Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review analyses the therapeutic usefulness of Delta(9)-tetrahydrocannabinol and its potential to induce adverse reactions on humans. During the last 30 years an enormous amount of research was carried out resulting in the disclosure of the cannabinoid system in Central Nervous System, with its CB(1) and CB(2) receptors, and the agonist anandamide. Under the clinical point of view, Delta(9)-THC produces some therapeutic benefits which are beyond reasonable doubt. Thus, the effects on nausea/emesis due to cancer chemotherapy, as appetite promoter, on some painful conditions and on symptoms of multiple sclerosis are clearly demonstrated. Delta(9)-THC is not devoid of ill effects. On the cognitive domain it impairs the human capacity to discriminate time intervals and space distances, vigilance, memory and the performance for mental work. On the psychic area Delta(9)-THC may induce unpleasant reactions such as disconnected thoughts, panic reactions, disturbing changes in perception, delusions and hallucinatory experiences. However, the long term effects on the psyche and cognition are not known as there are no reports of prolonged use of Delta(9)-THC. Actually, it has been proposed by WHO that Delta(9)-THC should be rescheduled to schedule IV of the United Nations Convention on Psychotropic Drugs, as it does not constitute a substantial risk to public health and its abuse is rare if at all.
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PMID:The good and the bad effects of (-) trans-delta-9-tetrahydrocannabinol (Delta 9-THC) on humans. 1599 Jan 41

Several disease-modifying agents (DMAs) are approved for the treatment of multiple sclerosis, including three interferon (IFN)-beta products, glatiramer acetate and mitoxantrone. This article reviews the adverse event profiles of these DMAs based on the pivotal phase III trials, and provides practical guidelines for managing adverse effects. In general, the most common adverse events associated with IFN beta therapy are flu-like symptoms, including fever, chills and myalgias, and headache. The flu-like symptoms typically resolve within 24 hours and may be mitigated by over-the-counter anti-inflammatory agents. Adverse events related to glatiramer acetate therapy include injection-site reactions and a systemic reaction consisting of flushing, chest tightness, palpitation, anxiety or dyspnoea. The systemic reaction is transient (30 seconds to 30 minutes) and self-limited. Mitoxantrone may cause nausea, vomiting, alopecia, amenorrhoea and myelosuppression; isolated cases of acute leukaemia and dose-related cardiotoxicity have been reported in the literature. Longer-term tolerability data on mitoxantrone as a treatment for multiple sclerosis are needed. It is important for physicians to counsel patients on DMA-related adverse effects, most of which are transient and of mild-to-moderate severity. Various strategies that can be employed to prevent or manage these adverse effects and lessen their impact on the patient are discussed.
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PMID:US FDA-approved disease-modifying treatments for multiple sclerosis: review of adverse effect profiles. 1574 Jan 78

For about 5,000 years, cannabis has been used as a therapeutic agent. There has been growing interest in the medical use of cannabinoids. This is based on the discovery that cannabinoids act with specific receptors (CB1 and CB2). CB1 receptors are located in specific brain areas (e.g. cerebellum, basal ganglia, and hippocampus) and CB2 receptors on cells of the immune system. Endogenous ligands of the cannabinoid receptors were also discovered (e.g. anandamids). Many physiologic processes are modulated by the two subtypes of cannabinoid receptor: motor functions, memory, appetite, and pain. These innovative neurobiologic/pharmacologic findings could possibly lead to the use of synthetic and natural cannabinoids as therapeutic agents in various areas. Until now, cannabinoids were used as antiemetic agents in chemotherapy-induced emesis and in patients with HIV-wasting syndrome. Evidence suggests that cannabinoids may prove useful in some other diseases, e.g. movement disorders such as Gilles de la Tourette's syndrome, multiple sclerosis, and pain. These new findings also explain the acute adverse effects following cannabis use.
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PMID:[The endogenous cannabinoid system. Therapeutic implications for neurologic and psychiatric disorders]. 1577 59

