse headache (MOH). We measured the kinetic of platelet 5-HT uptake (maximal velocity, Vmax and the Michaelis-Menten constant, Km in patients with overuse of triptans (tMOH, n = 15) or analgesics (aMOH, n = 14) before and after drug withdrawal, as well as in headache-free healthy subjects (n = 15) and patients with episodic migraine (EM, n = 16). Vmax was increased similarly in both, tMOH and aMOH compared to healthy subjects and patients with EM and normalized after withdrawal in parallel to the improvement of headache frequency. Average Km was similar in all groups at baseline and not affected by the withdrawal. The data demonstrate a transient increase of SERT activity in patients with analgesic and triptan induced MOH but do not allow to differentiate whether the increase of serotonin uptake is caused by regular intake of analgesics or triptans or is a consequence of frequent headache attacks.
J Headache Pain 2008 Apr
PMID:Increased activity of serotonin uptake in platelets in medication overuse headache following regular intake of analgesics and triptans. 1833 May 4

Acute pancreatitis (AP) is a rapidly onset inflammation of the pancreas. Clinical characteristics of AP are severe pain in the upper abdomen and at least a threefold elevation of pancreatic enzymes in the blood. Many conditions predispose to AP; the most common are gallstones and chronic alcohol abuse which account for 75% of acute pancreatitis in the United States. Medications are an infrequent but important and rising cause of acute pancreatitis and contribute about 2% of the cases. Over 100 drugs have been implicated as a cause for AP, mostly from case and anecdotal reports. Documentation of drug-induced pancreatitis (DIP) is more definite if other likely causes of pancreatitis are not present, if there is recovery after drug withdrawal, and if pancreatitis recurs with reintroduction of the drug. In addition, some medications reported to have caused AP have obvious patterns of presentation, including the time from initiation to the development of disease (latency). The authors describe two large reviews of the literature which have classified drugs that have been reported to cause AP based on the published weight of evidence for each agent and the pattern of clinical presentation. Among adverse drug reactions, pancreatitis is often ignored because of the difficulty in implicating a drug as its cause. The physician should have a high index of suspicion for DIP.
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PMID:[Drug-induced pancreatitis]. 1962 37


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