Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A multicenter, open labeled, randomized early Phase II study for CGS 20267 was conducted at the doses 0.5 mg once daily and 1.0 mg once daily in postmenopausal women with advanced breast cancer. Sixty-four patients were randomly assigned to the doses of either 0.5 mg once daily (n = 33) or 1.0 mg once daily (n = 31). Thirty-one patients were eligible for 0.5 mg group, and 29 for 1.0 mg group. A total of 57 patients (30 in the 0.5 mg group and 27 in the 1.0 mg group) were eligible for the evaluation of efficacy. There were 3 CR, 5 PR, 5 stable disease (SD: NC lasting over 24 weeks), 7 NC and 10 PD in the 0.5 mg group. The objective response rate (ORR) was 26.7%. There were 4 CR, 7 PR, 8 SD, 3 NC and 5 PD in the 1.0 mg group. The ORR was 40.7%. A total of 57 patients (29 in the 0.5 mg group and 28 in the 1.0 mg group) were eligible for safety evaluation. Adverse clinical events related to CGS 20267 in the 0.5 mg group were headache, nausea, cold sweat, sleepiness and muscle ache in the lower extremities (2 patients, incidence rate 6.9%) whereas those in the 1.0 mg group were generalized itching and generalized hot feeling (2 patients, incidence rate 7.1%). All of the adverse events were grade 1 except the generalized itching which was grade 2. CGS 20267-related abnormalities in the laboratory tests for the 0.5 mg group were a decrease in WBC, and increases in GOT, GPT, LDH and gamma-GTP (5 patients, 14.3%) whereas those in the 1.0 mg group were increases in GPT, gamma-GTP, alkaline phosphatase, and total bilirubin (1 patient, 3.6%). The increases in GOT and GPT were grade 2, but others were grade 1. The data show both CGS 20267 0.5 mg once daily and 1.0 mg once daily to be effective and tolerable in the treatment of postmenopausal women with advanced breast cancer.
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PMID:[CGS 20267 (Letrozole), a new aromatase inhibitor: early phase II study for postmenopausal women with advanced breast cancer]. 1197 39

Heart failure during the immediate period of an acute myocardial infarction constitutes a major insult to this pathology; since, once installed, it is associate to ventricular dysfunction and expansion of the left ventricle. It can appear either early or delayed. Subsequent to the acute insult, the myocardium is subjected to diverse changes in its anatomical conformation and to diastolic and systolic alterations, which will affect the hemodynamic constants of the patient. Changes in the parietal ventricular architecture as well as at the neurohumoral level will also occur. The clinical signs of heart failure are: dyspnea, pallor, tachycardia, diaphoresis, cold skin, oliguria, somnolence, and gallop, which can be observed at the very beginning of the coronary occlusion. Its clinical identification, through in-hospital studies supported by adequate hemodynamic monitoring, is of utter relevance since it will lead to appropriate and fast treatment. The groups of patients with acute myocardial infarction with high risk for the development of cardiac failure are: patients with extensive Q wave infarction, diabetic, patients over 65 years of age, and those with a history of previous myocardial infarction(s). The cornerstone of treatment must be focused on reducing the myocardial ischemia, which can be achieved through the use of modern therapeutics and, given the case, pharmacological agents, coronary intervention procedures, or cardiac surgery must be taken into account. At present it is known that angiotensin converting enzyme inhibitors, betablockers, inotropics, are useful to improve ventricular function in patients with acute myocardial infarction.
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PMID:[Heart failure in acute myocardial infarction]. 1200 71

Coricidin products seemed to be one of the over-the-counter medications being reportedly abused by adolescents, as observed from the Texas Poison Center Network data. This retrospective chart review investigated the occurrence of abuse, developed a patient profile, and defined the clinical effects resulting from the abuse of Coricidin products. Data collected from the Texas Poison Center Network Toxic Exposure Surveillance System database included human exposures between 1998 and 1999, patients > or = 10y old, intentional use or abuse, and single substance ingestion of I of the tablet formulations of Coricidin. Thirty-three cases from 1998 and 59 cases from 1999 were reviewed. Of these cases, 85% met the inclusion criteria. Of the 7 medications searched, only 4 substances were coded for: Coricidin D, Coricidin D (long acting), Coricidin D (cold, flu & sinus) and Coriciding HBP. These contain a combination of dextromethorphan hydrobromide, chlorpheniramine maleate, phenylpropanolamine hydrochloride, and acetaminophen. Of the 78 cases, 63% were male and 38% were female. The mean age was 14.67 years, 77% being between 13 to 17 years old. Eighteen different symptoms were reported: tachycardia 50%, somnolence 24.4%, mydriasis and hypertension 16.7%, agitation 12.8%, disorientation 10.3%, slurred speech 9%, ataxia 6.4%, vomiting 5.1%, dry mouth and hallucinations 3.9%, tremor 2.6%, and headache, dizziness, syncope, seizure, chest pain, and nystagmus each 1.3%; 12.8% of the calls originated from the school nurse. The incidence of abuse reported increased 60% from 1998 to 1999. This worrisome trend suggests increased abuse of these products.
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PMID:A possible trend suggesting increased abuse from Coricidin exposures reported to the Texas Poison Network: comparing 1998 to 1999. 1204 73

