Since the first reports of AIDS, skin involvement has become a burdensome stigma for seropositive patients and a challenging task for dermatologist and infectious disease specialists due to the severe and recalcitrant nature of the conditions. Dermatologic manifestations in AIDS patients act as markers of disease progression, a fact that enhances the importance of understanding their pathogenesis.Broadly, cutaneous disorders associated with HIV type-1 infection can be classified as primary and secondary. While the pathogenesis of secondary complications, such as opportunistic infections and skin tumours, is directly correlated with a decline in the CD4+ T cell count, the origin of the certain manifestations primarily associated with the retroviral infection itself still remains under investigation.The focus of this review is to highlight the immunological phenomena that occur in the skin of HIV-1-seropositive patients, which ultimately lead to skin disorders, such as seborrhoeic dermatitis, atopic dermatitis, psoriasis and eosinophilic folliculitis. Furthermore, we compile the latest data on how shifts in the cytokines milieu, impairments of the innate immune compartment, reactions to xenobiotics and autoimmunity are causative agents in HIV-1-driven skin diseases. Additionally, we provide a thorough analysis of the small animal models currently used to study HIV-1-associated skin complications, centering on transgenic rodent models, which unfortunately, have not been able to fully unveil the role of HIV-1 genes in the pathogenesis of their primarily associated dermatological manifestations.

Erythema nodosum is the most common form of panniculitis and is characterized by tender erythematous nodules mainly in the lower limbs on the pretibial area. The exact cause of erythema nodosum is unknown, although it appears to be a hypersensitivity response to a variety of antigenic stimuli. Although the etiology is mostly idiopathic, ruling out an underlying disease is imperative before diagnosing primary erythema nodosum. Erythema nodosum can be the first sign of a systemic disease that is triggered by a large group of processes, such as infections, inflammatory diseases, neoplasia, and/or drugs. The most common identifiable causes are streptococcal infections, primary tuberculosis, sarcoidosis, Behçet disease, inflammatory bowel disease, drugs, and pregnancy. We propose a diagnostic algorithm to optimize the initial work-up, hence initiating prompt and accurate management of the underlying disease. The algorithm includes an initial assessment of core symptoms, diagnostic work-up, differential diagnosis, and recommended therapies. Several treatment options for the erythema nodosum lesions have been previously reported; nevertheless, these options treat the symptoms, but not the triggering cause. Making an accurate diagnosis will allow the physician to treat the underlying cause and determine an optimal therapeutic strategy.

Our results support the recommendation for assessing insulin resistance and cardiovascular-related features and disorders in all young males with stage III or higher AGA, according to the Hamilton-Norwood classification.

Worldwide, more than 1.9 billion adults are overweight, and around 600 million people suffer from obesity. Similarly, ~382 million individuals live with diabetes, and 40–50% of the global population is labeled at “high risk” (i.e., prediabetes). The impact of these two chronic conditions relies not only on the burden of illnesses per se (i.e., associated increased morbidity and mortality), but also on their increased cost, burden of treatment, and decreased health-related quality of life. For this review a comprehensive search in several databases including PubMed (MEDLINE), Ovid EMBASE, Web of Science, and Scopus was conducted. In both diabetes and obesity, genetic, epigenetic, and environmental factors overlap and are inclusive rather than exclusive. De facto, 70–80% of the patients with obesity and virtually every patient with type 2 diabetes have insulin resistance. Insulin resistance is a well-known pathophysiologic factor in the development of type 2 diabetes, characteristically appearing years before its diagnosis. The gold standard for insulin resistance diagnosis (the euglycemic insulin clamp) is a complex, invasive, costly, and hence unfeasible test to implement in clinical practice. Likewise, laboratory measures and derived indexes [e.g., homeostasis model assessment of insulin resistance (HOMA-IR-)] are indirect, imprecise, and not highly accurate and reproducible tests. However, skin manifestations of insulin resistance (e.g., acrochordons, acanthosis nigricans, androgenetic alopecia, acne, hirsutism) offer a reliable, straightforward, and real-time way to detect insulin resistance. The objective of this review is to aid clinicians in recognizing skin manifestations of insulin resistance. Diagnosing these skin manifestations accurately may cascade positively in the patient’s health by triggering an adequate metabolic evaluation, a timely treatment or referral with the ultimate objective of decreasing diabetes and obesity burden, and improving the health and the quality of care for these patients.

These results demonstrate the clinical benefit of combining A/BPO with lymecycline in the treatment of moderate to severe acne vulgaris.

