Leprosy is caused by Mycobacterium leprae and has been known since biblical times. It
is still endemic in many regions of the world and a public health problem in Brazil.
The prevalence rate in 2011 reached 1.54 cases per 10,000 inhabitants in Brazil. The
mechanism of transmission of leprosy consists of prolonged close contact between
susceptible and genetically predisposed individuals and untreated multibacillary
patients. Transmission occurs through inhalation of bacilli present in upper airway
secretion. The nasal mucosa is the main entry or exit route of M. leprae. The deeper
understanding of the structural and biological characteristics of M. leprae, the
sequencing of its genome, along with the advances in understanding the mechanisms of
host immune response against the bacilli, dependent on genetic susceptibility, have
contributed to the understanding of the pathogenesis, variations in the clinical
characteristics, and progression of the disease. This article aims to update
dermatologist on epidemiological, clinical, and etiopathogenic leprosy aspects.
An intense inflammatory infiltrate in AC was predictive of an adjacent invasive SCC. In this study, the p53 protein immunoreactivity was not a marker of malignant transformation.
Dermatitis herpetiformis (DH) or Duhring-Brocq disease is a chronic bullous disease
characterized by intense itching and burning sensation in the erythematous papules
and urticarial plaques, grouped vesicles with centrifuge growth, and tense blisters.
There is an association with the genotypes HLA DR3, HLA DQw2, found in 80-90% of
cases. It is an IgA-mediated cutaneous disease, with immunoglobulin A deposits
appearing in a granular pattern at the top of the dermal papilla in the sublamina
densa area of the basement membrane, which is present both in affected skin and
healthy skin. The same protein IgA1 with J chain is found in the small intestinal
mucosa in patients with adult celiac disease, suggesting a strong association with
DH. Specific antibodies such as antiendomysium, antireticulina, antigliadin and,
recently identified, the epidermal and tissue transglutaminase subtypes, as well as
increased zonulin production, are common to both conditions, along with
gluten-sensitive enteropathy and DH. Autoimmune diseases present higher levels of
prevalence, such as thyroid (5-11%), pernicious anemia (1-3%), type 1 diabetes (1-2%)
and collagen tissue disease. The chosen treatment is dapsone and a gluten-free
diet.
Leprosy is a chronic infectious condition caused by Mycobacterium
leprae(M. leprae). It is endemic in many regions of the world and a
public health problem in Brazil. Additionally, it presents a wide spectrum of
clinical manifestations, which are dependent on the interaction between M.
leprae and host, and are related to the degree of immunity to the bacillus. The
diagnosis of this disease is a clinical one. However, in some situations
laboratory exams are necessary to confirm the diagnosis of leprosy or classify
its clinical form. This article aims to update dermatologists on leprosy,
through a review of complementary laboratory techniques that can be employed for
the diagnosis of leprosy, including Mitsuda intradermal reaction, skin smear
microscopy, histopathology, serology, immunohistochemistry, polymerase chain
reaction, imaging tests, electromyography, and blood tests. It also aims to
explain standard multidrug therapy regimens, the treatment of reactions and
resistant cases, immunotherapy with bacillus Calmette-Guérin (BCG) vaccine and
chemoprophylaxis.
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