Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Itching is usually manifested by scratching. It is lacking before three months of age. The practitioner must determine whether itching is generalised or localised and whether a skin disease is present. The main skin diseases responsible for generalised itching are scabies, atopic dermatitis, urticaria and papular urticaria. When itching is localised, contact dermatitis or pediculosis are usually responsible. Diagnosis rests on careful analysis of symptoms. In patients without skin lesions, an external cause (irritation, environment) or an internal cause (cholestasis, chronic uraemia, lymphoma, drug and psychological problems) should be considered. Therapy should be causal when possible. If not, antihistaminic drugs should be used.
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PMID:[Pruritus in children]. 793 81

Intense, generalized pruritus associated with mycosis fungoides was relieved using subcutaneous naloxone but intensified when changed to the new oral opioid antagonist, naltrexone. Rechallenge again led to worsening in pruritus. This unexpected adverse effect is surprising as naltrexone and naloxone are currently thought to work via similar opioid receptor binding. The worsening of the itch may have been due to adaptation in opioid receptor expression induced by prolonged naloxone therapy, possibly highlighting differential opioid receptor affinity between naltrexone and naloxone, or may have represented an idiosyncratic adverse reaction. Naltrexone and naloxone have been reported to reduce pruritus due to cholestasis, uraemia, morphine epidurals, and possibly atopic dermatitis and urticaria. Naltrexone has the convenience of oral administration and a longer half-life. The role of the opioid system and naltrexone in pruritus is reviewed.
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PMID:Naltrexone: a case report of pruritus from an antipruritic. 943 14

In origin, itch can be cutaneous ("pruritoceptive", e.g. dermatitis), neuropathic (e.g. multiple sclerosis), neurogenic (e.g. cholestasis), mixed (e.g. uraemia) or psychogenic. Although itch of cutaneous origin shares a common neural pathway with pain, the afferent C-fibres subserving this type of itch are a functionally distinct subset: they respond to histamine, acetylcholine and other pruritogens, but are insensitive to mechanical stimuli. Histamine is the main mediator for itch in insect bite reactions and in most forms of urticaria, and in these circumstances the itch responds well to H(1)-antihistamines. However, in most dermatoses and in systemic disease, low-sedative H(1)-antihistamines are ineffective. Opioid antagonists relieve itch caused by spinal opioids, cholestasis and, possibly, uraemia. Ondansetron relieves itch caused by spinal opioids (but not cholestasis and uraemia). Other drug treatments for itch include rifampicin, colestyramine and 17-alpha alkyl androgens (cholestasis), thalidomide (uraemia), cimetidine and corticosteroids (Hodgkin's lymphoma), paroxetine (paraneoplastic itch), aspirin and paroxetine (polycythaemia vera) and indometacin (some HIV+ patients). If the remedies specified fail, paroxetine and mirtazapine should be considered. Ultraviolet B therapy, particularly narrow-band UVB, may be superior to drug treatment for itch in uraemia.
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PMID:Itch: scratching more than the surface. 1265 79

Apolizumab (Hu1D10), a humanized monoclonal anti- Human leukocyte antigen -DR beta-chain antibody, mediates apoptosis of chronic lymphocytic leukemia (CLL) cells in vitro. We conducted a phase I/II dose-escalation study of thrice-weekly apolizumab (1.5, 3.0, 5.0 mg/kg/dose) for 4 weeks in relapsed CLL. Two of six patients at 5.0 mg/kg/dose developed treatment-related dose-limiting toxicity (aseptic meningitis, hemolytic uremia). Other toxicities included infusion toxicity, urticaria, and headache. Eleven patients were enrolled in a phase I/II expansion to evaluate the maximum tolerated dose (MTD) of 3.0 mg/kg/dose. In total, 23 patients were enrolled (22 CLL, 1 ALL). Nineteen patients with CLL were treated at or above the MTD. One partial response was observed, and three patients had stable disease exceeding 6 months. Pharmacokinetic analysis demonstrated a dose-dependent C(max) increase and serum antibody accumulation after week 1 of therapy. Given the toxicity and lack of efficacy in this and other trials in lymphoma and solid tumors, further development of apolizumab was discontinued.
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PMID:A phase I/II dose escalation study of apolizumab (Hu1D10) using a stepped-up dosing schedule in patients with chronic lymphocytic leukemia and acute leukemia. 1988 43

Several antiepileptic drugs (AEDs) are approved by the US Food and Drug Administration for the treatment of bipolar disorder (valproic acid, divalproex, lamotrigine, carbamazepine) and some cutaneous neuropathic pain syndromes (carbamazepine, gabapentin, pregabalin). The AEDs may be effective in the management of (1) chronic pruritus, including pruritus due systemic disease, including uremia, neuropathic pain, neuropathic pruritus, and complex cutaneous sensory syndromes, especially where central nervous system (CNS) sensitization plays a role; (2) management of emotional dysregulation and the resultant repetitive self-excoriation or other cutaneous self-injury in patients who repetitively stimulate or manipulate their integument to regulate emotions (prurigo nodularis, lichen simplex chronicus, skin picking disorder, trichotillomania); (3) management of dermatologic clinical manifestations associated with autonomic nervous system activation (hyperhidrosis, urticaria, flushing; these often occur in conjunction with psychiatric disorders with prominent autonomic activation and dysregulation, eg, social anxiety disorder, posttraumatic stress disorder); and (4) when certain anticonvulsants have a direct therapeutic effect (eg, in psoriasis); currently the use of AEDs for such cases is largely experimental. Gabapentin (dosage range 300-3600 mg daily) is the most widely studied AED mood stabilizer in dermatology and is especially effective in situations where CNS sensitization is a mediating factor. Further larger-scale controlled studies of AEDs in dermatology are necessary.
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PMID:Use of antiepileptic mood stabilizers in dermatology. 3044