The results suggest that, whilst accepted causes do affect onset of melasma, a combination of these factors often triggers this disorder. These factors may provide further insights into how physicians can manage individual melasma cases, support recommendation of preventative measures and even anticipate treatment results and recurrence.

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Objective/Aim To examine approaches to therapy for melasma in Latin Americans and to propose treatment algorithms for patients with mild, moderate and severe melasma.Background Melasma is prevalent in up to 10% of the Latin American population. It is found in all racial groups and is

After resolution of melasma with TC, maintenance therapy over 6 months was successful in preventing relapse in over half of the patients who entered maintenance phase. Prescribing medicines should be adapted to patients based on melasma severity.

Latin-Americans have a heterogeneous ancestry that is defined by their place of domicile, while Hispanics are defined as those persons of Spanish descent. These two groups have a diverse range of skin phototypes and pigmentation and are prone to an increased incidence of melasma and post-inflammatory hyperpigmentation. Little research has been conducted to evaluate the frequency, course, effects, tolerability and treatment response of skin diseases in Hispanic and Latin-American populations. From the limited data that are available it is considered that the treatment of melasma in these two groups does not differ from the general population. First-line therapy of melasma should consist of effective topical therapies, mainly a fixed triple combination of hydroquinone, retinoic acid and fluocinolone acetonide. Where patients have either sensitivity or triple combination therapy is unavailable, other compounds with dual ingredients may be considered as an alternative. Options for second-line therapy include peels either alone or in combination with topical therapy. Lasers should rarely be used in the treatment of melasma and then only as third-line therapy in cases of melasma which is resistant to all other therapies. If applied, skin type must be taken into account. Irritation and sensitivity can be a concern in darker-skinned Hispanic patients and for this reason, the risk of post-inflammatory hyperpigmentation (PIH) following treatment should be considered.

Background: The flare up phenomenon has most frequently been described with nickel. Not many cases of flare up to drugs have reported in the literature, however we have reported it with different medications. Methods and results: A 31-year-old woman developed an adverse reaction with an antibiotic during her childhood. Prick test with penicillin (100,000 IU/ml), penicilloyl polylysine (PPL), minor determinant mixture (MDM), amoxicillin (200 mg/ml), ampicillin (200 mg/ml) and cephalotin (200 mg/ml), and intradermal test to the same substances diluted in saline were all negative immediately. We performed an oral challenge test with 500 mg of amoxicillin. Twelve hours later, the intradermal test to PPL and MDM became positive (PPL 10 × 10 mm, MDM 8 × 7 mm). All patch tests were positive after 72 hours with erythema, vesicles and infiltration and the patient also had exanthema with pruritus on her entire body. Conclusions: We present one patient with delayed allergic reaction caused by amoxicillin and penicillin, that we all know as Flare up. We suggest that this phenomenon of Flare up occurs by a Type IV mechanism mediated by T-cells without participation of IgE antibodies. The betalactam hypersensitivity mechanism which has usually been described is an IgE mediated reaction, but there are other not very well known mechanisms that are responsible for the delayed reactions.

Background: Acrylates are used in a wide variety of products such as solvents, adhesives, paints, printing ink, soft contact lenses, porcelain nails, and methacrylates (used by dentists and orthopedists). Currently there are various types of acrylic compounds: acrylates, cyanoacrylates (such as tissue adhesives and home glues), and methacrylates (prostheses and dental and orthopedic fillings). The sensitization mechanism is unknown, but the allergy is believed to be due to a non-IgE mediated phenomenon, since a late asthmatic response occurs. Various cases of acrylate-induced asthma have been reported, especially in dentists and persons using glues or paints containing this substance. Material and methods: We present the case of a 52-year-old man who had been working in graphic arts for the previous 7 years. For the previous 2 years he had experienced persistent cough with a sensation of drowning, dyspnea that increased with moderate exertion, and nasal obstruction despite continuous treatment. The symptoms first appeared after an episode of acute respiratory difficulty associated with weight loss, pulmonary infiltrates, and eosinophilia. Peak expiratory flow (PEF) was measured during work and sick leave, and specific bronchial challenge with acrylates was performed in a bronchial chamber. Results: The PEF improved on weekends and sick leave. The challenge test provoked a late astmatic response and the non-specifc bronchial hyperreactivity increased after the test. As well in the sputum samples there was a increase of eosinophil amount.

We consider that there are patients with tolerance to low dosages of COX-2 inhibitors who show a reaction on increasing the administered dosage, which means that their tolerance should be taken into account and checked in the long term.