Joana Antunes

Mechanisms of Action of Topical Corticosteroids in Psoriasis

Psoriasis is a lifelong, chronic, and immune-mediated systemic disease, which affects approximately 1–3% of the Caucasian population. The different presentations of psoriasis require different approaches to treatment and appropriate prescriptions according to disease severity. The use of topical therapy remains a key component of the management of almost all psoriasis patients, and while mild disease is commonly treated only with topical agents, the use of topical therapy as adjuvant therapy in moderate-to-severe disease may also be helpful. This paper focuses on the cutaneous mechanisms of action of corticosteroids and on the currently available topical treatments, taking into account adverse effects, bioavailability, new combination treatments, and strategies to improve the safety of corticosteroids. It is established that the treatment choice should be tailored to match the individual patients needs and his/her expectations, prescribing to each patient the most suitable vehicle.

Autoimmune thyroiditis presenting as interstitial granulomatous dermatitis

A 54-year-old female presented with recurrent, widespread, erythematous, painful plaques, over a 3-month period. Skin biopsy was compatible with interstitial granulomatous dermatitis. Additional investigation revealed hypothyroidism and positive anti-thyroid antibodies. Normalization of thyroid function and high-potency topical corticosteroids provided only transitory improvement of the dermatosis. Interstitial granulomatous dermatitis is a histologic inflammatory reaction, with variable cutaneous expression. It has been reported in association with several drugs, lymphoproliferative diseases and autoimmune disorders, such as rheumatoid arthritis, systemic lupus erythematosus and vasculitis, but association with autoimmune thyroiditis is rare. Optimal therapy for this condition is yet to be established, but topical corticosteroids have been a mainstay of treatment. In most cases, this disease is characterized by flares and remissions.

Occupational airborne contact dermatitis caused by usnic acid in a domestic worker

6. Sands MF, Blume JW, Schwartz SA. Successful treatment of 3 patients with recurrent idiopathic angioedema with omalizumab. J Allergy Clin Immunol. 2007;120:979-81. 7. Metz M, Maurer M. Omalizumab in chronic urticaria. Curr Opin Allergy Clin Immunol. 2012;12:406-11. 8. Rodríguez-Trabado A, Fernández Pereira LM, Romero-Chala S, García-Trujillo JA, Cámara Hijón C. Monitoring omalizumab treatment efficacy in chronic urticaria by the basophil activation test. Allergol Immunopathol (Madr). 2011 [Epub ahead of print]. 9. Lemoli E, Piconi S, Fusi A, Borgonovo L, Borelli M, Trabattoni D. Immunological effects of omalizumab in chronic urticaria: a case report. J Investig Allergol Clin Immunol. 2010;20: 252--4. 10. Sánchez-Machín I, Iglesias-Souto J, Franco A, Barrios Y, González R, Matheu V. T cell activity in successful treatment of chronic urticaria with omalizumab. Clin Mol Allergy. 2011;9:11. M. Rodríguez-Rodríguez ∗, D. Antolin-Amerigo, J. Barbarroja-Escudero, M.J. Sánchez-González, M. Alvarez-Mon

Clastogenic Plasma Factors in Psoriasis—Comparison of Phototherapy and Anti–TNF-α Treatments

As previously described, Psoralen plus UVA (PUVA) therapy induces chromosome damage in psoriatic patients. This study evaluates whether these effects are transitory or persistent. In addition, we studied these effects after narrowband UVB (nUVB) and anti‐tumor necrosis factor (TNF)‐α treatments. Among 40 responder patients, 10 received PUVA, 10 nUVB, 10 Infliximab and 10 Etanercept. Disease activity was determined with Psoriasis Area and Severity Index. Chromosomal breakage was evaluated by the clastogenic factor (CF) test. Potential clastogenic agents, malondialdehyde (MDA) and TNF‐α were measured. Before treatment, the plasma‐adjusted clastogenic scores (ACS) of patients were increased. During treatment, a further increase in ACS was observed in both phototherapy groups. Chromosome damage persisted for PUVA patients at week 32, while it diminished after nUVB to ACS values lower than before treatment. MDA and TNF‐α values were also increased at baseline. MDA decreased during treatment in all groups, but without reaching normal levels. Plasma TNF‐α remained unchanged in PUVA and nUVB but decreased in both anti–TNF‐α treatment groups. Psoriasis is accompanied by CF‐induced chromosomal breakage that increases during PUVA and nUVB treatments. Plasma clastogenic activity persisted in the follow‐up after PUVA, while after nUVB ACS returned to values even lower than baseline. Clastogenic activity during the induction phase with anti–TNF‐α remained unchanged.

The importance of patch tests in the differential diagnosis of adverse drug reactions

Exudative erythema multiforme is an acute self-limited skin disease often associated with infections (usually viral), and also with systemic diseases and drugs. We report the case of a 39-year-old woman diagnosed with systemic lupus erythematosus, who presented at the emergency clinic with exudative erythema multiforme which started 10 days after taking amoxicillin and clavulanic acid for tonsillitis together (almost simultaneously) with the pneumococcal vaccine. Rowells syndrome was also considered to be a possibility. Skin patch tests were carried with the standard battery of patches (GPEDC) and the active ingredients of the suspected drugs (Chemotechnique ®), with readings at D2 and D3. The tests were positive for amoxicillin 10% pet (++), ampicillin 10% pet (+ +) and penicillin G potassium 10% pet (+). We accepted the diagnosis of erythema multiforme due to amoxicillin, confirmed by patch testing.

