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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective study was carried out in 40 infants, age 1 to 24 months, with urticaria. Acute urticaria was seen most frequently (85%), followed by recurrent (10%) and chronic disease (5%). Several clinical features such as frequency of angioedema and hemorrhagic lesions appeared to be specific to urticaria in infants. An underlying cause was identified or suspected in 65% of cases: foods in 25%, and drugs and infections in 37.5%. Under 6 months of age, all infants had acute urticaria and 75% had cow's milk allergy. After 6 months of age, the main causes were drug intake (mostly aspirin and amoxicillin) and/or infections (mainly viral) (50%). Atopy was not overrepresented (20%), although a possible link between atopy and recurrent urticaria was noted. After a follow-up of 2 to 7.5 years, 96% of patients were symptom free. Thus, our results indicate that clinical and etiologic features of urticaria in infants are somewhat different from those of adults and children.
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PMID:Urticaria in infants: a study of forty patients. 235 24

An increasing incidence of strongyloidosis must be expected in European countries as a result of the increasing numbers of immigrants, as well as holiday-makers returning from tropical regions. In addition to gastrointestinal symptoms, dermatological complaints are predominant. Only rarely are cutaneous symptoms the only clinical manifestation of disease. The penetration of filariform larvae may cause "ground itch." In cases of chronic disease, larva currens is the most obvious sign and consists of linear urticarial wheals evoked by larva migration. The most common non-specific symptoms are rashes, pruritus and urticaria. A further symptom of strongyloidosis, intensely itching prurigo, is described in a 20-year-old female Thai. Remission was achieved following tiabendazole therapy.
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PMID:[Prurigo and further diagnostically significant skin symptoms in strongyloidosis]. 335 53

Gram-negative osteomyelitis frequently responds poorly to conventional therapy. Ciprofloxacin displays excellent in vitro activity against gram-negative bacilli and offers the potential for outpatient therapy. In this ongoing study, ciprofloxacin therapy is being evaluated for the treatment of gram-negative osteomyelitis. Twenty-three patients (16 men and seven women) have been treated under the protocol (750 mg orally twice daily for 1.5 to six months), and 14 patients have completed therapy. All patients had either growth on bone cultures from an open or percutaneous biopsy, or an arthrocentesis to confirm the diagnosis. Involved sites included ankle or tibia (seven patients), vertebra (four patients), hip (five patients), metatarsal (four patients), phalanx (two patients), and metacarpal (one patient); 16 patients had chronic disease, and seven patients had acute disease. Patients had a total of 28 gram-negative bacilli, 12 gram-positive cocci, and one anaerobic gram-negative rod, for an average of 1.8 pathogens per patient. Eighteen of the 28 gram-negative bacilli were Pseudomonas species. The geometric mean minimal inhibitory concentration for all the gram-negative bacilli was 0.15 microgram/ml. The geometric mean minimal inhibitory concentration for the gram-positive isolates was 0.41 microgram/ml. All patients who completed therapy experienced a cure, with a mean follow-up of 6.1 months. Infections in all patients, except for two who are still taking ciprofloxacin, are resolving, both clinically and radiologically. One patient who was not eligible for the protocol experienced a superinfection with methicillin-resistant Staphylococcus aureus. Side effects have included urticaria, lethargy, nausea, and transient elevations of liver and renal function test results. Overall, ciprofloxacin therapy was well tolerated. This study suggests that ciprofloxacin holds promise for the outpatient treatment of gram-negative osteomyelitis.
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PMID:Oral ciprofloxacin therapy for gram-negative bacillary osteomyelitis. 355 43

Thirty-nine patients with cold urticaria seen over a 12-year-period were re-examined. All but 12 still had positive skin tests for cold and only five of these had shown a spontaneous cure. Fourteen patients were prone to collapse on cold exposure. The incidence of atopy in this group was comparable to that in control groups. Cold urticaria is an extremely chronic disease. The mean disease duration was 9.3 years. Serum antibodies to Epstein-Barr virus, measles virus, cytomegalovirus (CMV), varicella-zoster virus (VZV), herpes simplex virus (HSV), Chlamydia psittaci and Mycoplasma pneumoniae were determined in all 39 patients and compared with control groups. The EBV-antibody patterns (heterophile antibodies and different types of EBV-specific antibodies) showed no evidence of current or of recent primary or secondary infection with EBV. Complement fixing antibody titres to measles virus, CMV, HSV and Mycoplasma pneumoniae were significantly higher in cold urticaria patients than in controls. The existence of a basic immuno-regulatory defect responsible for both the cold urticaria and the elevated antibody levels is proposed.
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PMID:Cold urticaria and virus infections: a clinical and serological study in 39 patients. 395 51

