Granuloma annulare--a genetic disorder that sustain an incomplete foreign-body granuloma reaction.

Granuloma annulare (GA) is a common dermatosis characterized by an annular arrangement of erythematous papules, plaques, rarely nodules or patches. It is a type of non-infectious granuloma with unknown etiology. Hypothesis. The immune reaction always begins with the foreign-body granuloma formation. However, if during the process the antigen is recognized as too small the immune reaction stops the granuloma development. In the case of GA the dysfunctional control mechanism continues to sustain the granulomatous formation. Because the target does not exist anymore, the initiated process starts the "search" for a new target (circular spreading). Different histological and clinical presentations depends on which gene of the control mechanism is dysfunctional, while the distribution depends on the type of antigen and its distribution at the start of the immune reaction. The disappearance of GA after biopsy, that occurs in some cases, could be attributable to the specific defective gene involved (the biopsy can disrupt only some type of GA). So, new therapies for solitary GA formations could be directed to the disruption and creation of a new and healthy immune response from the point of disruption. A comparative analysis of the gene expression of GA and the foreign-body granuloma in the same patient, and GA among different patients could clarify which genes are involved in granulomatous formations. The cells affected by those genetic defects are probably histiocytes and lymphocytes (both always present in GA). Because of some similarity, necrobiosis lipoidica could also be a specific type of GA.

Defective induction of senescence during wound healing is a possible mechanism of keloid formation.

UNLABELLED: Keloids are a hyperproliferative response of connective tissue in response to trauma. The mechanism by which this occurs is poorly understood and currently no successful treatment exists. HYPOTHESIS: Senescent fibroblasts form during wound repair, as the result of oxidative stress. They have a major role in the control of fibroblast proliferation and extracellular matrix synthesis, acting as inhibitors. The defective induction of stress-induced senescent phenotype (SIPS) creates an insufficient number of senescent cells, diminishing the inhibitor effect, causing the uncontrolled hyperproliferation and keloid formation. In the proposed mechanism of keloid formation, fibroblasts have a major role, but it is also possible that other cells are involved, like keratinocytes and melanocytes. Accepting the hypothesis to be correct, a therapy that induces senescence can be used to prevent the keloid formation. Current therapies are only partially effective because they either induce senescence in too few cells or in enough number of cells, but at the same time inducing death (apoptosis and necrosis) of other cells. Dead cells are probably the source of a new repair cycle (proliferation), therefore the process of keloid formation is only postponed but not blocked. A more efficient prevention of keloid formation could be achieved using specific drugs or physical methods that induce senescence and not cell death. Therapies based on photodynamic and PUVA therapy, capable to induce predominantly cell senescence, can be possibly effective. The magnitude of oxidative stress, created during photodynamic therapy, can be reduced and used to produce sublethal doses, to cause senescence instead of cell death. Except standard photosensitizers, other drugs could be used, that are not so powerful in inducing oxidative stress, i.e. amphotericin B in combination with UV light.

Delayed onset of warts over tattoo mark provoked by sunburn.

Multiple warts in a 32-year-old-man are reported that developed after tattooing and remaining exclusively confined to that area. The tattooing was done 2.5 years earlier by a professional tattoo artist. It was previously a lesion-free tattoo, but when damaged by sunburn developed multiple skin warts. The ability of a latent virus to induce warts after cutaneous ultraviolet exposure was discussed.

The epidemiology of Microsporum canis infections in Rijeka area, Croatia.

The aim of the study was to analyze the Microsporum canis infections in the Rijeka area, Croatia, observed between 1990 and 2001. A total of 724 cases of dermatophytosis caused by M. canis were diagnosed in 320 individuals with the tinea capitis and 404 with tinea corporis. The M. canis infections constituted 32.8% of all dermatophytes isolated during the study period.

Treatment of early syphilis with azithromycin.

