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Abstract Fluoroscopy-induced chronic radiation dermatitis (FICRD) is a complication of fluoroscopy-guided intervention. Unlike acute radiation dermatitis, FICRD is different as delayed onset and usually appears without preexisting acute dermatitis. Unfortunately, the chronic and progressive pathology of FICRD makes it difficult to treat, and some patients need to receive wide excision and reconstruction surgery. Due to lack of standard treatment, investigating underlying mechanism is needed in order to develop an effective therapy. Herein, the Hippo pathway is specifically identified using an RNA-seq analysis in mild damaged skin specimens of patients with FICRD. Furthermore, specific increase of the Yes-associated protein (YAP1), an effector of the Hippo pathway, in skin region with mild damage plays a protective role for keratinocytes via positively regulating the numerous downstream genes involved in different biological processes. Interestingly, irradiated-keratinocytes inhibit activation of fibroblasts under TGF-β1 treatment via remote control by an exosome containing YAP1. More importantly, targeting one of YAP1 downstream genes, nuclear receptor subfamily 3 group C member 1 (NR3C1), which encodes glucocorticoid receptor, has revealed its therapeutic potential to treat FICRD by inhibiting fibroblasts activation in vitro and preventing formation of radiation ulcers in a mouse model and in patients with FICRD. Taken together, this translational research demonstrates the critical role of YAP1 in FICRD and identification of a feasible, effective therapy for patients with FICRD. Key messages • YAP1 overexpression in skin specimens of radiation dermatitis from FICRD patient. • Radiation-induced YAP1 expression plays protective roles by promoting DNA damage repair and inhibiting fibrosis via remote control of exosomal YAP1. • YAP1 positively regulates NR3C1 which encodes glucocorticoid receptor expression. • Targeting glucocorticoid receptor by prednisolone has therapeutic potential for FICRD patient.

Herpes zoster (HZ), which is caused by reactivation of the latent varicella zoster virus, was not listed as a side effect of any vaccines until the introduction of coronavirus disease 2019 (COVID-19) vaccine. This study used a nationwide population database to examine whether the HZ risk is increased after receiving the influenza vaccination.This population-based retrospective self-controlled case series evaluated the association between influenza vaccine exposure and HZ risk. Data were collected from Taiwan's National Health Insurance Research Database between 2015 and 2017. Patients with HZ diagnosed within 6 months before and after receiving the influenza vaccination were included. After receiving the influenza vaccine, the first 15 and 30 days were defined as risk intervals, while the other periods were defined as control intervals. Poisson regression was used to compare the incidence rate ratio (IRR) for HZ during the risk interval vs. the control interval.In total, 13,728 patients were diagnosed with HZ before and after receiving the influenza vaccine. The IRR for days 1-15 was significantly higher (IRR = 1.11; 95% confidence interval [CI], 1.02-1.20), but insignificant for days 1-30 (IRR = 1.04; 95% CI, 0.98-1.10). In a subgroup analysis, the IRRs were significantly higher in participants, including 50-64 years old (1.16; 95% CI, 1.02-1.33), males (1.14; 95% CI, 1.01-1.28), and healthier individuals (i.e., no history of cancer or autoimmune diseases).There was a slight increase in risk of HZ in people receiving influenza vaccine in the first 1-15 days after vaccination.

SR-T100 gel, containing solamargine extracted from Solanum undatum (synonym: Solanum incanum), had good therapeutic effects on actinic keratosis (AK) in human and ultraviolet B-induced papilloma in mice. This study aimed to investigate the immunohistochemical changes in the human skin after SR-T100 treatment. An immunohistochemical study was performed and the changes in photocarcinogenesis and photoaging markers after 16-week SR-T100 gel treatment were documented. SR-T100 gel treatment for 16 weeks resulted in complete remission in nine AK lesions and partial remission in four AK lesions. SR-T100 gel abolished the expression of mutant p53 and SOX2 and restored the expression of NOTCH1. Additionally, SR-T100 gel improved wrinkling in human skin, while restoring the expression of lamin B1 and increasing synthesis of new elastic fibers. SR-T100 gel had therapeutic effects on photocarcinogenesis and photoaging of photodamaged skin with AK.

