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)

This study describes the probably eleventh case, mentioned in literature, of acquired heat contact uticaria in an otherwise healthy young woman. With regard to true contact induction heat contact urticaria clearly differs from the more common cholinergic uticaria. On the other hand, heat contact urticaria is completely analogous to cold uticaria because of the exposure area, reversible blocking by unphysiological prolonged heating of the skin, sensitivity to antihistamines and resistance to corticosteroids. In this case, whealing of the skin occurred on exposure to heating of 39 degrees C for 5 min. With a temperature of 44-46 degrees C, The shortest time for wheal induction was 3-5 sec. At 70 degrees C, the shortest time for maximal reaction was only a split second. An "optimal temperature" for wheal induction could not be determined. Local anaesthesia with 2% Xylocain caused a considerable blocking of wheals. Histamine and cholinergic drugs showed normal skin reactions after intradermal injection. Antihistamines administered parenterally or perorally were highly effective. Corticosteroids, however, given systemically in high doses proved to be ineffective. During our observations, a spontaneous remission appeared with a clinical symptom-free state; on unphysiological high temperature stimulus, however, contact uticaria could still be demonstrated. The pathogenetic uniformity of sporadic heat contact urticaria and problems of therapeutical controls are discussed.
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PMID:[Clinical and experimental observations on idiopathic urticaria due to the contact with heat]. 0 89

The physician should be familiar with preventive measures for acute urticaria or its most severe form, anaphylaxis, and with the general principles of management. Treatment does not differ basically whether given in a nonmedical setting, the emergency room, or the office, except for the availability of special supplies and equipment, such as oxygen, if needed. In all cases, a history should be obtained quickly, the patient should be examined to confirm the diagnosis, and epinephrine should be administered. Hospitalization is indicated in severe cases with systemic symptoms. Once the acute episode has been treated, the physician must decide whether further investigation is necessary. Quite often a presumptive etiologic diagnosis is made on the basis of the history. Allergy testing is not part of the routine evaluation of the patient with urticaria.
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PMID:Managing acute urticaria. 0 81

Urticaria is a problem often as vexing to the physician as to the patient. The approach to the patient with hives first demands a search for the etiology, whether endogenous and triggered by emotions or occult systemic disease, exogenous and triggered by allergy to inhaled or ingested antigens, or physical and due to abnormal sensitivity to heat, cold, light, or pressure. Often a fruitless search, the diagnostic evaluation must be accompanied by appropriate symptomatic therapy requiring familiarity with the antihistamines and their relative advantages in the various forms of urticaria. Elimination diets are of diagnostic as well as therapeutic value: pencillin-free, yeast-free, and salicylate-free diets are particularly useful. Therapeutic trials of tetracycline, nystatin and griseofulvin may be helpful, while corticosteroids and specific desensitization are rarely of value.
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PMID:Urticaria. 0 33

Antihistamines are a diverse group of drugs which possess the ability to inhibit various histaminic actions. By and large, they bear a certain structural resemblance to histamine, and act principally to prevent histamine-receptor interaction through competition with histamine for histamine receptors. Consequently, they are helpful therapeutically in preventing, rather than reversing, histaminic actions. Individual antihistaminic drugs act to inhibit histaminic action at one or another histamine receptor (H1 or H2-receptor), but not at both receptors. The large number of antihistaminics which have been available for many years and employed chiefly as 'antiallergic' drugs are classified as H1-receptor inhibitors; they are most effective therapeutically in inhibiting manifestations of histamine-induced wheal and erythema formation and pruritus. H2-receptor inhibitors, agents which are able to inhibit histamine-induced gastric acid secretion, have been developed more recently. Antihistaminics in general and H1-receptor inhibitors in particular, exert a wide variety of pharmacological activities. Their use is frequently accompanied by undesirable side-effects, notably CNS depression, dryness of mucous membranes, and gastrointestinal effects. Used judiciously and in proper dosage, antihistaminic drugs are helpful in the control of allergic disorders, allergic rhinitis and urticaria in particular; newly developed H2-receptor inhibitors show therapeutic promise in the treatment of peptic ulceration.
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PMID:Antihistamines: pharmacology and clinical use. 0 70