A high incidence of anaphylactic reactions has been observed in patients undergoing therapeutic plasma exchange. In three of 22 patients who underwent multiple exchanges, urticaria, bronchospasm, and hypotension developed during a course of plasma exchange that responded to treatment with steroids, antihistamines, and epinephrine. Fatal pulmonary microvascular occlusion with platelets and granulocytes developed in an additional patient eight hours following an apheresis procedure involving albumin replacement. The mechanism for the latter complication is not known but did not appear to invoke complement activation. This unexpectedly high risk of potentially fatal complications must be considered when a course of therapeutic apheresis, particularly involving treatment of a chronic disease, is planned.
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PMID:Complications of therapeutic apheresis, including a fatal case with pulmonary vascular occlusion. 685 81

The term "food allergy" refers to adverse immunologic reactions to food. Food allergy is usually mediated by IgE antibody directed to specific food proteins, but other immunologic mechanisms can also play a role. The primary target organs for food allergic reactions are the skin, the gastrointestinal tract and the respiratory system. Both acute reactions (hives and anaphylaxis) and chronic disease (asthma, atopic dermatitis and gastrointestinal disorders) may be caused or exacerbated by food allergy. The foods most commonly causing these reactions in children are milk, egg, peanuts, soy, wheat, tree nuts, fish and shellfish; in adults, they are peanuts, tree nuts, shellfish and fish. The diagnosis of food allergy requires a careful search for possible causes, confirmation of the cause(s) with supporting tests, including specific tests for IgE (i.e., prick skin tests, radioallergosorbent tests) and, in some cases, oral food challenges. Treatment consists of elimination of the causal food(s) along with medical treatment, including the prompt self-administration of epinephrine in the event of a serious reaction.
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PMID:Manifestations of food allergy: evaluation and management. 1046 16

Chronic urticaria is above all a cutaneous disease, affecting the skin, a visible organ, which plays a privileged role in relational life. Like any chronic disease, it raises two principal problems: preservation of the quality of life and therapeutic compliance. In chronic urticaria, psychological factors intervene on several levels: the doctor-patient relationship, the urticarian crisis itself, the onset and/or the aggravation of the disease, and the psychosocial consequences of urticaria. The role of psychological factors in the onset and/or the aggravation of the disease is variously estimated, generally based on retrospective studies and without consensus between the authors. On the other hand, the psychosocial impact of the disease is regularly mentioned: 30 to 40 p. 100 of the patients presenting with an associated depressive state. Quality of life is especially impaired in case of an associated physical urticaria. These data plead in favour of taking into account the psychological factors involved in the disease in order to propose, combined with the classical treatments of chronic urticaria and before the use of heavier treatments, a psychological treatment, i.e. a prescription of psychotropic drugs (especially antidepressants), alone or associated to a psychotherapy (a relaxation technique for example), without forgetting health education sessions.
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PMID:[Psychological factors in chronic urticaria]. 1284 12

A growing body of evidence shows that at least 40% of patients with unexplained (idiopathic) chronic urticaria have clinically relevant functional autoantibodies to the high-affinity IgE receptor on basophils and mast cells. The term "autoimmune urticaria" is used for this subgroup of patients presenting with continuous ordinary urticaria. This article reviews the evidence for the autoimmune hypothesis and other nonantibody serum histamine-releasing factors in the etiopathogenesis of urticaria; defines autoimmune urticaria; looks at how autoimmune urticaria fits into existing classifications of urticaria; proposes diagnostic criteria that may be useful to the clinician; and reviews the management implications for patients with this subset of chronic disease.
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PMID:Autoimmune urticaria. 1512 Jan 46

Paroxetine (Paxil) is a widely prescribed antidepressant of the selective serotonin reuptake inhibitor (SSRI) class for which multiple cutaneous adverse effects have been reported, including urticaria, ecchymoses, vasculitis, and pruritus. In contrast, fluoxetine (Prozac) is the only SSRI previously reported to cause urticarial vasculitis. Urticarial vasculitis is a chronic disorder marked by recurrent episodes of erythematous, indurated wheals that histologically manifest the features of leukocytoclastic vasculitis. This case represents the first reported incidence of paroxetine-induced urticarial vasculitis, and highlights the need to consider the entire SSRI class as s as a potential cause of the condition.
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PMID:Urticarial vasculitis secondary to paroxetine. 1737 54

A case of solar urticaria is presented, followed by a discussion of the clinical characteristics, pathophysiology, diagnosis, and management of this disease. Special emphasis is given to clinical pearls and pitfalls for the practicing allergist. Solar urticaria is a physical urticaria that can be difficult to diagnose and distinguish from other photodermatoses. There are some characteristic features that are important to remember when evaluating a patient with suspected solar urticaria. Testing can be difficult without the assistance of an experienced dermatologist because there are several different wavelengths of light that can lead to a patient's symptoms. Solar urticaria tends to be a chronic disease with a low 5-year resolution rate but can usually be effectively managed with multiple antihistamines.
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PMID:Solar urticaria. 1984 10


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