Old generation H1-type antihistamines are the standard therapeutic option for acquired cold urticaria (ACU), but adverse effects are common. New antihistamines are well tolerated but efficacy is often poor. The present study aims to evaluate efficacy and safety of cinnarizine in the treatment of ACU patients intolerant to old antihistamines and resistant to new drugs. We studied 14 patients (4 males and 10 females). Mean duration of the disease was 48.9 (range 7-102) months. Cold cube test was positive in 78.6 % of patients. Cold urticaria was idiopathic in 10 (71.4 %) patients. Cryoglobulins were detected in the serum of 4 cases (28.6 %). Cinnarizine (25 mg t.i.d.) was administered for 3 months, and then it was gently tapered off and stopped within 2 months. A complete or good response was obtained in 8 (57.1 %) and 2 (14.3 %) patients, respectively. Only two patients were unresponsive (21.4 %). Tapering off or stopping cinnarizine was followed by the relapse of cold urticaria in 7 cases (50.0 %). These patients were amenable to a second treatment cycle. Six patients (42.9 %) had a persistent remission. A patient interrupted the therapy because of severe vertigo. Three patients reported mild and transitory adverse effects including epigastralgia, weight gain and drowsiness. In conclusion, cinnarizine at high doses may be considered as an effective and well-tolerated treatment for ACU.
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PMID:Cinnarizine is a useful and well-tolerated drug in the treatment of acquired cold urticaria (ACU). 1260 83

We report a 25-year-old man presenting with high fever, dyspnoea and somnolence. The presence of severe diffuse interstitial pneumonia with extrapulmonary symptoms, such as myositis and subclinical haemolysis, strongly suggested an infection by Mycoplasma pneumoniae. This diagnosis was supported by high titres of cold agglutinins and a positive Coombs test, and directly confirmed by specific IgM serological tests. After initiation of the appropriate antimicrobial treatment mechanical ventilation could be avoided and the patient showed a slow but complete clinical recovery. This diagnosis should be considered in any febrile patient with hypoxaemia and diffuse interstitial pneumonia, and rapid initiation of appropriate antibiotic treatment seems to be crucial for a favourable outcome.
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PMID:Severe diffuse interstitial pneumonia due to Mycoplasma pneumoniae in a patient with respiratory insufficiency. 1276 31

From folk medicine and anecdotal reports it is known that Cannabis may reduce pain. In animal studies it has been shown that delta-9-tetrahydrocannabinol (THC) has antinociceptive effects or potentiates the antinociceptive effect of morphine. The aim of this study was to measure the analgesic effect of THC, morphine, and a THC-morphine combination (THC-morphine) in humans using experimental pain models. THC (20 mg), morphine (30 mg), THC-morphine (20 mg THC+30 mg morphine), or placebo were given orally and as single doses. Twelve healthy volunteers were included in the randomized, placebo-controlled, double-blinded, crossover study. The experimental pain tests (order randomized) were heat, cold, pressure, single and repeated transcutaneous electrical stimulation. Additionally, reaction time, side-effects (visual analog scales), and vital functions were monitored. For the pharmacokinetic profiling, blood samples were collected. THC did not significantly reduce pain. In the cold and heat tests it even produced hyperalgesia, which was completely neutralized by THC-morphine. A slight additive analgesic effect could be observed for THC-morphine in the electrical stimulation test. No analgesic effect resulted in the pressure and heat test, neither with THC nor THC-morphine. Psychotropic and somatic side-effects (sleepiness, euphoria, anxiety, confusion, nausea, dizziness, etc.) were common, but usually mild.
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PMID:The analgesic effect of oral delta-9-tetrahydrocannabinol (THC), morphine, and a THC-morphine combination in healthy subjects under experimental pain conditions. 1449 23

The purpose of this research trial is to assess the effectiveness and tolerability of tizanidine in neuropathic pain. In an open-label study, patients with neuropathic pain received 1 to 4 mg of tizanidine once daily for 7 days, followed by weekly dose escalation of 2 to 8 mg to his/her effective or maximum tolerated dose or a maximum of 36 mg over an 8-week period. Treatment effects were assessed, using average weekly pain scores as well as biweekly scores for patient global assessment of pain relief, the neuropathic pain scale, and wisconsin brief pain inventory. Frequency and severity of adverse events were examined also. Twenty-three patients were enrolled. The mean average weekly pain score at baseline was 6.9, which decreased by 1.7 points at the end of week 8 to 5.2 (p < or =.01). A total of 15 patients (68%) reported that their pain relief was improved or much improved with tizanidine therapy, and 2 of these patients became completely pain-free. The following neuropathic pain qualities were significantly lower at week 8 compared with baseline: intense, sharp, hot, dull, cold, sensitive, unpleasant, and deep pain. There was a significant decline in pain quantity and interference of pain on quality of life from baseline to week 8. The mean effective or maximum tolerated dose was 23 mg/day (range 6 to 36 mg/day). Side effects consisted primarily of dizziness/lightheadedness (52%), drowsiness (48%), fatigue/weakness (43%), dry mouth (39%), gastrointestinal upset (30%), and sleep difficulty (22%). One patient developed significant elevation in liver function tests (LFTS) With symptoms at week 4. Tizanidine therapy was discontinued. LFTS returned to normal in 3 weeks. Tizanidine might be an effective treatment for neuropathic pain, offering an alternative for patients poorly responsive to other medications. A larger, randomized placebo-controlled trial is recommended. In addition, comparative studies with alternative agents should be sought.
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PMID:Effectiveness of tizanidine in neuropathic pain: an open-label study. 1462 12