Appearance of de novo dysplastic spitzoid compound naevus in an adalimumab-treated psoriatic patient: case report and review of the possible causal relationship with TNF-α blockers.

Anti-TNF-α therapies have proved to be beneficial in moderate to severe plaque-type psoriasis. Nonetheless, one of the core safety issues associated with tumour necrosis factor (TNF)-α blockers is their still poorly defined potential to increase the risk of malignancy. Moreover, there is an increased risk of skin cancer associated with previous conventional systemic therapies for psoriasis, including methotrexate, cyclosporine and psoralen UV A therapy, and these may confer an additional risk in patients undergoing anti-TNF-α therapy. We report an unusual case of a pigmented macule arising in an adalimumab-treated patient and discuss its differential diagnosis of Spitz naevus versus malignant melanoma (MM). A review of the published cases of malignant lesions in patients with psoriasis receiving anti-TNF-α therapies is also presented.

Allergic hypersensitivity to Deflazacort

1. Textiles and shoes. In: Fisher’s contact dermatitis. 6th ed. Hamilton, Ontario: Bc Decker Inc.; 2008. p. 339--69. 2. Warshaw EM, Schram SE, Belsito DV, DeLeo VA, Fowler Jr JF, Maibach HI, et al. Shoe allergens: retrospective analysis of cross-sectional data from the North American contact dermatitis group, 2001--2004. Dermatitis. 2007;18:191. 3. Fleming AJ. The provocative test for assaying the dermatitis hazards of dyes and finishes used on nylon. J Invest Dermatol. 1948;10:281--91. 4. Edward Gaul L, Underwood GB. Primary irritants and sensitizers used in fabrication of footwear. Arch Derm Syphilol. 1949;60 Pt I:649--75. 5. Leppard BJ, Parhizgar B. Contact dermatitis to PPD rubber in Maleki shoes. Contact Dermatitis. 1977:91--3. 6. Johansen JD, Frosch PJ, Lepoittevin J-P. Contact dermatitis. 5th ed. Berlin: Springer; 2011. p. 545--76. 7. Lepoittevin JP, Le Coz C. Chimie des colorants vestimentaries. In: Libbey J, editor. Progrès en Dermato-allergologié. GERDA; 1999. p. 133--42. 8. Seidenari S, Mantovani L, Manzini BM, Pignatti M. Crosssensitizations between azo-dyes and para-amino compounds. A study of 236 azo-dye sensitive subjects. Contact Dermatitis. 1997;36:91--6. 9. Dooms-Goossens A. Textile dye dermatitis. Contact Dermatitis. 1992;27:321--3. 10. Goon AT, Gilmour NJ, Basketter DA, White IR, Rycroft RJ, McFadden JP. High frequency of simultaneous sensitivity to Disperse Orange 3 in patients with positive patch tests to para-phenylenediamine. Contact Dermatitis. 2003;48: 248--50.

A randomized controlled clinical trial to assess the impact of motivational phone calls on therapeutic adherence in patients suffering from psoriasis

Adherence to topical therapies in psorasis remains suboptimal, with an average adherence of 50–60% (Augustin, Holland, Dartsch, Langenbruch, & Radtke, 2011; Hambly et al., 2017). New strategies to optimize adherence are needed to improve therapeutic success. Motivational phone-calls (MPCs) were shown to improve adherence to skin topical treatments (Feldman et al., 2017), but this strategy has not been tested in psoriasis.

Post-Kala-azar dermal leishmaniasis due to Leishmania donovani in Europe – Case report

condition will be needed to confirm this hypothesis. There seems to be no apparent genotype/phenotype correlation in patients with DSH. Carriers with identical mutations can show different clinical features and severity, indicating the contribution of environmental or extrinsic factors on disease development. Viral infection frequently induces increased levels of IFN in the peripheral blood and other tissues. In the present case, it is possible that the high IFN condition induced by systemic viral infection and encephalitis caused the patient’s latent shortage of ADAR1 enzymatic ability to become apparent, triggering the development of the DSH phenotype. Notably, the IFN-inducible p150 isoform of ADAR1 was recently revealed to suppress the replication of paramyxoviruses and orthomyxoviruses. Thus, a loss-of-function mutation of the ADAR1 p150 isoform might be a risk factor for severe infection by measles and other viruses. Further accumulation of cases and experimental data will be needed to elucidate the exact link between DSH with ADAR1 mutations and viral infection.

Atypical cutaneous mycobacteriosis co-infection with pulmonary tuberculosis in an immunocompetent patient

ejd.2011.1441 Auteur(s) : Joana Antunes joana_antunes@yahoo.com, Paulo Filipe, David Pacheco, Rita Travassos Dermatology Department, Hospital de Santa Maria, Av. Prof. Egas Moniz, 1649-035 Lisbon, Portugal Atypical mycobacterial infections are caused by mycobacteria other than Mycobacterium tuberculosis and M. leprae. Almost all atypical mycobacteria have been implicated in skin diseases [1]. M. avium-intracellulare complex (MAI) consists of M. avium, M. intracellulare and other unidentified species, [...]