A novel fractional laser system with differential-wavelength modified optically pumped semiconductor technology can produce a pure 585 nm wavelength as pulsed dye laser, which has been used to treat vascular, pigmented skin lesions. Besides, this new laser modality also showed promising results for verruca plana in our experience. In this brief report, we present three cases of facial flat warts treated by this novel 585 nm diode laser.

Hintergrund und ziele Die histopathologische Diagnose eines Fluoroskopie-induzierten Rontgenulkus (RU) kann eine Herausforderung darstellen, insbesondere wenn keine Informationen uber eine vorausgegangene Strahlenexposition vorliegen. Die wichtigste Differenzialdiagnose ist die zirkumskripte Sklerodermie (ZS). Ziel dieser Studie war die Identifikation klinischer und histopathologischer Merkmale, mit deren Hilfe sich RU und ZS unterscheiden lassen. Patienten und methodik Wir fuhrten eine retrospektive Studie an 25 Proben von 15 Patienten mit RU und 21 Proben von 21 Patienten mit ZS durch. Die klinischen Befunde und histopathologischen Merkmale wurden analysiert. Ergebnisse Dreizehn von 15 RU-Patienten (86,7 %) hatten sich wegen einer koronaren Herzkrankheit einer Angioplastie unterzogen, bei elf Patienten befanden sich die Lasionen unterhalb des rechten Schulterblatts. Im Vergleich zu ZS-Patienten zeigten sich bei RU-Patienten haufiger nichtentzundliche Infiltrate (28 %), atypische „bizarre“ Fibroblasten (100 %), Sklerosen (48 %), Teleangiektasien (96 %), Gefasschaden (64 %) und Verlust von Hautanhangsgebilden (100 %). Bei der ZS waren bizarre Fibroblasten selten (14 %), wahrend Teleangiektasien (62 %) und Verlust von Hautanhangsgebilden (62 %) unterschiedlich haufig auftraten. Der Verlust von CD34+ -Zellen und die Kompression elastischer Fasern waren nicht geeignet, um zwischen RU und ZS zu unterscheiden. Schlussfolgerungen Hautlasionen im rechten subskapularen Bereich mit Nachweis von bizarren Fibroblasten, Sklerosen, Teleangiektasien und Verlust von Hautanhangsgebilden in der Histologie sind sehr charakteristisch fur Strahlenschaden im Zusammenhang mit einer Durchleuchtung bei Angiographie.

Background and objectives Histopathologic diagnosis of fluoroscopy-induced radiation ulcer (FIRU) can be challenging if the past history of radiation exposure is unknown. Morphea is the most important differential diagnosis. This study was intended to identify clinical and pathologic features that can be used to distinguish FIRU from morphea. Patients and methods We performed a retrospective study on 25 specimens from 15 patients with FIRU and 21 specimens from 21 patients with morphea. Clinical findings and pathological features were analyzed. Results Thirteen of 15 patients (86.7 %) with FIRU underwent angioplasty for coronary artery disease, and eleven patients had lesions in the right subscapular area. Compared with morphea, FIRU patients were more likely to display non-inflammatory infiltrates (28 %), bizarre fibroblasts (100 %), sclerosis (48 %), telangiectasia (96 %), vascular damage (64 %), and loss of skin appendages (100 %). In morphea, bizarre fibroblasts were rare (14 %), while telangiectasia (62 %) and loss of skin appendages (62 %) were variable. Loss of CD34+ cells and compression of elastic fibers could not be used to distinguish between FIRU and morphea. Conclusions Skin lesion in the right subscapular area with presence of bizarre fibroblasts, sclerosis, telangiectasia, and loss of cutaneous appendages as seen with histology are highly characteristic of the radiation damage associated with fluoroscopic angiography.

