Early diagnosis of leprosy remains primarily clinical, based on recognition of skin lesions with altered sensation and peripheral nerve involvement. However, complementary tests play crucial roles in confirming uncertain cases, guiding operational classification, detecting subclinical neural involvement, and distinguishing late reactions from relapse. This review synthesizes the practical application of diagnostic methods available to dermatologists. Slit-skin smear microscopy demonstrates high specificity but limited sensitivity in paucibacillary forms, while histopathology reveals the characteristic immunopathological spectrum, with perineural acid-fast bacilli being pathognomonic for leprosy. Molecular detection by PCR enhances diagnosis in paucibacillary cases (34%‒80% sensitivity) but cannot distinguish viable from non-viable bacilli, limiting its utility in post-treatment assessment. Anti-PGL-1 serology aids contact surveillance, with seropositive individuals showing 3.5-fold increased risk of developing disease, though sensitivity remains below 30% in tuberculoid forms. For neural evaluation, Semmes-Weinstein monofilament testing provides a standardized tactile threshold assessment, while the histamine test maps autonomic dysfunction, particularly valuable in indeterminate forms. Electrodiagnostic studies reveal early subclinical changes and monitor reaction-related neural deterioration. Peripheral nerve ultrasonography demonstrates superior sensitivity over palpation for detecting thickening (97.4% vs. 30% concordance) and identifies inflammatory activity through Doppler assessment. When evaluating post-treatment complications, an integrated approach combining bacteriological index trajectory, histopathological patterns, PCR cycle threshold values, and serological trends enables reliable differentiation between therapeutic failure, late reactions, and relapse. No single laboratory test confirms early leprosy in isolation; clinical dermato-neurological expertise remains paramount, with complementary tests interpreted within the epidemiological context to optimize diagnostic accuracy and therapeutic decisions.

Mycosis Fungoides (MF) is the commonest type of primary cutaneous T-Cell lymphomas representing about 50% of all lymphomas arising primarily in the skin. Janus kinases are non-receptor intracellular tyrosine kinases that play an important role in the pathogenesis of variant skin disorders and several hematological malignancies. The aim of this study was to investigate the gene expression of Janus Kinase-1 (JAK1) and Janus Kinase-3 (JAK3) in the skin of different types of MF patients using Real-time Quantitative Reverse Transcription Polymerase Chain Reaction (RT-PCR). The current study included 53 patients with MF, and 53 control samples. RT-PCR for JAK1 and JAK3 was done in the skin specimens obtained from patients and controls. Both JAK1 and JAK3 fold changes showed stepwise upregulation in lesional MF skin than normal control skin, with statistically significant increase in MF patients than healthy controls (p<0.001 and < 0.001 respectively). JAK1 was significantly upregulated in early-stage MF than JAK3 (p<0.001). Limitations of this study include the small sample size of some mycosis fungoides variants, such as erythrodermic MF. Further studies are needed to clarify the functional role of Janus kinase signaling pathways in MF pathogenesis. Both JAK1 and JAK3 play a role in the pathogenesis of MF. JAK1 may have a pathogenic role, particularly in the early stage of cutaneous T-cell lymphoma. This potentiates the idea of using JAK1 and JAK3 inhibitors for MF treatment.

BackgroundCutaneous Leishmaniasis (CL) affects up to 1.2 million people annually, mainly in resource-limited regions. Meglumine antimoniate, the standard treatment, is limited by systemic toxicity, injectable administration, and increasing resistance. Miltefosine, an oral alternative, offers practical advantages, although comparative efficacy and safety data remain inconsistent.ObjectiveTo compare the efficacy and safety of miltefosine versus meglumine antimoniate for New World CL.MethodsThe authors systematically searched PubMed, Embase, Scopus, and the Cochrane Library for randomized controlled trials directly comparing miltefosine and meglumine antimoniate. Risk Ratios (RRs) with 95% Confidence Intervals (95% CIs) were calculated using random-effects models. Heterogeneity was assessed with the I² statistic. Risk of bias was evaluated using the Cochrane RoB-2 tool. Certainty of evidence was assessed using the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) approach.ResultsEight trials involving 898 patients (502 treated with miltefosine, 396 with meglumine antimoniate) were included. Miltefosine showed significantly higher cure rates at two months (RR = 0.83; 95% CI: 0.71–0.98; I2 = 0%). Differences at six months were not statistically significant. Gastrointestinal side effects were more frequent with miltefosine, whereas hepatic enzyme elevations, arthralgia (RR = 10.08; 95% CI: 2.36–43.12), and fever (RR = 2.98; 95% CI: 1.53–5.80) were more common with meglumine antimoniate.Study LimitationsHigh heterogeneity, short follow-up, small sample sizes, and interstudy variability may limit precision.ConclusionMiltefosine shows superior early response and a safer systemic profile. However, the certainty of evidence, as assessed by GRADE, ranged from very low to high across outcomes, and long-term data remain limited, highlighting the need for further high-quality studies with extended follow-up.

