Repeated hand urticaria due to contact with fishfood.
BACKGROUND: The etiology of urticaria is often difficult to determine. However, in case of repeated circumstance-connected urticaria, the reason may be easily clarifyable. CASE: A 51-year-old healthy woman repeatedly experienced occupational hand urticaria when handling fish food. An unexpected reason for the urticaria was found in that the fishfood contained histamine as a "contaminant". CONCLUSIONS: In fishfood batches, biological degradation can produce histamine and possibly other toxic substances that can lead to occupational health problems. (+info)
Genetic linkage of the Muckle-Wells syndrome to chromosome 1q44.
The Muckle-Wells syndrome (MWS) is a hereditary inflammatory disorder characterized by acute febrile inflammatory episodes comprising abdominal pain, arthritis, and urticaria. Progressive nerve deafness develops subsequently, and, after several years, the disease is complicated by multiorgan AA-type amyloidosis (i.e., amyloidosis derived from the inflammatory serum amyloid-associated protein) (MIM 191900) with renal involvement and end-stage renal failure. The mode of inheritance is autosomal dominant, but some sporadic cases have also been described. No specific laboratory findings have been reported. The genetic basis of MWS is unknown. Using a genomewide search strategy in three families, we identified the locus responsible for MWS, at chromosome 1q44. Our results indicate that the gene is located within a 13.9-cM region between markers D1S2811 and D1S2882, with a maximum two-point LOD score of 4. 66 (recombination fraction.00) at D1S2836 when full penetrance is assumed. Further identification of the specific gene that is responsible for MWS will therefore provide the first biological element for characterizing MWS, other than doing so on the basis of its variable clinical expression. (+info)
Acquired lipoprotein lipase deficiency associated with chronic urticaria. A new etiology for type I hyperlipoproteinemia.
Type I hyperlipoproteinemia (type I HLP) is a rare disorder of lipid metabolism characterized by fasting chylomicronemia and reduced postheparin plasma lipoprotein lipase (LPL) activity. Most cases of type I HLP are due to genetic defects in the LPL gene or in its activator, the apolipoprotein CII gene. Several cases of acquired type I HLP have also been described in the course of autoimmune diseases due to the presence of circulating inhibitors of LPL. Here we report a case of type I HLP due to a transient defect of LPL activity during puberty associated with chronic idiopathic urticaria (CIU). The absence of any circulating LPL inhibitor in plasma during the disease was demonstrated. The LPL genotype showed that the patient was heterozygous for the D9N variant. This mutation, previously described, can explain only minor defects in the LPL activity. The presence of HLP just after the onset of CIU, and the elevation of the LPL activity with remission of the HLP when the patient recovered from CIU, indicate that type I HLP was caused by CIU. In summary, we report a new etiology for type I HLP - a transient decrease in LPL activity associated with CIU and with absence of circulating inhibitors. This is the first description of this association, which suggests a new mechanism for type I HLP. (+info)
Inhibition of aminopeptidase P potentiates wheal response to bradykinin in angiotensin-converting enzyme inhibitor-treated humans.
Bradykinin is a nonapeptide that contributes to the cardioprotective effects of angiotensin-converting enzyme (ACE) inhibitors. During ACE inhibition, an increased proportion of bradykinin is degraded through non-ACE pathways. Studies in animals suggest that aminopeptidase P (EC 126.96.36.199) may contribute to the metabolism of bradykinin. The purpose of the present study was to determine the contribution of aminopeptidase P to the degradation of bradykinin in humans in the presence and absence of ACE inhibition. To do this, we measured the wheal response to intradermal injection of bradykinin (0, 1, or 10 nicrog) in the presence or absence of intradermal administration of the specific aminopeptidase P inhibitor apstatin (5 or 10 microg) and oral administration of the ACE inhibitor quinapril (10 mg) in six healthy subjects. Both bradykinin (ANOVA; F = 101.18, P <.001) and apstatin alone (F = 7.01, P =.049) caused a wheal of dose-dependent size. There was no significant interaction between apstatin and bradykinin (F = 4.94, P =.175). Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P <.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041). The effect of quinapril was significantly potentiated by coinjection of 10 microg of apstatin (effect of apstatin; F = 21.60, P =.006), such that there was significant interactive effect of quinapril and apstatin (F = 20.83, P =.006) on the wheal response to bradykinin. Collectively, these data suggest that aminopeptidase P plays a minor role in the degradation of bradykinin in human skin in the absence of ACE inhibition but contributes significantly to the degradation of bradykinin in the presence of ACE inhibition. (+info)
Pharmacodynamic interaction of eltanolone and alfentanil during lower abdominal surgery in female patients.