Psoriasis is a complex genetic disease, which has previously been associated with numerous single nucleotide polymorphisms (SNPs) that are implicated in various processes, including skin barrier functions and in the regulation of inflammatory and immune responses. The present study aimed to investigate the genotypic and allelic frequencies of 32 SNPs at 24 genetic loci, and their association with psoriasis in a Mexican population. These SNPs, which were associated with psoriasis in previous studies, included the following genes: Major histocompatibility complex class I-C (HLA-C), interleukin (IL)-12B, IL-23R, IL-23A, IL-28RA, tumor necrosis factor (TNF)-α, ring finger protein-114 (RNF114), cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1, late cornified envelope 3B/3C, signal transducer and activator of transcription 4, LINC01185, interferon induced with helicase C domain 1, IL-13, TNF-α-induced protein 3 (TNFAIP3), TNFAIP3 interacting protein 1, endoplasmic reticulum aminopeptidase 1, TNF receptor-associated factor interacting protein 2, Leptin, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha, F-box and leucine-rich repeat protein 19, nitric oxide synthase 2, cluster of differentiation 40, nuclear receptor coactivator 5, and ADAM metallopeptidase domain 33. A total of 32 male and 14 female subjects with a clinical diagnosis of chronic plaque psoriasis, as well as 103 control subjects, were analyzed. Molecular analyses were performed using TaqMan® assays in a TaqMan® OpenArray® Genotyping system. Results were analyzed using the Golden Helix SNP and Variation Suite 7 program. Of the 32 SNPs, six were associated with an increased risk of developing psoriasis, including: HLA-C rs10484554 [allele T: odds ratio (OR) 3.51], IL-12B rs3212227 (allele T: OR 1.88), IL-12B rs3213094 (allele C: OR 1.94), HLA complex group 27 rs1265181 (allele C: OR 2.83), annexin A6 rs17728338 (allele A: OR 2.41), and RNF114 rs6125829 (allele G: OR 1.98). Fisher's exact test detected statistical significance; however, following false discovery rate and Bonferroni correction, this association was no longer significant (threshold for genome-wide significance, P<1.56×10−3). SNPs that were associated with an increased risk of psoriasis in the present study have previously been associated with psoriasis in European, American, and Asian populations. In order to establish genome-wide significance, future studies must analyze a greater sample size. To the best of our knowledge, the present pilot study is the first to investigate the association between these 32 SNPs and psoriasis in a Mexican Mestizo population.

This is a narrative review of azathioprine. This medication is immunomodulatory and immunosuppressive, and it has been used widely through different medical specialties to modify disease. It has been proven useful for several dermatoses and it has encountered success when used as an off-label indication for other dermatologic diseases. Its mechanism of action is described thoroughly, as well as precautions for monitoring adequate levels in patients using it. Dermatologists should also be aware of the possible adverse events it may present. In dermatology it can be used in bullous and autoimmune diseases, and in other conditions, including intractable pruritus, atopic dermatitis, photodermatoses, psoriasis, and others. Azathioprine offers an alternative as a steroid-sparing agent and this review helps dermatologists prescribe it safely to all patients who require it.

An 86-year-old female patient from northeast Mexico presented with diffuse lepromatous leprosy (DLL). Sequence analysis of four genes (rrs, rpoB, sigA, and hsp65) from the skin biopsy specimen identified "Mycobacterium lepromatosis." This is the first independent confirmation of a case of DLL due to M. lepromatosis. CASE REPORTIn 2005, an 86-year-old female with no prior medical history of leprosy was admitted to our hospital due to a 10-day bout of distal cyanosis of the extremities (Fig. 1). Physical examination also showed generalized dermatosis characterized by diffuse infiltration of the skin, predominantly in the face, with thickening of the superciliary region and ears plus an accompanying absence of eyebrows and eyelashes. In the rest of the body, the skin had an atrophic "cigarette paper"-like appearance and diminished or absent body hair. The neurological examination revealed extensive areas of dysesthesia. The areas of diffuse lepromatous leprosy (DLL) associated with Lucio's phenomenon were characterized by a purpuric appearance, with necrosis and ulceration in some of the areas, leading to sloughing in acral sites such as fingers and toes. A presumptive diagnosis of cryoglobulinemia versus other vasculitis disorders was considered, and laboratory examination showed microcytic hypochromic anemia, thrombocytosis, leukocytosis, and a rheumatoid factor of 80. A skin biopsy was performed and treatment with pentoxifylline initiated. During the first week, the rheumatologist prescribed cyclophosphamide, but the patient did not improve and developed necrosis in areas that were previously cyanotic (Fig. 1). The skin biopsy specimen showed vasculitis with thrombosis and perivascular and periadnexial lymphocytic infiltrates (Fig. 2) as well as numerous acid-fast bacilli, leading to diagnosis of diffuse lepromatous leprosy (DLL) and Lucio's phenomenon. Treatment with prednisone and multidrug therapy for multibacillary leprosy was initiated. The patient improved after 10 days of treatment, was discharged after 2 weeks in stable condition, but died at home 3 months later of unknown cause.Leprosy is one of the oldest recorded human afflictions. Depending upon the immune response mounted against the bacilli, the disease presents with a broad clinical spectrum. At one pole are the tuberculoid (TT) patients, with effective T cell-mediated immunity resulting in very low bacterial numbers, while at the other, the lepromatous (LL) patients mount an ineffective humoral response and exhibit a high bacillary load. Other unstable forms, with characteristics between these poles, can also be observed. A particular variation of lepromatous leprosy involving diffuse nonnodular lesions is more frequent in Mexico and the Caribbean than in any other part of the world (2). This variation has been referred to as diffuse lepromatous leprosy (DLL) or Lucio's phenomenon (6, 11).All these forms of leprosy have been attributed to various host responses to the causative pathogen, Mycobacterium leprae. However, M. leprae exhibits exception...