We report a pediatric case of multiple sclerosis mimicking malignant brain tumor. A 11-year-old male presented with high fever, vomiting and partial convulsion of left lower extremity followed by left visual impairment. Magnetic resonance imaging (MRI) revealed a mass lesion in the right frontal lobe with significant peripheral edema. Incomplete ring-like enhancement by gadolinium administration was also noted. Open biopsy of the lesion was undertaken that provided pathological confirmation of demyelinating changes. Luxol fast blue stain and Bodian stain demonstrated extensive myelin loss and good preservation of axons. The patient was given intravenous high-dose methyl-prednisolone and sequential oral low-dose prednisone, which improved his neurological status progressively. The lesion was dramatically decreased in size and finally disappeared. Although many tumor-like demyelinating lesions were reported previously, pediatric cases of multiple sclerosis mimicking malignant brain tumor are extremely rare. Pathological examinations including Luxol fast blue stain and Bodian stain are essential for exact diagnosis.
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PMID:[A pediatric case of multiple sclerosis mimicking malignant brain tumor]. 1622 80

A 46-year-old man with multiple sclerosis had severe generalised pain for which treatment with paracetamol, ibuprofen, gabapentin and methyl-prednisolone had been unsuccessful. In addition normocytic anaemia without haemolysis and with a normal iron load was found. Due to bright red rectal blood loss and nausea, vomiting, weight loss, anorexia, abdominal pain and constipation a colonoscopy was planned. However, before this was performed, manual slide differentiation of a blood smear showed basophilic stippling and it turned out that the patient had been taking Ayurvedic medication up to one month before presentation. A moderately severe lead intoxication was diagnosed: 0.77 mg/l. The herbal medication had a very high lead content. The patient was successfully treated with the oral lead chelator 23-dimercaptosuccinic acid. Traditional and folk remedies often are important causes of lead poisoning.
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PMID:[Chronic lead intoxication associated with Ayurvedic medication]. 1640 16

The effect ofcannabis can be explained on the basis of the function of the cannabinoid receptor system, which consists of CB receptors (CB1, CB2), endoligands to activate these receptors and an enzyme--fatty acid amidohydrolase--to metabolize the endoligands. The endoligands of the cannabinoid receptor system are arachidonic acid-like substances, and are called endocannabinoids. Indications exist that the body also contains arachidonic acid-like substances that inhibit fatty acid amido hydrolase. Various cannabinoids have diverse effects on the receptors, functioning as agonists, antagonists or partial antagonists, as well as affecting the vanilloid receptor. Many known effects ofcannabis can be explained on the basis of this mechanism of action as can the use ofcannabis in various conditions including multiple sclerosis, Parkinson's disease, glaucoma, nausea, vomiting and rheumatoid arthritis.
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PMID:[The mechanism of action of cannabis and cannabinoids]. 1646 12

4-aminopyridine (4-AP) is an orphan drug in the United States. It enhances neuronal conduction at synapses and is indicated in the treatment of selected neuromuscular disorders, including multiple sclerosis and myasthenia gravis, among others. Its documented toxicity generally has been limited to central nervous system (CNS) hyperexcitation and gastrointestinal upset. In this case, a 56-year-old man accidentally overdosed on an unknown amount of generic 4-AP. This history was unknown by his family and unavailable to initial providers. Approximately 1 h after ingestion, his son found him diaphoretic, vomiting, and having unintelligible speech. In the ensuing 2-3 h, the patient became moderately hypothermic (32.8 degrees C; 91 degrees F), developed atrial fibrillation with a rapid ventricular response, and had neurological changes that were confused with an acute cerebrovascular accident. After a 36-h stay in the intensive care unit that included mechanical ventilation, cardioversion, passive rewarming, and an extensive medical workup, the patient recovered without sequelae. After extubation he stated that he thought he may have ingested too much 4-AP after rubbing a large amount of it against a sore tooth to take advantage of its local analgesic properties. This case of 4-AP overdose resulting in atrial fibrillation with rapid ventricular response, hypothermia, and acute neurological changes mistaken for an acute cerebrovascular accident is an unusual one. This case shows that overdose of 4-AP can cause or mimic several serious medical conditions, and that a detailed history and physical examination are essential for uncovering unusual diagnoses.
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PMID:An unusual case of 4-aminopyridine toxicity. 1656 54