A research has been carried out on a total of 121 persons with survival post-drug shock (DS), which registered 192 DS. Mention should be made of their predominance in the feminine sex (85 per cent) and their maximum frequency between the ages of 21-50 (average age 34). DS was the first adverse reaction to drugs in 71 per cent of the cases. Therefore DS unpredictability is very frequent. A retrospective study suggested the role of risk factors which should help the doctor to prevent DS (personal allergic antecedents, antecedents of adverse reactions to drugs, neuroses, disorders of endocrine glands, feminine sex, etc.). In 1970, the clinical concept of shock imminence (SI) was formulated and it is applied to various etiologies (drugs, insect stings, food). The existence of SI was identified in the case history of 14 per cent of the persons with DS. SI is a syndrome which includes all clinical manifestations with imminent potential of transformation into shock condition, and represents the stage precursory to the setting up of shock. The utility of SI diagnosis is maximum if it also includes the causal factor (e.g. SI by penicillin or aspirin). The clinical image of SI may vary from the monosymptomatic aspect (urticaria, vomiting, diarrhoea, headaches, etc.) to the one with complex symptomatology (mixed form). Usually the symptoms are dramatic and depend on the administration of a certain drug (often in SI of allergic origin) or of various drugs (mainly on non-immunologic form). The absence of vascular collapse differentiates SI from shock. Differential diagnosis is more difficult in border cases with a slight diminution of blood pressure. SI can be diagnosed especially in several circumstances: when the first adverse drug reaction is dramatic; when the first allergic-type reaction to a drug occurs; when the repetition of drug reactions is amplified in intensity or frequency; when it occurs in persons with risk factors. The differential diagnosis of SI is made with a crude or minimum shock and with pre-shock condition. The advantages of SI diagnosis are the institution of efficient treatment with rapid recoverability and the prevention of subsequent shock to the respective drug.
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PMID:Imminent shock; a useful diagnosis in drug pathology. 1 47

A 45-year-old man had solar urticaria that was activated by visible light. Passive transfer of the reactivity with the patient's serum to the skin of normal recipients was accomplished. Results of reverse passive transfer studies were negative. The patient developed an urticarial wheal at the site of injection of his own serum that had been previously exposed to light in vitro. The experimental data suggested that his condition was attributable to an allergic response. Systemic administration of reserpine was of some therapeutic value, and increasing exposure to natural sunlight was associated with substantial in crease in his tolerance to sunlight. Unfortunately, the possible loss of reactivity that may occur in the natural course of the disease makes substantiation of the therapeutic effects difficult.
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PMID:Solar uticaria. Photoallergen in a patient's serum. 1 39

A high antihistaminic activity of quinuclidyl-3-diphenylcarbinol (phencarol) has been ascertained. In pharmacological experiments phencarol is superior to dimedrol (diphenhydramine), both as concerns its antihistaminic activity and the duration of its action. Unlike dimedrol and diprazine (promethazine) it has no inhibitory effect on the central nervous system. With its clinical use phencarol is effective in treating urticaria, Quincke's edema and allergic skin reactions. The drug is well tolerated by the patients and does not produce any inhibitory or soporific action. Phencarol has an authorized permission to be used for medical purposes.
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PMID:[Phencarol--an antihistaminic preparation from the quinuclidylcarbinol group]. 1 61

Patients with urticaria and angioedema admitted to CHMC were analyzed. The most common etiologic factor for the urticaria was infection (in 45% of the cases), while drugs or medications were responsible in 10% of patients. Almost half of the children received corticosteroids for the treatment of their urticaria.
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PMID:The hospitalized child with urticaria. 1 60

In a group of patients with a syndrome consisting of recurrent episodes of urticaria, arthralgia, abdominal pain, and (rarely) glomerulonephritis, examination of skin biopsy specimens showed necrotizing venulitis. An elevated erythrocyte sedimentation rate was the most common laboratory abnormality. Analyses of serum immunoglobulins revealed random abnormalities of immunoglobulin levels, and assessment of the complement system showed two groups of patients--some with hypocomplementemia and others with a normal complement system. In those with hypocomplementemia, there were low levels of C1q, C4 and, occasionally, C3, compatible with activation of the classic complement pathway. Although the cause of this syndrome is unknown, the complement profiles suggest that more than one mechanism of vascular damage may be operative.
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PMID:Chronic urticaria as a manifestation of necrotizing venulitis. 1 67

A 10-year-old asthmatic boy began to suffer from urticarial rash and moderately severe bronchospasm after 8 weeks' treatment with disodium cromoglycate. Initially, DSCG had helped to control his asthmatic attacks, and steroid therapy could be discontinued. Inhalation provocation test with DSCG aerosol, 4 months after stopping DSCG treatment, showed an immediate-type 1 response and urticaria. A repeat provocation test, under antihistaminic cover , failed to produce similar response. When DSCG was withdrawn, urticaria vanished and the child remained symptom-free. Disodium cromoglycate is regarded as the possible aetiological agent.
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PMID:Asthma and urticaria during disodium cromoglycate treatment. A case report. 1 95


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