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Objectives: Chilblain lupus erythematosus (LE) is a rare chronic cutaneous lupus erythematosus (CCLE) characterized by the appearance of violaceous plaques in acral regions most exposed to cold. The isolated form affects middle-aged women, while the familial form manifests in early childhood and is associated with mutations in the TREX1 gene. Result(s): A 13-year-old adolescent, with no relevant family history, was referred in March 2021 for suspected chilblain-like lesions associated with COVID-19 infection. The patient presented with multiple violaceous papules on hands and feet. The lesions were slightly painful. Small hyperkeratotic papules were also observed on finger pads. Physical examination also revealed some aphthae affecting the lips. No other systemic symptoms were reported. A skin biopsy and blood tests were performed due to presumed chilblain LE with probable systemic involvement. Histology revealed basal vacuolar damage and intense perivascular and periadnexal lymphocytic inflammatory dermal infiltrate. Remarkably, mucin was noted among the collagen bundles. Leukopenia and positive ANA antibodies (titre 1:320) were detected. Complement levels were normal. SARS-CoV2 infection was ruled out. Skin lesions disappeared within 1 month under topical corticosteroids. Hydroxychloroquine was afterwards started by Rheumatology without recurrence of skin symptoms until last follow-up. Discussion(s): We present an uncommon case of an adolescent with systemic LE presenting as chilblain LE. Chilblain LE can be accompanied by other discoid CCLE. It can progress to systemic LE in up to 20% of patients, especially when concomitant CCLE is present. This rare presentation of CCLE should be differentiated from typical chilblain and other resembling lesions, such as SARS-CoV2-associated chilblain and acral purpuric lesions (COVID toes). The Mayo Clinic diagnostic criteria can be helpful, particularly in this last SARS-CoV2 outbreak scenario, when the reporting of similar skin lesions has been significant.
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Case Report: A 28 year old male with a past medical history of hypothyroidism and positive ANA presented to an outpatient dermatology clinic with a diffuse pruritic rash two weeks after the administration of his first Moderna COVID booster vaccine. He denied any other accompanying symptoms such as fever or chills as well as any similar rashes to prior doses of the Moderna COVID vaccine. The rash consisted of pink erythematous minimally scaly papules, thin plaques and patches involving the left and right dorsal hands, forearms, wrists, face, neck and left shoulder. The remainder of the patient's skin including the bilateral lower extremities, the eyelids, conjunctiva and oral mucosa was clear. The patient denied any similar rashes in the past. The patient denied any allergies to medications, or food or environmental allergies. He denied any notable contact allergen exposures, including to soaps, lotions, and cosmetic products. The patient also denied any significant family history or past surgical history. The patient was on Armour Thyroid for hypothyroidism and testosterone for low levels since age eighteen. The patient was started on cetirizine 10 mg once daily for the rash with minimal improvement. Autoimmune workup for the rash was notable for an elevated anti-RNP and as the patient's past medical history included Raynaud's phenomenon and ANA positivity for ten years, the patient was diagnosed with mixed connective tissue disease (MCTD). Autoimmune conditions can often have an indolent course, where symptoms progressively develop and worsen. MCTD is an autoimmune overlap syndrome that can consist of the following three connective tissue diseases: systemic lupus erythematosus, scleroderma, and polymyositis. Millions of individuals across the world are receiving COVID vaccines to protect themselves and members of their community, and it is of utmost importance that we continue to investigate adverse events. Although of low incidence, these rare effects have the ability to impact large numbers of people within both healthy and immunocompromised populations. It is critical that we examine and document them in a rigorous manner, to ensure safe vaccine delivery and reassure the public about vaccine safety overall.
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Monkey pox, a zoonotic disease with clinical symptoms resembling smallpox, unexpectedly broke out and spread over the world after the outbreak of COVID-19, severely affecting several of the continents of the world. Monkey pox is currently a member of the genus otrhopox virus, which is a member of the sub family chorodoxvirinae. According to the available knowledge, small mammals and rodents have all been identified as potential sources of the monkey [ox virus]. The disease is characterized by a short febrile illness with lymphadenopathy followed by a rash which spreads centrifugally and passes through phases of macules, papules, vesicles, and pustules. Recovery occurs in most patients within 2-4 wk. Complications are more likely in children, pregnant women, and the immunocompromised. Specific diagnosis is by detection of viral DNA by PCR.Tecovirimat, brincidofovir, and cidofoviir are the medications used to treat monkey pox, immunoglobulin and new compounds are the vaccinations. This review will introduce a general overview of MPXV and describe the epidemiology, clinical features, evaluation, and treatment of monkey pox patients.Copyright © Journal of Global Trends in Pharmaceutical Sciences.