BackgroundPsoriasis is a chronic, immune-mediated disease with a significant genetic component. The HLA-C*06:02 allele is one of the most strongly associated with the disease, particularly influencing early onset and severity. There are few current data on genetics in a Brazilian population with psoriasis.ObjectiveThis study aimed to investigate the genetic associations between human leucocyte antigen (HLA) alleles and psoriasis in a Brazilian admixed population.MethodsThe authors conducted HLA class I and II genotyping in 144 patients with psoriasis and compared the results with those of 720 controls. Additionally, the authors calculated the Psoriasis Area and Severity Index (PASI) and recorded whether the patient had current or previous systemic treatment for psoriasis and the age of disease onset.ResultsHLA-B*13:02g, B*15:01g, B*37:01g, B*38:01g, B*57:01g, B*57:02g, B*13:02g, C*01:02g, C*06:02g, C*12:03g, C*18:01g, DRB1*01:02g, DRB1*04:08g and DPB1*04:01g alleles were associated with an increased risk of psoriasis (after the Bonferroni correction factor, only the HLA-C*06:02 remained significant). And HLA-DRB1*15:03g conferred protection against psoriasis after Bonferroni correction. Alleles significantly associated with PASI score < 10 were A*34:02g (p = 0.037) and B*50:01g (p = 0.037), while the allele related to PASI > 10 was DRB1*01:01g (p = 0.049). When comparing the age of disease onset, the following alleles were significantly associated with early onset psoriasis (before 30 years of age): B*44:03g (p = 0.010) and C*07:02g (p = 0.022).Study limitationsThe sample size was small compared with other international publications, and the subgroup of patients with mild disease was less represented; however, the combination of analytical approaches (univariate tests, PCA, and correction for multiple comparisons) reinforces the robustness of the work.ConclusionThe present findings highlight the genetic complexity of psoriasis in a diverse population and suggest that it may not be directly linked to specific genetic factors. Further research is required to explore the environmental and genetic interactions that contribute to psoriasis pathogenesis.

BackgroundMycosis fungoides is the commonest type of cutaneous T-Cell lymphoma. Janus kinases are intracellular tyrosine kinases that have recently been proven to have a crucial role in the pathogenesis and progression of several dermatological and malignant diseases.ObjectiveThe aim of this study was to investigate the immunohistochemical expression of Janus Kinase-1 (JAK1) and Janus Kinase-3 (JAK3) in the skin of mycosis fungoides .MethodsThe current study included 46 patients with early-stage MF, and 7 patients with late-stage MF, and 53 control samples. Immunohistochemical staining using JAK1 and JAK3 monoclonal antibodies was done in the skin specimens obtained from patients and controls. The evaluation of JAK1 and JAK3 gene expression using RT-PCR will be included in part 2 of the study.ResultsJAK1 immunohistochemical expression was nuclear, and JAK3 was cytoplasmic in MF patients. Immunoreactivity scores for JAK1 and JAK3 in MF patients were significantly increased compared to healthy controls (p < 0.001 and < 0.001, respectively). JAK1 and JAK3 immunoreactivity scores were significantly higher in the tumor than in the patch and plaque stages of MF (P7 = 0.001 and 0.004, respectively).Study limitationsThis study is limited by the relatively small sample size of some clinical variants of mycosis fungoides, particularly advanced forms such as erythrodermic and tumor-stage MF. Further studies are needed to evaluate JAK1 and JAK3 expression following therapeutic interventions, including phototherapy and JAK inhibitors.ConclusionsJAK1 and JAK3 were significantly expressed in MF skin lesions in comparison to normal controls. JAK1 and JAK3 were more expressed in the tumor stage than patch and plaque stage MF, suggesting that JAK1 and JAK3 could play a crucial role in MF pathogenesis, progression, and prognosis.