Chronic urticaria and hormones: Is there a link?

BACKGROUND: While the role of oestrogens in bradykinin angioedema (AE) has been clearly demonstrated, scarce data are available about the role of sex hormones in chronic urticaria (CU). OBJECTIVES: To gather information from a population of women with various forms of CU [chronic spontaneous urticaria (CSU), including a subtype of isolated histaminic AE and a classic subtype of association of wheals and AE, and exclusive inducible urticaria (IU)] about the impact of sex hormones and reproductive factors on their symptoms. METHODS: This was a cross-sectional study comprising interviews of 200 women consulting for CU at nine centres throughout France between May and July 2013. The dermatologists filled in an online questionnaire on the impact of reproductive factors (puberty, contraception and pregnancy) and hormonal treatments on the course of CU, including CSU and IU, in the presence of the women. RESULTS: Most of the women did not experience CU before puberty and if so, puberty did not influence the course of CU. Only 16 women had experienced a pregnancy during CU which caused a worsening of symptoms in four. Hormonal contraception was associated with aggravation in a minority of women, mostly women with CSU (10%). Women with isolated histaminic AE did not exhibit any female sex hormone dependency. CONCLUSIONS: It would appear that sex hormones act as a trigger in only a small subset of women with CU. Nevertheless, this should be taken into account to improve patient management.

[Pathophysiology of urticaria]. / Physiopathologie de l'urticaire.

Urticaria is a dermal edema resulting from vascular dilatation and leakage of fluid into the skin in response to molecules released from mast cells. The major mediator responsible for urticaria is histamine. However, the clinical spectrum and pattern of lesions indicate that other molecules, including prostaglandins, leukotrienes, cytokines, and chemokines, produced at different times after mast cell activation contribute to the polymorphism of this symptom and the variable evolution of this disease. It is a common practice to distinguish immunological and nonimmunological urticaria. Immunological urticaria is a hypersensitivity reaction mediated by antibodies and/or T-cells that results in mast cell activation. Although immunoglobulin (Ig) E-mediated type I hypersensitivity (HS) was long postulated to be the major immunological pathway associated with mast cell activation, interaction between IgEbound mast cells and allergens is unlikely to be the mechanism by which urticaria develops in most patients. It is now well established that urticaria may result from the binding of IgG auto-antibodies to IgE and/or to the receptor for IgE molecules on mast cells, thus corresponding to a type II HS reaction. These auto-immune urticarias represent up to 50 % of patients with chronic urticaria. Mast cell activation can also result from type III HS through the binding of circulating immune complexes to mast cell-expressing Fc receptors for IgG and IgM. Finally, under certain circumstances, T-cells can induce activation of mast cells, as well as histamine release (type IV HS). Nonimmunological urticarias result from mast cell activation through membrane receptors involved in innate immunity (e.g., complement, Toll-like, cytokine/chemokine, opioid) or by direct toxicity of xenobiotics (haptens, drugs). In conclusion, urticaria may result from different pathophysiological mechanisms that explain the great heterogeneity of clinical symptoms and the variable responses to treatment.

[Heart failure and stasis ulcer: A significant association (prospective study of 100 cases)]. / Insuffisance cardiaque et ulcère de stase : une association significative (étude prospective de 100 cas).

BACKGROUND: Risk factors for stasis ulcers have been poorly studied. We conducted a three-year controlled prospective study of the usual risk factors [venous insufficiency (VI), obesity, phlebitis] and of other factors suggested by our experience, such as heart failure (HF). PATIENTS AND METHODS: Both in-patients and out-patients referred for stasis ulcers were included. The diagnosis of stasis ulcer was based on clinical criteria: venous insufficiency, cutaneous signs and/or severe leg oedema. Doppler ultrasound was performed systematically if the lesions showed no dramatic improvement within two months of treatment to eliminate arterial ulcers. VI, liver cirrhosis, heart failure, deep venous thrombosis, obesity, after-effects of leg injury, homolateral artificial hip and knee joints, and consumption of anti-leukaemia or leg-oedema-eliciting drugs were the criteria analysed by clinical examination or by consulting the information in the hospital records. Data were analyzed using SPSS/PCv12 software. Chi(2) and Fischer's exact tests were to compare cases and controls, who were identical in age, gender, and department of initial contact for reasons other than leg ulcers, stasis eczema or lipodermatosclerosis. RESULTS: We included 100 cases and 200 control subjects. Most were out-patients and only 4% were hospitalized in cardiology. Univariate analysis showed that stasis ulcer was significantly associated (p < 10(-4)) with VI (71% of cases versus 32.5% of control subjects), HF (44% versus 11%), obesity (44% versus 21.5%), after-effects of injury (17% versus 0%), and to a lesser extent, with artificial knee joints (7% versus 2.5%; p = 0.04). Multivariate analysis showed that stasis ulcer was strongly associated with VI (OR=5.5; 3-9.9) and HF (OR=4.7; 2.1-10.4). HF (right 16%, left 11%, global 57%, unspecified 16%) was also significantly associated with bilateral localization of leg ulcers (p = 10(-4)) but not with delayed healing (> 6 months). DISCUSSION: This study highlights two risk factors for stasis ulcer: artificial knee joints (in the univariate analysis only) and HF. An increase in leg oedemas is probably an important mechanism but we suggest the role of hypoxaemia in patients with isolated left HF. We advise an internist approach in the management of venous leg ulcers, which we prefer to name stasis ulcers, before having ruled out a general disease. In particular, we recommend a consultation with a cardiologist in the event of doubt.

