Forty patients with rosacea were entered into a study comparing clarithromycin with doxycycline in the systemic treatment of mild and severe rosacea. The patients, 25 women and 15 men, aged from 26 to 62 years, were subdivided into two homogeneous groups with regard to age, sex, and disease seventy. The first group of 23 patients, 14 women and 9 men, was treated with 250 mg of clarithromycin for 4 weeks twice daily, and then with 250 mg once daily for the following 4 weeks. The second group of 17 patients, 11 women and 6 men was treated with 100 mg of doxycycline for 4 weeks twice daily, and then with 100 mg once a day for the following 4 weeks. Both objective and subjective evaluations of the dermatosis were performed prior to therapy and after 4, 6, and 8 weeks of treatment.

Although the pathophysiology of chronic urticaria is not fully understood, it is possible that dysfunctioning of peripheral cutaneous nerve fibres may be involved. It has also been suggested that fibromyalgia syndrome, a multi-symptomatic chronic pain condition, may be associated with alterations and dysfunctioning of peripheral cutaneous nerve fibres. The aim of this study was to determine whether patients with chronic urticaria are also affected by fibromyalgia syndrome. A total of 126 patients with chronic urticaria were investigated for fibromyalgia syndrome. An unexpectedly high proportion (over 70%) had fibromyalgia syndrome. The corresponding proportion for 50 control dermatological patients was 16%, which is higher than previously published data for the Italian general population (2.2%). It is possible that dysfunctional cutaneous nerve fibres of patients with fibromyalgia syndrome may release neuropeptides, which, in turn, may induce dermal microvessel dilatation and plasma extravasation. Furthermore, some neuropeptides may favour mast cell degranulation, which stimulates nerve endings, thus providing positive feedback. Chronic urticaria may thus be viewed in many patients, as a consequence of fibromyalgia syndrome; in fact, skin neuropathy (fibromyalgia syndrome) may trigger neurogenic skin inflammation (chronic urticaria).

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Fas-L molecules expressed by in vitro stimulated T cells may be critically involved in suicidal activation-induced cell death (AICD) of such cells through engagement of their Fas receptors. A similar suicide of T cells was postulated to occur even in vivo, to eliminate dangerous activated lymphocytes; however, the demonstration of suicidal AICD of T cells in healthy humans in vivo is still lacking. We therefore investigated the possible occurrence of Fas-L-linked suicidal apoptosis of T cells in normal human peripheral blood. For this purpose, we took advantage of immunoelectron microscopy, which allows simultaneous visualization of the morphological apoptotic cellular changes together with surface expression of Fas-L molecules. Very few T lymphocytes were observed showing the ultrastructural features of apoptotic lymphocytes; these occasional apoptotic T cells, together with the majority of the normal T cell population, expressed the Fas molecule on the plasma membrane, as expected. Interestingly, the apoptotic cells were also Fas-L-positive, whereas normal T cells were Fas-L-negative. Such Fas-L-associated T cell suicide operating in vivo in healthy individuals is presumably able to suppress immune responses and prevent autoreactivity, thus maintaining the homeostasis of human blood.