Treatment of Pain in Keloids Using Only a Long-Pulsed 1064 nm Nd:YAG Laser.

BACKGROUND AND OBJECTIVE: Keloids are benign lesions arising from overproduction of the extracellular matrix and abnormal collagen deposition by dermal fibroblasts. This altered wound healing typically occurs in response to dermal trauma. Keloid treatment poses a challenge due to the variable nature of treatment response, which can be affected by the size, appearance, and associated symptoms of erythema, pruritus, and pain. Recently, successful treatment of keloids has been reported using the Nd:YAG laser in conjunction with 5-fluorouracil and intralesional corticosteroids. We present a series of patients with symptomatic keloids, who we treated with only a 1064 nm Nd:YAG laser. STUDY DESIGN/MATERIALS AND METHODS: Eight patients of Fitzpatrick skin types I-VI presented for treatment of keloids with associated symptoms of pain. The keloids were most commonly located on the trunk, and seven patients had intralesional steroid injections prior to presentation with persistence of symptoms. Patient treatment consisted of two passes under a long-pulsed 1064 nm Nd:YAG laser with a 10 mm spot size, a fluence of 18-19 J/cm2 , and 60 ms pulse duration every 3-8 weeks. Patient-reported pain scores were collected before and after treatment. RESULTS: Following treatment, transient erythema and mild edema were noted at the treatment site. All patients reported improvement in the symptoms of pain, with an average of a 5-point reduction using a 10-point scale (R: 2-10). Five out of eight patients had total resolution of their pain. An average of 3.25 treatments (R:1-5) were needed for patients to first notice an improvement in the pain. A Wilcoxon signed-rank test showed that treatment with a 1064 nm laser elicited a statistically significant improvement in pain in individuals with keloids (Z = 2.46, P = 0.01). No patients in our study suffered any scarring or pigment changes as a result of these treatments. CONCLUSION: Keloids are a common condition with variable rates of treatment satisfaction. Lasers have been used in an attempt to improve clinical appearance and associated symptoms. We report a significant reduction in pain for patients treated exclusively with a 1064 nm Nd:YAG laser. Lasers Surg. Med. © 2020 Wiley Periodicals LLC.

Immunoglobulin and Complement Immunohistochemistry on Paraffin Sections in Autoimmune Bullous Diseases: A Systematic Review and Meta-analysis.

ABSTRACT: Immunohistochemistry (IHC) on formalin-fixed, paraffin-embedded tissue has been proposed as a potential tool in the diagnosis of autoimmune bullous diseases (AIBDs) in lieu of standard direct immunofluorescence (DIF) microscopy. To comprehensively determine the diagnostic accuracy of immunoglobulin and complement IHC for diagnosis of AIBDs, we conducted a systematic review and multivariate Bayesian model-based meta-analysis of the literature. Quality and heterogeneity assessment of studies was performed using the Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) checklist and the I2 index, respectively. Electronic searches using PubMed from April 1964 to July 2020 identified 14 articles meeting predetermined inclusion and exclusion criteria. Median sensitivities with 95% credible intervals in pemphigus and pemphigoid were 0.24 (0.01-0.89) and 0.22 (0.02-0.77) with immunoglobulin G (IgG), 0.77 (0.39-0.95) and 0.25 (0.02-0.85) with IgG4, 0.11 (0.02-0.32) and 0.86 (0.56-0.98) with C3d, and 0.84 (0.56-0.97) and 0.75 (0.37-0.94) with C4d, respectively. Specificities were 1.00 (0.00-1.00) with IgG, 0.98 (0.89-1.00) with IgG4, 0.99 (0.97-1.00) with C3d, and 0.99 (0.97-1.00) with C4d. The risk of bias and heterogeneity among studies was a serious problem, decreasing the level of evidence. Our work suggests that, in selected cases, paraffin-based IHC may be a helpful procedure to screen for AIBDs, especially when specialized laboratories and/or biopsy specimens for DIF do not exist. Nevertheless, more studies with a refined quality design are needed to explore the true usefulness of this diagnostic method in AIBDs.

Cutaneous metastases: A great imitator.

Neoplastic cells originating from a primary cancer can uncommonly spread to the skin, where they suggest a poor prognosis for the patient. In women, melanoma, breast, ovarian, oral cavity, and lung are the most common primary sources; in men, melanoma, lung, colon, and squamous cell carcinoma of the head and neck predominate. The classic presentation of cutaneous metastases is a firm, painless, flesh-colored to an erythematous dermal nodule (or nodules); however, several other presentations, including inflammatory, cicatricial, and bullous lesions, have been reported. Cutaneous metastases may also mimic benign conditions such as lipomas, hemangiomas, or cellulitis. A high degree of clinical suspicion is necessary, and the diagnosis is confirmed by biopsy, which may also be used to establish the primary malignancy if unknown, as the histopathologic appearance of the metastatic tissue may mimic the primary tumor. Treatments include excision of the metastases, chemotherapy, immunotherapy, radiation, and/or palliative care.