An open, noncomparative study was performed to establish the efficacy of azithromycin in the treatment of early syphilis. Sixteen patients were treated with oral azithromycin: 1g the first day and then 500 mg for the following 8 days. Two patients were excluded from the study, leaving 14 patients for the evaluation of the efficacy. Venereal Disease Research Laboratory (VDRL) negativity was observed in 3 out of 6 patients treated for primary syphilis after 3 months and in all patients after 6 months. Two of 8 patients treated for manifest or early latent secondary syphilis had VDRL negativity after 3 months and 4 patients after 6 months. This study demonstrates that azithromycin is effective in the treatment of early syphilis. Two patients experienced gastrointestinal side effects which did not require treatment interruption.

Azithromycin compared with minocycline in the treatment of acne comedonica and papulo-pustulosa.

This open study was conducted in 72 outpatients with acne vulgaris, to compare the clinical efficacy and tolerability of azithromycin and minocycline. Azithromycin was administered as a single oral dose (500 mg/day) for 4 days in four cycles every 10 days and minocycline was administered 100 mg daily for 6 weeks. Improvement was assessed 6 weeks after initiation of treatment with a four-graded scale. A satisfactory clinical response was observed in 75.8% of the patients treated with azithromycin and in 70.5% of those treated with minocycline. There were no significant differences between these two acne treatments in terms of reduction of the number of lesions (p> 0.05). Both agents were well tolerated and mild side effects were reported in 10.3% of azithromycin and 11.7% of minocycline treated patients. We conclude that azithromycin is at least as clinically effective and well tolerated as minocycline as treatment of facial comedonic and papulopustular acne.

Comparative trial of azithromycin and ciprofloxacin in the treatment of gonorrhea.

This single-blind (investigator) comparative study was designed to determine the efficacy and tolerability of 1 g of azithromycin vs 500 mg of ciprofloxacin both given as a single oral dose in patients with gonorrhea, who were constantly on the move. One hundred eight patients (59 men and 49 women) with clinically suspected gonococcal infection, confirmed by Gram-stain and culture, were enrolled. Data of 50 patients treated with azithromycin and 51 with ciprofloxacin were evaluable for efficacy and tolerability at the end of the study. After 2 weeks clinical and microbiological cure rates were 96.0% (48 out of 50) for the patients treated with azithromycin and 92.15% (47 out of 51) for the patients treated with ciprofloxacin (p > 0.05). Adverse reactions were reported in 5 patients treated with azithromycin and 6 with ciprofloxacin. In conclusion, 1 g azithromycin is at least as clinically and microbiologically effective and well tolerated as 500 mg of ciprofloxacin in the treatment of gonococcal infections. The drug is particularly useful for sailors and people constantly on the move.

Postcoital fixed drug eruption in a man sensitive to trimethoprim-sulphamethoxazole.

We describe a 34-year-old patient with a probable fixed drug eruption caused by trimethoprim-sulphamethoxazole, having developed the eruption after sexual intercourse with his wife, who was taking the drug. The patient was known to be allergic to trimethoprim-sulphamethoxazole by history, and the lesion then recurred at the same site when the drug was administered orally to his wife. To the best of our knowledge, this is the first report describing postcoital fixed drug eruption. Physicians should thus be aware of unusual and atypical forms of fixed drug eruption. Fixed drug eruption (FDE) is an unusual form of adverse drug reaction, in which one or more lesions appear in precisely the same place or places each time the precipitating drug is administered. The entity was first described by Bourns in 1889, but Brocq then coined the name some years later. FDE may occur anywhere on the skin or mucous membranes, but more frequently occurs on the genitalia and lips. Lesions are usually sharply demarcated patches which quickly become urticarial and sometimes vesicular in the centre. Itching or burning may also be present. Lesions generally leave prolonged postinflammatory hyperpigmentation. The exact pathogenesis of FDE has not been determined, but recent reports have underlined the importance of T lymphocytes, mast cells, keratinocytes and cytokines in the origin of the lesions. We now report a case of FDE apparently caused by trimethoprim-sulphamethoxazole in a male after intercourse with his wife, who was taking the drug. Such FDE, caused by contact with a drug seemingly present in the vaginal fluid, has not been previously described in the literature as far as we know.