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Purpose of study A 32-years old male with known multi-system sarcoidosis in remission for 5 years off treatment presented to the emergency room with complaints of generalized weakness, hematemesis, epistaxis, and bruises. Physical examination was notable for petechiae, ecchymosis along with papules and plaques suggestive of active sarcoid skin lesions on his extremities. Laboratory workup was significant for thrombocytopenia 3000/uL, acute kidney injury with sub-nephrotic proteinuria. Peripheral blood smear did not show evidence of hemolysis and direct Coombs test was negative. Infectious workup including COVID-19, HIV, and hepatitis serologies were negative. Computed Tomography (CT) of chest, abdomen, and pelvis showed mild splenomegaly and an increased number of sub-centimeter hilar and mediastinal lymph nodes. The patient was treated with dexamethasone 40 mg daily for 4 days and intravenousimmunoglobulins (IVIG-2 gm/kg) for possible Immune Thrombocytopenic Purpura (ITP) with improvement in platelet count to 42000/uL by day 3. His workup for AKI and sub-nephrotic proteinuria was negative apart from a positive ANA (1: 160) with low complements. The anti-phospholipid antibody panel was negative. The ACE level was markedly elevated (>80U/L). The patient could not get a renal biopsy due to severe thrombocytopenia. He was discharged but was re-admitted in 15 days for severe thrombocytopenia of 1000/uL, epistaxis, and bruising. We continued high dose steroids along with IVIG 1 gm/kg for refractory ITP with minimal response and started anti-CD20 agent (Rituximab) 375 mg/m2 weekly with thrombopoietin-receptor agonist (Eltrombopag). His platelets count improved in response to treatment and subsequent renal biopsy showed focal and segmental glomerulosclerosis along with mild interstitial fibrosis, tubular atrophy thought to be from long standing sarcoidosis. There was also evidence of focal arteriosclerosis with no evidence of granulomas, immune complex, complement, or IgG4 deposition. Given skin lesions, thrombocytopenia, extensive lymphadenopathy, and renal involvement with markedly elevated ACE levels the overall picture was consistent with active multi-system sarcoidosis. His platelet count increased to 177,000/uL at the time of discharge. Currently, the patient is on slow steroid taper along with Eltrombopag 25 mg every other day without any recurrence of his symptoms so far. Methods used We described one case of sarcoidosis with hematologic and renal involvement. Summary of results Our patient developed hematologic and renal complications approximately 6 years after being diagnosed with sarcoidosis. Initially, he did not demonstrate sufficient clinical response to IVIG and high dose steroids. However, after a course of anti-CD20 agent (Rituximab) and with the addition of thrombopoietin-receptor agonist (Eltrombopag) he showed improvement of platelet count and stabilization of the renal function. Currently, the patient is receiving maintenance therapy with Prednisone 7.5 mg daily along with Eltrombopag 25 mg twice weekly with no recurrence of ITP and stable renal function. A further decision on whether the patient needs another cycle of Rituximab will be determined by the patient's clinical course. Conclusions Highly variable manifestations of Sarcoidosis can pose a significant diagnostic and therapeutic challenge as can be seen from our case. ITP is a rare hematological manifestation of sarcoidosis and addition of anti-CD20 agents should be considered in refractory cases.
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Background. Prior research has shown that viruses may trigger JDM, although the degree to which COVID-19 may serve as a trigger for JDM remains unknown. We present two case reports of JDM occurring after COVID-19 infection. We also provide case numbers of new JDM diagnoses pre-and post-COVID-19 as well as an analysis of JDM population characteristics pre-and post-COVID-19. A 5year-old female developed upper respiratory infection (URI) symptoms and was diagnosed with COVID-19 in December of 2020. She developed Gottron's sign, heliotrope rash, and weakness resulting in admission in February of 2021. She had elevated CK, AST, ALT, LDH, and aldolase. Her CMAS (childhood myositis assessment scale) was 24. An MRI showed diffuse myositis. Myositis specific antibody (MSA) testing revealed a positive MJ antibody. She was diagnosed with JDM and started on steroids, methotrexate, hydroxychloroquine, and IVIG with improvement. The second patient was a 4year-old female who was diagnosed with COVID-19 in October 2020. In January 2021, she developed heliotrope rash and Gottron's papules. She developed decreased exercise tolerance in May 2021 found to have elevated Aldolase and LDH. Her CMAS was 34. An MRI showed diffuse myositis. MSA testing was significant for a positive P155/140 antibody. She was started on hydroxychloroquine, steroids, IVIG and methotrexate with improvement. Due to the aforementioned cases a retrospective analysis was performed assessing the characteristics of JDM pre-and post-COVID-19 at Lurie Children's Hospital. Methods. The Cure JM biorepository houses clinical data, laboratory data, and patient samples obtained at the onset of JDM. The following information was obtained from newly diagnosed JDM patients: MSA, DAS (disease activity score), flow cytometry results, vWF antigen, neopterin, CMAS, capillary end row loop(ERL), LDH, Aldolase, ESR, CRP, IgG, complements, ANA, and age at diagnosis. We identified 10 patients with a diagnosis of JDM from January 1st 2020 -July 1st 2021 who were designated as the post-COVID-19 group. This population was compared to a total of 51 patients diagnosed with JDM between Jan 1st 2010 and December 31st 2019 who were designated as the pre-COVID-19 group. Data analysis was performed using Welch T-testing. Research enrollment was impacted due to the COVID-19 pandemic. To better assess JDM rates, chart review and EMR reports were obtained to determine the total number of JDM diagnoses. Results. T-testing showed no significant change in DAS, ERL count, T or B cell flow cytometry, vWF antigen, CK, CMAS, CRP, Aldolase, LDH, IgG, complements or ANA titer between the pre-and post-COVID-19 JDM groups. The analysis showed a significant change in NK cell population with a decrease in the absolute NK cell number (pre 163, post 90.75. P value 0.03), and NK cell percentage (pre 6.6%, post 3.625%, P value 0.008). Both of the patients presented in this case report showed a low NK cell number (1% and 3% respectively). The total number of new JDM cases rose from an average of 6.3 cases per year to an average 9 cases per year from January 1st 2020 to December 31st 2021. Conclusion. This study provides two case reports of COVID-19 likely triggering JDM. This study also shows a modest increase in the number of new JDM cases since the onset of the pandemic. Interestingly, the NK cell population in the post-COVID-19 JDM patients were significantly decreased. NK cells have multiple roles in not only immune regulation, but also the immune response to viruses. This study suggests that NK cells play a role in the development of in virally mediated JDM, specifically in cases triggered by COVID-19. Future studies will be important to further delineate the function of NK cells in these patients. Markers of JDM disease severity, including DAS, Neopterin, CK, and CMAS, did not significantly change in our institution's JDM population after the onset of the COVID-19 pandemic.