Background: Heart failure (HF) is one of the important complications of acute myocardial infarction (AMI), but the epidemiology, associated risks and outcomes have not been well investigated in the era of broad use of fluoroscopy-guided angiographic intervention. Methods: We analysed 161,384 subjects who had experienced the first episode of AMI during 1 January 2000 and 31 December 2012 using the Taiwan National Health Insurance Research Database. Results: During the index AMI hospitalization, 23.6% of cases developed HF. Female, ≥65 years-old, non-ST-segment elevation type of MI, diabetes mellitus (DM), peripheral vascular occlusion disease (PAOD), chronic obstructive pulmonary disease (COPD), atrial fibrillation, and ventricular tachycardia/fibrillation (VT/VF) were associated with higher risks of developing HF. HF cases had inferior survival outcomes compared to non-HF cases in both the short and long term. Among those HF patients, ≥65 years, DM, PAOD, and VT/VF were associated with worse outcomes. On the contrary, coronary reperfusion intervention and treat-to-target pharmacologic treatment were associated with favourable survival outcomes. Conclusions: HF remains common in the modern age and poses negative impacts in survival of AMI patients. It highlights that prudent prevention and early treatment of HF during AMI hospitalization is an important medical issue.

Backgrounds: Reducing radiation exposure is the basic principle for performing percutaneous coronary intervention (PCI). Many studies have confirmed the effect of radiation protection for medical staff, but studies about the effectiveness of protection for patients and real measurement of radiation dose in patients’ specific organs are lacking. Aim: To measure the radiation doses absorbed by patients’ radiosensitive organs during PCI and the effectiveness of radiation protection. Methods: A total of 120 patients were included and allocated into three groups as the ratio of 1:1:2. A total of 30 patients received PCI at 15 frames rate per second (fps), 30 patients at 7.5 fps, and 60 patients wore radiation protective hat and glasses during PCI at 7.5 fps. The radiation doses were measured at right eyebrow (lens), neck (thyroid), back (skin), and inguinal area (genital organs) by using thermoluminescent dosimeters (TLDs). Results: Dose-area product (DAP) reduced by 58.8% (from 534,454 ± 344,660 to 220,352 ± 164,101 mGy·cm2, p &lt, 0.001) after reducing the frame rate, without affecting successful rate of PCI. Radiation doses measured on skin, lens, genital organs, and thyroid decreased by 73.3%, 40.0%, 40.0%, and 35.3%, respectively (from 192.58 ± 349.45 to 51.10 ± 59.21, 5.29 ± 4.27 to 3.16 ± 2.73, 0.25 ± 0.15 to 0.15 ± 0.15, and 17.42 ± 12.11 to 11.27 ± 8.52 μSv, p &lt, 0.05). By providing radiation protective equipment, radiation doses at lens and thyroid decreased further by 71.8% and 65.9% (from 3.16 ± 2.73 to 0.89 ± 0.79, 11.27 ± 8.52 to 3.84 ± 3.49 μSv, p &lt, 0.05). Conclusions: By lowering the frame rate and providing protective equipment, radiation exposure in radiosensitive organs can be effectively reduced in patients.

ImportanceAlthough influenza vaccination has been associated with Guillain-Barré syndrome (GBS), the findings among studies of older adult populations are inconsistent.ObjectiveTo determine the risk of GBS after influenza vaccination among older adults.Design, Setting, and ParticipantsThis cross-sectional study incorporated a self-controlled case series design. Days 1 to 7, days 1 to 14, and days 1 to 42 after influenza vaccination were identified as risk intervals; days 8 to 180, days 15 to 180, and days 43 to 180 comprised the corresponding control interval. Population-based data were obtained from Taiwan’s National Health Insurance research database between January 1, 2003, and December 31, 2017. Data were analyzed from November 1, 2021, through February 28, 2022. Adults 65 years or older who developed GBS within 180 days after influenza vaccination were enrolled.ExposureGovernment-funded seasonal influenza vaccination.Main Outcomes and MeasuresOnset of GBS during risk intervals after influenza vaccination compared with control intervals using Poisson regression to calculate incidence rate ratio (IRR).ResultsOf 13 482 122 adults aged 65 years or older who received an influenza vaccination, 374 were hospitalized for GBS. The mean (SD) age of the study population was 75.0 (6.1) years; 215 (57.5%) were men and 159 (42.5%) were women. In terms of comorbidities, 33 adults (8.8%) had cancer and 4 (1.1%) had autoimmune diseases. The IRRs for GBS during days 1 to 7, days 1 to 14, and days 1 to 42 were 0.95 (95% CI, 0.55-1.61; P = .84), 0.87 (95% CI, 0.58-1.29; P = .48), and 0.92 (95% CI, 0.72-1.17; P = .49), respectively. No results showed statistical significance. Similarly, no significant differences in IRRs were noted for the overall risk interval (ie, days 1-42) in subgroup analyses pertaining to different age groups (65-74 years [0.93 (95% CI, 0.66-1.31)], 75-84 years [0.85 (95% CI, 0.58-1.26)], and ≥85 years [1.10 (95% CI, 0.57-2.11)]), sex (men, 0.97 [95% CI, 0.71-1.33; P = .87]; women, 0.85 [95% CI, 0.58-1.23; P = .39]), Charlson Comorbidity Index (1.03 [95% CI, 0.77-1.38; P = .84]), or comorbidities (cancer, 0.68 [95% CI, 0.28-1.64; P = .39]; autoimmune disease, 1.10 [95% CI, 0.11-10.53; P = .94]).Conclusions and RelevanceThese findings suggest that influenza vaccination did not increase the risk of GBS among adults aged 65 years or older in Taiwan regardless of postvaccination period or underlying characteristics.