Cannabis sativa L. preparations have been used in medicine for millenia. However, concern over the dangers of abuse led to the banning of the medicinal use of marijuana in most countries in the 1930s. Only recently, marijuana and individual natural and synthetic cannabinoid receptor agonists and antagonists, as well as chemically related compounds, whose mechanism of action is still obscure, have come back to being considered of therapeutic value. However, their use is highly restricted. Despite the mild addiction to cannabis and the possible enhancement of addiction to other substances of abuse, when combined with cannabis, the therapeutic value of cannabinoids is too high to be put aside. Numerous diseases, such as anorexia, emesis, pain, inflammation, multiple sclerosis, neurodegenerative disorders (Parkinson's disease, Huntington's disease, Tourette's syndrome, Alzheimer's disease), epilepsy, glaucoma, osteoporosis, schizophrenia, cardiovascular disorders, cancer, obesity, and metabolic syndrome-related disorders, to name just a few, are being treated or have the potential to be treated by cannabinoid agonists/antagonists/cannabinoid-related compounds. In view of the very low toxicity and the generally benign side effects of this group of compounds, neglecting or denying their clinical potential is unacceptable--instead, we need to work on the development of more selective cannabinoid receptor agonists/antagonists and related compounds, as well as on novel drugs of this family with better selectivity, distribution patterns, and pharmacokinetics, and--in cases where it is impossible to separate the desired clinical action and the psychoactivity--just to monitor these side effects carefully.
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PMID:Cannabinoids in health and disease. 1828 1

Medicinal cannabis, cannabis extracts, and other cannabinoids are currently in use or under clinical trial investigation for the control of nausea, emesis and wasting in patients undergoing chemotherapy, the control of neuropathic pain and arthritic pain, and the control of the symptoms of multiple sclerosis. The further development of medicinal cannabinoids has been challenged with problems. These include the psychoactivity of cannabinoid CB1 receptor agonists and the lack of availability of highly selective cannabinoid receptor full agonists (for the CB1 or CB2 receptor), as well as problems of pharmacokinetics. Global activation of cannabinoid receptors is usually undesirable, and so enhancement of local endocannabinoid receptor activity with indirect cannabimimetics is an attractive strategy for therapeutic modulation of the endocannabinoid system. However, existing drugs of this type tend to be metabolized by the same enzymes as their target endocannabinoids and are not yet available in a form that is clinically useful. A potential solution to these problems may now have been suggested by the discovery that paracetamol (acetaminophen) exerts its analgesic (and probably anti-pyretic) effects by its degradation into an anandamide (an endocannabinoid) reuptake inhibitor (AM404) within the body, thus classifying it as pro-drug for an indirect cannabimimetic. Given the proven efficacy and safety of paracetamol, the challenge now is to develop related drugs, or entirely different substrates, into pro-drug indirect cannabimimetics with a similar safety profile to paracetamol but at high effective dose titrations.
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PMID:Pro-drugs for indirect cannabinoids as therapeutic agents. 1885 92

Two cannabinoids receptors have been characterised in mammals; cannabinoid receptor type 1 (CBI) which is ubiquitous in the central nervous system (CNS), and cannabinoid receptor type 2 (CBII) that is expressed mainly in immune cells. Cannabinoids have been used in the treatment of nausea and emesis, anorexia and cachexia, tremor and pain associated with multiple sclerosis. These treatments are limited by the psychoactive side-effects of CBI activation. Recently CBII has been described within the CNS, both in microglia and neuronal progenitor cells (NPCs), but with few exceptions, not by neurons within the CNS. This has suggested that CBII agonists could have potential to treat various conditions without psycho-activity. This article reviews the potential for CBII agonists as treatments for neurological conditions, with a focus on microglia and NPCs as drug targets. We first discuss the role of microglia in the healthy brain, and then the role of microglia in chronic neuroinflammatory disorders, including Alzheimer's disease and Parkinson's disease, as well as in neuroinflammation following acute brain injury such as stroke and global hypoxia. As activation of CBII receptor on microglia results in suppression of the proliferation and activation of microglia, there is potential for the anti-inflammatory properties of CBII agonist to treat neuropathologies that involve heightened microglia activity. In addition, activating CBII receptors may result in an increase in proliferation and affect migration of NPCs. Therefore, it is possible that CBII agonists may assist in the treatment of neuropathologies by increasing neurogenesis. In the second part of the article, we review the state of development of CBII selective drugs with an emphasis on critical aspects of CBII agonist structural activity relationship (SAR).
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PMID:The development of cannabinoid CBII receptor agonists for the treatment of central neuropathies. 2023 42


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