We have studied the influence of eltanolone on intraoperative alfentanil requirements in 18 female patients undergoing lower abdominal surgery receiving target-controlled infusions of eltanolone and alfentanil. While target concentrations of eltanolone were maintained constant, target concentrations of alfentanil changed in response to the presence or absence of responses. With serum eltanolone concentrations increasing from 500 to 2000 ng ml-1, the EC50 of alfentanil for suppression of responses to surgical stimulation decreased from 233 to 9 ng ml-1. The findings suggest that the interaction between eltanolone and alfentanil is synergistic. (+info)
Additive-induced urticaria: experience with monosodium glutamate (MSG).
In patients with chronic urticaria, the incidence of reactions to any additives, including monosodium glutamate (MSG), is unknown. Although many studies have investigated the association of additives and urticaria, most have been poorly designed. This study sought to determine the prevalence of reactions to additives, including MSG, in patients with chronic urticaria using a rigorous protocol. We studied 65 subjects (44 women, 21 men; ages 14-67). All had urticaria for >6 wk without discernible etiology. Subjects with active urticaria were studied while they were taking the lowest effective dose of antihistamine. Screening challenges to the 11 additives most commonly associated with exacerbations of chronic idiopathic urticaria were performed in a single-blind fashion. The dose of MSG given was 2500 mg. Skin scores were obtained to determine a positive reaction in an objective manner. Subjects with a positive screening challenge were rechallenged (at least 2 wk later) with a double-blind, placebo-controlled protocol as in-patients in our General Clinical Research Center. Two subjects had positive single-blind, placebo-controlled challenges, but neither had a positive double-blind, placebo-controlled challenge. We conclude, with 95% confidence, that MSG is an unusual (<3% at most) exacerbant of chronic idiopathic urticaria. (+info)
Identification of a locus on chromosome 1q44 for familial cold urticaria.
Familial cold urticaria (FCU) is a rare autosomal dominant inflammatory disorder characterized by intermittent episodes of rash with fever, arthralgias, conjunctivitis, and leukocytosis. These symptoms develop after generalized exposure to cold. Some individuals with FCU also develop late-onset reactive renal amyloidosis, which is consistent with Muckle-Wells syndrome. By analyzing individuals with FCU from five families, we identified linkage to chromosome 1q44. Two-point linkage analysis revealed a maximum LOD score (Zmax) of 8.13 (recombination fraction 0) for marker D1S2836; multipoint linkage analysis identified a Zmax of 10. 92 in the same region; and haplotype analysis defined a 10.5-cM region between markers D1S423 and D1S2682. Muckle-Wells syndrome was recently linked to chromosome 1q44, which suggests that the two disorders may be linked to the same locus. (+info)
Medical surveillance of allergy in laboratory animal handlers.
Allergic disease is a serious occupational health concern for individuals who have contact with laboratory animals. The principal respiratory symptoms include allergic rhinitis, conjunctivitis, and asthma. Urticaria (" hives") is the most common skin manifestation. The overall prevalence of allergic disease among laboratory animal handlers is about 23%, and respiratory allergy is much more common than skin allergy. Various studies have found annual incidence rates ranging from 2% to 12%. Prevention of animal allergy depends on control of allergenic material in the work environment. Personal protective equipment such as air filtering respirators should be used in addition to the other exposure control technologies where conditions require. Pre-placement evaluation and periodic medical surveillance of workers are important pieces of the overall occupational health program. The emphasis of these medical evaluations should be on counseling and early disease detection. The article gives recommendations for the content of the medical evaluations. (+info)