Periodontitis in oral pemphigus and pemphigoid: A systematic review of published studies.

Periodontitis and autoimmune bullous diseases, including pemphigus vulgaris and mucous membrane pemphigoid, are immunoinflammatory disorders leading to microbial plaque- and autoantibody-elicited tissue injury of the oral cavity, respectively. Evidence indicates that these autoimmune conditions may represent a risk factor for periodontitis, but no systematic evaluation exists to corroborate this assumption. A systematic literature review of periodontal status in pemphigus and pemphigoid was conducted. Electronic searches using PubMed from inception to July 2016 identified 10 studies meeting predetermined inclusion and exclusion criteria. Most reported some correlation between poor periodontal health and both oral pemphigus vulgaris and mucous membrane pemphigoid. Some demonstrated beneficial effects of oral hygiene procedures on periodontal parameters and clinical disease severity of the established blistering diseases. Inconsistent results were found between studies and within analyzed patient cohorts, likely because of methodological shortcomings. This review preliminarily suggests that patients with oral pemphigus vulgaris and mucous membrane pemphigoid appear somewhat more susceptible to periodontitis, which in turn may potentially trigger the bullous disorders. These patients should be encouraged by dermatologists to pursue collaborative professional periodontal follow-up with dentists. The true relationship and mutual interaction between both diseases needs to be more comprehensively addressed in well-designed prospective studies.

Fixed drug eruption related to fluconazole.

Fixed drug eruption (FDE) is a type of cutaneous drug reaction that occurs at the same sites upon re-exposure to specific medications. Herein we discuss the case of a 23-year-old man with a FDE to fluconazole.

Bed bugs and possible transmission of human pathogens: a systematic review.

The global population of bed bugs (Cimex lectularius and Cimex hemipterus, family Cimicidae) has undergone a significant resurgence since the late 1990s. This is likely due to an increase in global travel, trade, and the number of insecticide-resistant bed bugs. The global bed bug population is estimated to be increasing by 100-500 % annually. The worldwide spread of bed bugs is concerning, because they are a significant socioeconomic burden and a major concern to public health. According to the United States Environmental Protection Agency, bed bugs are "a pest of significant health importance." Additionally, 68 % of U.S. pest professionals reported that bed bugs are the most challenging pest to treat. Upwards of 45 disease pathogens have been reported in bed bugs. Recent studies report that bed bugs may be competent vectors for pathogens, such as Bartonella quintana and Trypanosoma cruzi. However, public health reports have thus far failed to produce evidence that major infectious disease outbreaks have been associated with bed bugs. Since many disease pathogens have previously been reported in bed bugs and the worldwide bed bug population is now drastically increasing, it stands to reason to wonder if bed bugs might transmit human pathogens. This review includes a literature search on recently published clinical and laboratory studies (1990-2016) investigating bed bugs as potential vectors of infectious disease, and reports the significant findings and limitations of the reviewed studies. To date, no published study has demonstrated a causal relationship between bed bugs and infectious disease transmission in humans. Also, we present and propose to expand on previous hypotheses as to why bed bugs do not transmit human pathogens. Bed bugs may contain "neutralizing factors" that attenuate pathogen virulence and, thereby, decrease the ability of bed bugs to transmit infectious disease.

Mercury toxicity presenting as acrodynia and a papulovesicular eruption in a 5-year-old girl.

Acrodynia is a reaction that occurs in children who have been exposed to mercury. Mercury toxicity has systemic manifestations as well as cutaneous manifestations, which can appear similar to those found in a number of other diseases. We present a case of acrodynia caused by mercury exposure in a previously healthy 5-year-old girl who developed hypertension, palmoplantar pruritus, and a papulovesicular eruption.

Biochemical and functional characterization of CpMuc4, a Cryptosporidium surface antigen that binds to host epithelial cells.

