Increased urinary excretion of the histamine metabolite N tau-methylhistamine during acetylsalicylic acid provocation in chronic urticaria patients.

Seventeen chronic urticaria patients with a history suggestive of acetylsalicylic acid (ASA, Aspirin)-intolerance were challenged with ASA; only 2 patients showed marked clinical reactions. These clinical reactions were accompanied by a significant increase in the urinary excretion of the most important histamine metabolite, N tau-methylhistamine, in comparison with 15 non-responders (p less than or equal to 0.05) and placebo test. These results suggest an involvement of histamine in the pathogenesis of ASA-intolerance in chronic urticaria patients.

Water vapour loss threshold and induction of cholinergic urticaria.

A patient is described with cholinergic urticaria (CU) in whom the symptoms could be provoked by gustatory stimuli. The aim of this study was to investigate whether there is a threshold of sweating (monitored by skin water vapour loss (SVL) measurements) at which CU can be provoked. Provocations with lemon and sal-ammoniac liquorice induced transient sweating differing both in degree and duration. Only 'doubly salted' liquorice, which caused the most intense sweat response, resulted in urticarial lesions. This findings suggest a threshold dependency for the induction of CU. SVL measurement may be a useful method for the evaluation of sweating tests in CU patients.

Elevated levels of squamous cell carcinoma antigen in patients with a benign disease of the skin.

Squamous cell carcinoma antigen (SCC), formerly referred to as TA-4, is a tumor marker for SCC of the uterine cervix. Based on the findings in a patient with complete remission after treatment for cervical carcinoma, the authors decided to analyze the sera from patients with benign dermatoses. It was found that 83% (25/30) of the patients with psoriasis and 80% (12/15) of the patients with eczema had SCC levels in excess of the cut-off value of 2.5 ng/ml. In psoriasis the serum SCC level correlated positively with the body surface area affected by the disease (r = 0.64). Seven patients with miscellaneous skin disorders, all with an inflammatory component, showed high serum SCC levels as well. Thus the existence of an inflammatory skin disease or a hyperkeratotic skin disease with an inflammatory component interferes with the usefulness of the SCC antigen as a tumor marker in SCC of the uterine cervix.

Pemphigus-like eruption induced by d-penicillamine and captopril, in the same patient.

A patient suffering from rheumatoid arthritis and hypertension is described who developed pemphigus foliaceus during simultaneous treatment with d-penicillamine and captopril. Discontinuation of the d-penicillamine afforded some improvement, but skin symptoms still persisted after 3 months. When the captopril was discontinued as well, all lesions healed within 2 weeks. Our findings suggest that both these chemically related drugs might have been responsible for the pemphigus-like eruption in this patient.

Cold urticaria and virus infections: a clinical and serological study in 39 patients.

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.

Alpha 1-antitrypsin deficiency and PI typing in patients with chronic urticaria.

A group of 281 patients with chronic urticaria was classified into various subtypes and compared with 357 healthy controls for PI types of alpha1-antitrypsin. Total alpha 1-antitrypsin was measured by the Mancini technique, and PI types were determined by isoelectric focusing. The MZ phenotype and the Z gene frequency were significantly more frequent in the urticaria group. The Z gene predominated in the groups with cold urticaria and acquired angio-oedema. The total group of chronic urticaria patients showed a significant decrease in total alpha 1-antitrypsin compared with the control group (P less than 0.03). Deficiencies in alpha 1-antitrypsin may predispose to the development of certain types of urticaria and angio-oedema.

Immunohistochemical findings in a patient with penicillamine pemphigus.

This report describes the immunofluorescence (IF) findings in sequential skin biopsies and serum obtained during a follow-up study of a patient who developed pemphigus lesions after D-penicillamine treatment of arthritis. The distribution in the skin of IgG, IgM and C3 varied with the date, type and site of the biopsy sample. Thus IF patterns showed features of (a) pemphigus vulgaris, (b) pemphigus foliaceus and (c) pemphigus erythematosus. Indirect IF examination indicated the presence of circulating intercellular epithelial antibody of both the IgG and IgM class.

Protease inhibitors in plasma of patients with chronic urticaria.

The hypothesis that deficiencies of plasma protease inhibitors might play a role in the pathogenesis of chronic urticaria was evaluated. Plasma levels were measured in patients with urticaria and a matched control group for alpha1-antitrypsin, alpha2-macroglobulin, total trypsin-inhibiting capacity, kallikrein-inhibiting capacity, and the complement factors C1 esterase inhibitor, C3, and C4. A total of 92 patients with chronic urticaria or more than three months' duration was studied. Patients with acquired cold urticaria had significantly decreased levels of alpha1-antitrypsin and total antitrypsin activity. In patients with acquired angioneurotic edema, alpha1-antitrypsin levels and antichymotrypsin activities were lowered, with less significant decreases in anti-trypsin and antikallikrein activities. Levels of C1 esterase inhibitor , C3, and C4 were normal in all groups. There was no correlation between the increased sensitivity to intracutaneously administered kallikrein injection and deficiencies of of protease inhibitors.

Reactions to aspirin and food additives in patients with chronic urticaria, including the physical urticarias.

In 131 patients with chronic urticaria, including physical urticarias, oral provocation tests were done with aspirin. A total of thirty-one patients showed a reaction on aspirin challenge. Reactions were seen in 35% of patients with idiopathic urticaria, 52% of patients with cholinergic urticaria, and 43% of those with pressure urticaria. The patients with reactions to aspirin were also tested with tartrazine, sodium benzoate, 4-hydroxybenzoic acid, sodium- and phenyl salicylate and the analgesics indomethacin, paracetamol and mefanamic acid. In nineteen of twenty three aspirin sensitive patients, positive reactions to one or more of these substances were observed. Indomethacin and tartrazine had the highest scores. There was no statistically significant correlation between aspirin reactions and the presence of nasal polyposis, sinusitis, asthma or atopy.