[Impact of corticosteroid withdrawal in chronic urticaria: a prospective study of 17 patients]. / Effet de l'arrêt des corticoïdes au cours de l'urticaire chronique (étude prospective de 17 malades).

BACKGROUND: Although two reports have indicated benefits of oral steroids in acute urticaria, the 2003 French guidelines emphasized their inefficacy in the treatment of idiopathic chronic urticaria, and the lack of studies. We present the results of a prospective study in 17 patients presenting severe chronic urticaria who agreed to stop taking oral steroids over a one-year period. PATIENTS AND METHODS: This single-centre prospective study included adults (1) presenting chronic urticaria as defined by the French consensus conference committee on chronic urticaria (2003), (2) exhibiting at least two of the following three criteria: sleep disturbance due to itching, repeated angioedema, general symptoms; (3) unresponsive or mildly improved by antihistaminic (anti-H1) therapy; (4) receiving oral steroids at least three days per month. After inclusion in the study, oral steroids were stopped either immediately or gradually, on a case-by-case basis. Two different anti-H1 agents were prescribed at inclusion with follow-up visits two, four and 12 months after complete withdrawal of oral steroids. RESULTS: Seventeen patients were included (M/F sex-ratio: 0.54; mean age: 40 years). General signs (fever, arthralgia, various pains), delayed pressure urticaria, and idiopathic cutaneous vasculitis were noted respectively, in seven, nine and three cases. Oral steroids had been taken for three to 30 days per month before inclusion. Three patients had received prior treatment (e.g., immunosuppressants), with no improvement. After withdrawal of oral steroids, (1) 47% of patients presented a short relapse and/or worsening of chronic urticaria, (2) three patients dropped out of the study at four months (persistence of chronic urticaria unacceptable to patients, despite a clinical score showing mild response), (3) six (35%) had complete remission of chronic urticaria at 12 months, with delayed pressure urticaria in three of these cases, (4) eight (47%) had partial remission, five of whom had delayed pressure urticaria, (5) lasting remission of general symptoms. DISCUSSION: Our study shows that most cases of chronic urticaria are managed without oral steroids since inefficacy of anti-H1 drugs is generally only temporary. After withdrawal of oral steroids, a short increase in chronic urticaria was frequently observed with constant remission from extracutaneous signs and/or histological evidence of vasculitis. We suggest an active role of oral steroids in the failure of anti-H1 therapy. Moreover, oral steroids do not seem to confer any benefits in delayed pressure urticaria, and pending further prospective controlled studies, we recommend that these drugs be prescribed sparingly in chronic urticaria.

Giant foot schwannoma.

Schwannoma of the foot is rare; only 12 cases have been reported. A schwannoma is a benign neurogenic tumour derived from Schwann cells. The diagnosis is often delayed because the symptoms are mainly those of compression disorders. We describe a 7cm schwannoma of the heel in a 30-year-old man. Ten years earlier a schwannoma was removed from the same site. The recurrent lesion was widely excised and a medial plantar flap was used to repair the heel.

[Imputable cutaneous eruption caused by ticlopidine after implantation of a coronary endoprosthesis: why not continue treatment?]. / Eruption cutanée imputable à la ticlopidine après implantation d'une endoprothèse coronaire: pourquoi ne pas poursuivre le traitement?

BACKGROUND: The decision to interrupt a ticlopidine regimen in a patient who develops an adverse effect can be particularly difficult when discontinuing the drug could lead to a high risk situation. CASE REPORT: A 64-year old patient developed a skin rash after taking ticlopidine for coronary artery stenting. Stopping ticlopidine could have led to stent occlusion and no alternative therapy seemed to be suitable. We therefore decided to carry on the treatment under close clinical surveillance. The skin signs rapidly resolved. DISCUSSION: This cases shows that ticlopidine may be continued in patients who develop an adverse skin reaction. The rapid involution of the cutaneous signs in our patient demonstrated that the risk of discontinuing treatment can be greater than that of continuing.

[Perianal basal cell carcinoma. Apropos of 2 cases]. / Le carcinome basocellulaire périanal. A propos de 2 observations.

INTRODUCTION: Two cases of perianal basal cell carcinoma were reported. Less than 100 cases have been so far described. OBSERVATIONS: The first case was a pigmented tumour, in the second an erosive erythematous plaque somewhat similar to Paget's disease. COMMENTS: Basal cell carcinoma of the anal margin is about 15-fold less common than squamous cell carcinoma. The tumour is often ulcerated, sometimes infiltrative but metastasis never occurs. Histopathological findings are often close to what is observed in cloacogenic carcinoma. Surgical resection of the lesion is the best treatment but electrontherapy permitted lesion healing in one of our cases.