Introduction: Purpuric drug eruption (PDE) is an uncommon, clinically distinct side effect of epidermal growth factor receptor (EGFR) inhibitors. Patient concerns: Unlike acneiform eruption, which arises from hair follicles mainly in the head and neck area, PDE starts from xerosis cutis, primarily in the lower extremities and is not associated with hair follicles. Herein, we report 3 cases of 3 patients who had received EGFR inhibitor and were hospitalized for PDE later. The cases were characterized by painful late-onset palpable purpura with identifiable bacterial pathogens. Diagnosis: The patients were diagnosed with characteristic clinical presentations, that is, late onset, PDE locations mainly in the lower extremities, nonfollicular centricity, and laboratory findings with identifiable bacterial pathogens. Interventions: Systemic antibiotics and intensive moisturizer application were prescribed. Outcomes: All the patients were successfully treated within 6 to 9 days without discontinuation of EGFR inhibitors. Conclusion: Systemic antibiotics, topical emollient, and skin barrier repair should be included in the treatment regimens for PDE.

Relationship between radiation-induced skin ulceration (RSU) and variables in percutaneous coronary interventions (PCI) was rarely reported. RSU is a severe complication in PCIs, especially for chronic total occlusion (CTO) lesions. We investigated the RSUs and their risk factors in patients receiving CTO PCIs over a 2-year period. Data were analyzed using chi-square tests, t-tests and receiver operating characteristic (ROC) curve. Of 238 patients, 11 patients (4.6%) had RSUs all at right upper back. RSUs were significantly associated with use of left anterior oblique (LAO) views (100% vs. 47.1%, p 120, 180, or 240 minutes (p

Dengue virus (DENV)-mediated hair loss is one of the post-dengue fatigue syndromes and its pathophysiology remains unknown. Whether long-term or persistent infection with DENV in the scalp results in hair loss is unclear. In this study, we cultured human dermal fibroblasts (WS1 cells) and primary human hair-follicle dermal papilla cells (HFDPCs) in the long term with DENV-2 infection. The production of virion, the expression of inflammatory and anti-virus genes, and their signaling transduction activity in the infected cells were analyzed. DENV-2 NS3 protein and DENV-2 5&prime, UTR RNA were detected in fibroblasts and HFDPCs that were subjected to long-term infection with DENV-2 for 33 days. A significant amount of DENV-2 virion was produced by both WS1 cells and HFDPCs in the first two days of acute infection. The virion was also detected in WS1 cells that were infected in the long term, but HFDPCs failed to produce DENV-2 after long-term culture. Type I and type III interferons, and inflammatory cytokines were highly expressed in the acute phase of DENV infection in HFPDC and WS1 cells. However, in the long-term cultured cells, modest levels of anti-viral protein genes were expressed and we observed reduced signaling activity, which was correlated with the level of virus production changes. Long-term infection of DENV-2 downregulated the expression of hair growth regulatory factors, such as Rip1, Wnt1, and Wnt4. This in vitro study shows that the long-term infection with DENV-2 in dermal fibroblasts and dermal papilla cells may be involved with the prolonged-DENV-infection-mediated hair loss of post-dengue fatigue syndrome. However, direct evidence for viral replication in the human hair of a dengue victim or animal infection model is required.