Cryptosporidium spp. are intracellular apicomplexan parasites that cause outbreaks of waterborne diarrheal disease worldwide. Previous studies had identified a Cryptosporidium parvum sporozoite antigen, CpMuc4, that appeared to be involved in attachment and invasion of the parasite into intestinal epithelial cells. CpMuc4 is predicted to be O- and N-glycosylated and the antigen exhibits an apparent molecular weight 10kDa larger than the antigen expressed in Escherichia coli, indicative of post-translational modifications. However, lectin blotting and enzymatic and chemical deglycosylation did not identify any glycans on the native antigen. Expression of CpMuc4 in Toxoplasma gondii produced a recombinant protein of a similar molecular weight to the native antigen. Both purified native CpMuc4 and T. gondii recombinant CpMuc4, but not CpMuc4 expressed in E. coli, bind to fixed Caco-2A cells in a dose dependent and saturable manner, suggesting that this antigen bears epitopes that bind to a host cell receptor, and that the T. gondii recombinant CpMuc4 functionally mimics the native antigen. Binding of native CpMuc4 to Caco2A cells could not be inhibited with excess CpMuc4 peptide, or an excess of E. coli recombinant CpMuc4. These data suggest that CpMuc4 interacts directly with a host cell receptor and that post-translational modifications are necessary for the antigen to bind to the host cell receptor. T. gondii recombinant CpMuc4 may mimic the native antigen well enough to serve as a useful tool for identifying the host cell receptor and determining the role of native CpMuc4 in host cell invasion.

Psoriasis patients are enriched for genetic variants that protect against HIV-1 disease.

An important paradigm in evolutionary genetics is that of a delicate balance between genetic variants that favorably boost host control of infection but which may unfavorably increase susceptibility to autoimmune disease. Here, we investigated whether patients with psoriasis, a common immune-mediated disease of the skin, are enriched for genetic variants that limit the ability of HIV-1 virus to replicate after infection. We analyzed the HLA class I and class II alleles of 1,727 Caucasian psoriasis cases and 3,581 controls and found that psoriasis patients are significantly more likely than controls to have gene variants that are protective against HIV-1 disease. This includes several HLA class I alleles associated with HIV-1 control; amino acid residues at HLA-B positions 67, 70, and 97 that mediate HIV-1 peptide binding; and the deletion polymorphism rs67384697 associated with high surface expression of HLA-C. We also found that the compound genotype KIR3DS1 plus HLA-B Bw4-80I, which respectively encode a natural killer cell activating receptor and its putative ligand, significantly increased psoriasis susceptibility. This compound genotype has also been associated with delay of progression to AIDS. Together, our results suggest that genetic variants that contribute to anti-viral immunity may predispose to the development of psoriasis.

Protective effect of human endogenous retrovirus K dUTPase variants on psoriasis susceptibility.

Previous genetic and functional studies have implicated the human endogenous retrovirus K (HERV-K) dUTPase located within the PSORS1 locus in the major histocompatibility complex region as a candidate psoriasis gene. Here, we describe a variant discovery and case-control association study of HERV-K dUTPase variants in 708 psoriasis cases and 349 healthy controls. Five common HERV-K dUTPase variants were found to be highly associated with psoriasis, with the strongest association occurring at the missense single-nucleotide polymorphism (SNP) rs3134774 (K158R, P=3.28 × 10(-15), odds ratio =2.36 (95% confidence interval: 1.91-2.92)). After adjusting the association of the HERV-K dUTPase variants for the potential confounding effects of HLA alleles associated with psoriasis, the HERV-K SNPs rs9264082 and rs3134774 remained significantly associated. Haplotype analysis revealed that HERV-K haplotypes containing the non-risk alleles for rs3134774 and rs9264082 significantly reduced the risk of psoriasis. Functional testing showed higher antibody responses against recombinant HERV-K dUTPase in psoriasis patients compared with controls (P<0.05), as well as higher T-cell responses against a single HERV-K dUTPase peptide (P<0.05). Our data support an independent role for the HERV-K dUTPase on psoriasis susceptibility, and suggest the need for additional studies to clarify the role of this dUTPase in the pathogenesis of psoriasis.

Serum antibody responses to polymorphic Cryptosporidium mucin antigen in Bangladeshi children with cryptosporidiosis.

Cryptosporidium is a significant cause of diarrheal disease in children in developing countries. The sporozoite antigen Muc4 is important for infection of host cells, and could be a candidate vaccine antigen. However, this antigen is polymorphic between Cryptosporidium hominis and C. parvum. We investigated antibody responses to C. hominis Muc4 and C. parvum Muc4 antigen in children in Bangladesh infected with C. hominis. Antibody responses were compared between children with cryptosporidial diarrhea (cases) and uninfected children with diarrhea (controls). There was a significant IgM response to Muc4 from both species in cases compared with controls, which increased over time, and was higher in children with persistent diarrhea. Despite sequence polymorphisms, antibody responses to C. hominis Muc4 and C. parvum Muc4 were significantly correlated. These results suggest that the human antibody response to Muc4 is cross-reactive between species, but in young children does not mature to an IgG response within the period observed in this study.