RESUMO
Lyme disease is an emerging infection caused by the spirochete Borrelia burgdorferi. It is the most common vector-borne disease in the USA and Europe, and it is transmitted to humans through the bite of ticks of the genus Ixodes. Its animal reservoirs are the white-tailed deer, the white-footed mouse, and other small mammals. It is considered the new "great imitator", with its diagnosis being a major challenge. Traditionally it is divided into four stages, early localized disease, early disseminated, late disease, and the post-Lyme syndrome. Clinical manifestations may be both cutaneous and systemic, and can have cardiovascular, neurological, and musculoskeletal involvement. Diagnosis is based on clinical findings and can be confirmed by serologic studies (ELISA and Western Blot). The best preventive method is to avoid exposure to vectors. The aim of treatment with antibiotics (doxycycline and cephalosporins) is to relieve symptoms and prevent sequelae.
Assuntos
Doença de Lyme , Progressão da Doença , Humanos , Doença de Lyme/diagnóstico , Doença de Lyme/microbiologia , Doença de Lyme/terapia , Doença de Lyme/transmissãoRESUMO
Vitiligo is characterized by a skin depigmentation disorder resulting from an autoimmune response targeting melanocytes. Within the genetic factors involved in the development of the vitiligo immune response, various genes in the major histocompatibility complex (MHC) and non-MHC loci have been considered to be risk factors. The PTPN22 gene encodes for a lymphoid protein tyrosine phosphatase, a regulator of the activation and development of T-cells. The +1858C/T polymorphism has been associated to autoimmune disease susceptibility in different populations and could be implicated in the onset of vitiligo. To assess the possible association between the presence of PTPN22 +1858C/T and vitiligo, 187 patients with vitiligo and 223 control subjects were analyzed in the study. Genomic DNA was isolated using the salting-out method and samples were subjected to polymerase chain reaction-restriction fragment length polymorphism in order to detect the PTPN22 +1858C/T polymorphism. Causal associations were determined by χ2 test and their respective odds ratio (OR) was assessed in a 2×2 contingency table. The results showed an association between active vitiligo and the allele T load [P=0.0418; OR, 2.5706; 95% confidence interval (CI), 1.0040-6.5816], and active vitiligo-CT genotype (P=0.0389, OR, 2.6548; 95% CI, 1.0191-6.9156). In conclusion, the present data indicates a possible association between the PTPN22 +1858C/T genotype and a significant susceptibility of developing an active form of vitiligo.
RESUMO
INTRODUCTION: Frontal fibrosing alopecia (FFA) is a scarring alopecia characterized by progressive recession of the frontotemporal hairline. Current treatment is aimed at stopping progression, and the combination of dutasteride and pimecrolimus is the most effective therapy. Side effects associated with dutasteride are erectile dysfunction as well as breast tenderness and enlargement, while pimecrolimus produces a burning sensation. CASE REPORT: We present a 57-year-old postmenopausal female with a 3-year history of a scarring alopecic plaque in her frontotemporal region. Biopsy confirmed the diagnosis of FFA, and she was started on dutasteride 0.5 mg p.o. q.d., and later, topical pimecrolimus 1% b.i.d. was added. Eight months after initiating treatment, she showed hyperpigmentation on her metacarpophalangeal and interphalangeal joints, as well as on the cheeks and on the chin; dutasteride and pimecrolimus were discontinued. After 5 months of follow-up, her hyperpigmentation improved by 80% only by using photoprotection. CONCLUSION: Because of the variable clinical course of FFA, treatment is focused on halting its progression. Several therapeutic agents have been evaluated and the combination of dutasteride and pimecrolimus has shown a high response rate. There is no reported evidence of hyperpigmentation associated with this combination.
RESUMO
Pemphigus foliaceus (PF) is rarely described in the pediatric population with less than 40 cases reported in the literature. We report the case of an 11-year-old girl who was diagnosed with PF after 6 months of starting with symptoms and who responded well to therapy with oral dapsone. Although therapeutic guidelines for PF in children are lacking, oral corticosteroids in combination with dapsone have proven to be effective as first-line treatment in this setting.