Antiplatelet therapy is a key component in the treatment of acute coronary syndrome (ACS). The management of ACS has evolved considerably over recent years with the development of new and more potent antiplatelet agents. Clinical trials on ACS have demonstrated that potent antiplatelet agents can more effectively reduce cardiovascular events. However, there is a tipping point between safety and efficacy, beyond which the risk of bleeding and other adverse effects can outweigh the benefits of antiplatelet therapy. Striking a balance between safety and efficacy remains a major challenge. A consensus meeting of an expert panel composed of Taiwanese experts was held to provide recommendations for the management of adverse effects in patients with ACS receiving antiplatelet therapy. The common adverse effects of antiplatelet therapy include upper gastrointestinal bleeding, ecchymosis, hematuria, epistaxis and ticagrelor-related dyspnea. In this study, a literature review of these adverse events was performed and recommendations for the management were made.

β-Blockers are a standard therapy for acute myocardial infarction (AMI) due to their better short-term and long-term outcomes. However, β-blockers are often under-prescribed in chronic obstructive pulmonary disease (COPD) patients with AMI, since they are thought be related to bronchospasm. The aim of this study was to investigate the association between the usage of β-blockers and the risk of mortality in COPD patients after first AMI via a nationwide, population-based cohort study. In this retrospective study, we identified 186,326 patients with AMI diagnosed between January 2000 and December 2012, 23,116 of whom had COPD, from the National Health Insurance Research Database. A total of 7609 patients (32.92%) were prescribed β-blockers, while 15,507 were not. The β-blocker patients were stratified into selective and non-selective β-blocker groups. Multivariate Cox proportional hazards models were used to estimate adjusted hazard ratios (HR) with 95% confidence intervals (95% CI). Selective β-blocker use showed a reduced risk of mortality, as compared with patients without β-blockers (HR 0.93; 95% CI 0.89–0.98; p

Rituximab is associated with a higher incidence of Pneumocystis jirovecii pneumonia infection. Pneumocystis prophylaxis is advised in many immunocompromised populations treated with rituximab. However, the beneficial effect of pneumocystis prophylaxis in HIV-uninfected, rituximab-treated non-Hodgkin lymphoma (NHL) patients has not been assessed. Thus, we conducted this retrospective study to explore pneumocystis infection in HIV-uninfected NHL patients who received at least three courses of chemotherapy without haematopoietic stem cell transplantation using the Taiwan National Health Insurance Research Database. Patients who had rituximab-based chemotherapy were included in the experimental (rituximab) group, while the rest of the patients who did not receive any rituximab-based chemotherapy throughout the study period formed the control group. The prevalence rate of pneumocystis infection in the rituximab group (N = 7,554) was significantly higher than that in the control group (N = 4,604) (2.95% vs. 1.32%). The onset of pneumocystis infection occurred between 6 and 16 weeks after chemotherapy. Patients who had pneumocystis prophylaxis, whether or not they had a pneumocystis infection later in their treatment course, had significantly better first-year survival rates (73% vs. 38%). Regular pneumocystis prophylaxis should be considered in this group of patients.

Background Previous studies have shown that human sebum may play a role in barrier function but with much debate. Objective To elucidate the effects of human sebum on skin barrier function. Methods We used hairless mouse skin to study the functional and morphological alternation of epidermis after the application of human sebum. Results The results showed a significant increase in transepidermal water loss and erythema value, and a decrease in skin hydration, accompanied by epidermal hyperplasia with parakeratosis following sebum application. Nile red staining together with electron microscopic examination confirmed the underlying mechanisms for sebum-induced barrier disruption are related directly to the interaction of sebum with the intracellular lipid lamellae of the SC, thereby leading to the increase in the fluidity of SC intracellular lipids as demonstrated by ATR-FTIR measurement. An inflammatory reaction characterized by an enhanced cytokine cascade, including up-regulation of TNF-α, IL-1α and IL-6, was also observed. On the other hand, there were insignificant expression of thymic stromal lymphopoietin and unchanged serum levels of IgE, suggesting non-immunogenic stimulation by sebum treatment. Conclusion It may be concluded that inflammation induced by excess amount of sebum is more likely an irritant contact dermatitis rather than an allergic one. Moreover, these findings implicated possible relationships between sebum, irritant contact dermatitis, and seborrheic dermatitis.

