Heat contact urticaria is very rare and it is characterized by the development of wheal limited to the areas of heat contact. We report a case of heat contact urticaria in a 65-year-old women. The wheal was induced by hot bathing, washing in hot water or leaning on hot radiators. Symptoms started within 5 minutes of exposure and lasted 30 to 60 minutes. She had no systemic symptoms. The clinical diagnosis of localized heat urticaria was confirmed by experimental induction of localized wheals. Our investigation showed that the threshold temperature needed for induction of the heat urticaria was 39 degrees C. We tried to investigate the plasma levels of prostaglandin D2 and blood histamine before and after heat challenge. The patient showed marked improvement after a combination treatment of desensitizing by repeated exposure to heat and indomethacine.
Aged ; Case Report ; Female ; Heat/*adverse effects ; Human ; Prostaglandin D2/blood ; Urticaria/*etiology/therapy

OBJECTIVE: To detect the changes of leukotriene E4(LTE4), prostaglandin D2(PGD2), carboxypeptidase A3(CPA3) and platelet activating factor (PAF) in guinea pigs died from anaphylactic shock. METHODS: Guinea pigs were used for establishing anaphylactic shock models. The levels of LTE4, PGD2 and CPA3, and PAF were detected in urine, plasma, and brain tissues with ELISA kit, respectively. The significant biomarkers were selected comparing with control group. The changes of PGD2, CPA3 and PAF in the guinea pigs at time zero, 12 and 24 hours after death were observed and compared respectively. The effect of platelet activating factor acetylhydrolase (PAF-AH) to PAF in guinea pig brain was examined and compared. RESULTS: There were no statistically differences of LTE4 levels in urine observed between experimental group and control group. The levels of CPA3, PGD2 and PAF in the experimental group were significantly higher than that in the control group at 0 h. The levels of PAF at 12 and 24 hours after anaphylactic shock were significantly higher than that in the control group. The levels of PAF decreased significantly after pretreatment with PAF-AH. CONCLUSION LTE4 in urine cannot be selected as a biomarker to determine the anaphylactic shock. PGD2 and CPA3 in plasma, and PAF in brain tissue may be used as biomarkers to determine the anaphylactic shock. PAF-AH may be potentially useful for clinical treatment of anaphylactic shock.
1-Alkyl-2-acetylglycerophosphocholine Esterase/pharmacology* ; Anaphylaxis/prevention & control* ; Animals ; Brain/pathology* ; Carboxypeptidases/blood* ; Case-Control Studies ; Disease Models, Animal ; Egg Proteins/administration & dosage* ; Enzyme-Linked Immunosorbent Assay ; Female ; Guinea Pigs ; Leukotriene E4/urine* ; Male ; Mice ; Platelet Activating Factor/metabolism* ; Prostaglandin D2/blood* ; Time Factors