This review discusses the safety and tolerability of levetiracetam, as presented by the available literature, with attention paid to special populations. In Phase II/III trials, the adverse effects occurring more commonly in the treatment groups versus the placebo group were; somnolence (14.8 versus 8.4%), asthenia (14.7 versus 9.1%), infection (primarily common cold) (13.4 versus 7.5%), and dizziness (8.8 versus 4.1%). Adverse events usually appear within the first month after treatment initiation, are not dose-dependent, are mostly mild-to-moderate, generally resolve without medication withdrawal, and are transient when the medication is stopped. No significant changes in haematology and chemistry profiles or weight occurred. Hypersensitivity reactions were rare and no idiosyncratic event has been reported. Open-label studies have added patient data with other epileptic syndromes and from a wider patient pool, such as children and patients with prior psychiatric history. These studies have supported initial safety findings, but have reported increased behavioural adverse events in children and patients with a history of prior behavioural problems. Levetiracetam is proving to be safe and well-tolerated. So far, it appears to have a favourable safety profile in special populations, such as children, the elderly, and patients with hepatic dysfunction. Preliminary data in pregnancy are promising, but more data are needed on the impact of levetiracetam on the developing fetus and pharmacokinetic alterations caused in pregnancy. Adjustments in dosing are required for decreases in renal clearance.
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PMID:Levetiracetam safety profiles and tolerability in epilepsy patients. 1533 97

Gamma-hydroxybutyrate (GHB) is encountered in biological specimens as an endogenous neuromodulator, recreational drug, or therapeutic agent. Clinically, the drug is useful for the treatment of cataplexy. Illicit doses are typically 2-4 g, and the onset of action is rapid, occurring 15-30 min following oral ingestion. Dose-dependent effects include drowsiness, euphoria, dizziness, vomiting, respiratory depression, coma, and death. GHB was isolated from biological samples using a simple liquid-liquid extraction. The trimethylsilyl derivative (GHB-di-TMS) was analyzed using gas chromatography-mass spectrometry with positive chemical ionization. Deuterated internal standard and selective ion monitoring were used throughout. We report a GHB fatality involving a 35-year-old male who was partying with friends. Subjects at the party ingested unknown quantities of wine and GHB. A female companion at the party reported seeing the male alive before she herself passed out. She awoke to find the decedent cold and stiff. Postmortem specimens were submitted for comprehensive toxicology testing. No alcohol or common drugs of abuse were detected. A targeted analysis revealed GHB in urine, brain, vitreous fluid, femoral blood, heart blood, and liver at concentrations of 1665 mg/L, 102 mg/kg, 48 mg/L, 461 mg/L, 276 mg/L, and 52 mg/kg, respectively. Concentrations of the drug in urine and vitreous fluid are important in death investigations because of significant postmortem production of GHB in blood specimens. The cause of death was attributed to GHB intoxication, and the manner of death was accidental.
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PMID:Distribution of GHB in tissues and fluids following a fatal overdose. 1610 69

Thermoregulatory processes have long been implicated in the initiation of human sleep. In this paper, we review our own studies conducted over the last decade showing a crucial role for melatonin as a mediator between the thermoregulatory and arousal system in humans. Distal heat loss, via increased skin temperature, seems to be intimately coupled with increased sleepiness and sleep induction. Exogenous melatonin administration during the day when melatonin is essentially absent mimics the endogenous thermophysiological processes occurring in the evening and induces sleepiness. Using a cold thermic challenge test, it was shown that melatonin-induced sleepiness occurs in parallel with reduction in the thermoregulatory set-point (threshold); thus, melatonin may act as a circadian modulator of the thermoregulatory set-point. In addition, an orthostatic challenge can partially block the melatonin-induced effects, suggesting an important role of the sympathetic nervous system as a link between the thermoregulatory and arousal systems. A topographical analysis of finger skin temperature with infrared thermometry revealed that the most distal parts of the fingers, i.e., fingertips, represent the important skin regions for heat loss regulation, most probably via opening the arteriovenous anastomoses, and this is clearly potentiated by melatonin. Taken together, melatonin is involved in the fine-tuning of vascular tone in selective vascular beds, as circulating melatonin levels rise and fall throughout the night. Besides the role of melatonin as "nature's soporific", it can also serve as nature's nocturnal vascular modulator.
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PMID:Thermoregulatory effects of melatonin in relation to sleepiness. 1668 20


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