Previous evidence showed any radiation might carry a risk of skin or eye damage, malignant disease, or other hazards, which the U.S. radiation protection standards were also established based on this premise. However, most interventional cardiologists neglected the protection of radiation exposure

Background: Nail changes, including onychomadesis (nail shedding) and Beau&rsquo, s line, following hand-foot-mouth disease (HFMD) are a common emergence at the stage of late complications of HFMD. However, the exact mechanism is still unknown. Therefore, we conducted this study to elucidate the mechanism of nail changes following HFMD. Methods: We collected 11 patients suffering from onychomadesis following HFMD. Nail samples from all of them were collected. Real time reverse transcription polymerase chain reaction (RT-PCR) and sequencing for human enteroviruses (HEV) were performed. Throat swabs for RT-PCR and sequencing for HEV were performed for three cases. Results: RT-PCR demonstrated the presence of Coxackievirus A6 (CVA6) in nail samples from three patients and one with Echovirus. Conclusion: In conclusion, we believe that the major cause of onychomadesis following HFMD is that certain novel viruses, mostly CVA6, are virulent and may damage nail matrix. Direct injury caused by cutaneous lesions of HFMD around nail matrix is a minor cause. There are still other virulent HEV which may result in onychomadesis. In addition, the novel strain of CVA6 also causes atypical clinical presentations, such as adult involvement and delayed-onset palmar and plantar desquamation. Physicians should be familiar with atypical presentations caused by novel viruses to avoid misdiagnosis and even inform patients of the possibility of onychomadesis that may take place weeks later to reassure patients.

We used the oxygen and glucose deprivation (OGD) method in cultured astrocytes as an in vitro ischemic model. We investigated whether activation of group-II metabotropic glutamate receptors (mGluR2/3) can reverse OGD-induced impairment in astrocytic glutamate/aspartate transporter (GLAST) expression and elucidated the signaling pathways involving the GLAST expression. Cultured astrocytes exposed to OGD for 6 h resulted in significant reductions in the GLAST expression and extracellular glutamate clearance. These reductions were effectively restored by mGluR2/3 activation with mGluR2/3 agonists, LY379268 or DCG-IV, after the 6 h OGD insult. These mGluR2/3-mediated restorative effects were inhibited by selective mGluR2/3 antagonists LY341459 or EGLU. The mGluR2/3 activation also induced activations of signaling pathways including extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (PI3K) and nuclear transcription factor-κB (NFκB). These activations were prevented by blocking mGluR2/3 with LY341459, an mGluR2/3 antagonist. Furthermore, blocking ERK, PI3K and NFκB signaling pathways with U0126, LY294002 and pyrrolidine dithiocarbamate, respectively, significantly inhibited the mGluR2/3-mediated restorative effects. These results suggest that application of mGluR2/3 agonists after OGD insult can effectively reverse the OGD-reduced expression of GLAST proteins and restore clearance of extracellular glutamate by serially activating ERK/PI3K/NFκB signaling pathways in cultured astrocytes.

Severe forms of psoriasis that are refractory to conventional therapies are often difficult to manage. The mammalian target of rapamycin (mTOR) inhibitors potentially have versatile effects toward putative psoriatic pathologic pathways. Therefore, mTOR inhibitors may offer a range of new therapeutic options for patients with psoriasis. We describe a 55-year-old male renal transplant patient with refractory psoriasis. We adjusted his antirejection regimen and put him on everolimus (Certican(®); Novartis, Basel, Switzerland; a semisynthetic macrolide, belonging to the mTOR inhibitors family) with low-dose tacrolimus. This combination regimen maintained his graft function and successfully controlled his psoriasis. His skin lesions never recurred in the next 18 months. To our knowledge, this is the first report showing that the combination of everolimus and tacrolimus could be used to treat recalcitrant psoriasis. The relative benefit-risk profiles of such therapies worth further investigation.