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Background. Environmental factors such as infections and vaccines are known to trigger dermatomyositis (DM), and during the recent SARS-CoV-2 pandemic this has become even clearer. SARS-CoV-2 infection may share features with anti-MDA5 DM, such as rapidly progressive lung involvement, cutaneous lesions and cytokine release syndrome. A few case reports of DM following SARSCoV-2 vaccination have been published, suggesting the onset of an aberrant immune response leading to DM with specific autoantibody signatures and severe organ impairment. Methods. Clinical and laboratory data of the 2 case reports were obtained from electronic clinical charts in Humanitas Research Hospital (Rozzano, Milan, Italy). Autoantibody analysis was performed by protein-immunoprecipitation for anti-MDA5 and immunoblot for anti-Ro52 and TIF1gamma antibodies as per protocol. Results. Case report 1 is a 71-year-old woman who developed fever, cough, and anosmia, which resolved spontaneously in two weeks, but did not undergo a nasopharyngeal swab, while her relatives were diagnosed with SARS-CoV-2 infection. When symptoms improved, she developed arthralgia and skin lesions on her face, chest, and hands for which she started topical treatment, with negative SARSCoV-2 nasopharyngeal swab and positive serum test for IgG against SARS-CoV-2 spike protein. For the persistence of the skin rash and arthralgia, she was admitted to our Department in March 2021. Blood tests showed mild elevation of C reactive protein (2.1 mg/L -normal value NV<5), aspartate (84 UI/L) and alanine aminotransferase (133 UI/L -NV<35), ferritin (595 ng/ml -NV<306), troponin I (19 ng/L -NV<14), and BNP (251 pg/ml -NV<100) with normal complete blood cell count, creatine kinase, C3 and C4. IgG antibodies for SARS-CoV-2 spike protein were confirmed to be elevated (96 AU/ml -NV<15). Autoantibodies associated with connective tissue diseases were tested and only anti-MDA5 antibodies were positive at immunoprecipitation. A punch biopsy of a Gottron-like lesion on the left hand showed leukocytoclastic vasculitis. We observed reduced capillary density with neoangiogenesis and ectasic capillaries at the nailfold capillaroscopy. EKG and ecocardiography were normal, while cardiac magnetic resonance detected abnormalities in the parametric sequences, consistent with signs of previous myocarditis. A lung CT scan revealed pulmonary emphysema while respiratory function tests demonstrated reduced volumes (FVC 82%, FEV1 64%, inadequate compliance CO diffusion test). Based on the biochemical and clinical findings, a diagnosis of anti-MDA5-associated DM with skin and heart involvement was made and treatment with low-dose methylprednisolone (0.25 mg/kg daily) and azathioprine 100 mg was started, then switched to mycophenolate because not effective on skin lesions. Case report 2 is an 84-year-old woman with history of colon cancer (surgical treatment) and oral lichen treated with low doses steroids in the last 2 years. After the 2nd dose of SARS-CoV-2 mRNA vaccination, in March 2021 she developed skin rash with V-sign, Gottron's papules, periungueal ulcers, muscle weakness and fatigue, thus she performed a rheumatologic evaluation. Blood tests showed mild elevation of creatine kinase (484 UI/L, NV <167), CK-MB (9.6ng/ml, NV <3.4), BNP (215 pg/ml -NV<100) with normal values of complete blood cell count, C3 and C4. Anti-Ro52kDa and TIF1gamma were positive at immunoblot, thus we confirmed a diagnosis of DM. The clinical evaluation also showed active scleroderma pattern at nailfold capillaroscopy, normal echocardiography, bronchiectasia but not interstitial lung disease at lung CT, and normal respiratory function tests (FVC 99%, FEV1 99%, DLCO 63%, DLCO/VA 81%). A PET-CT scan was performed to exclude paraneoplastic DM, and treatment with steroids and mycophenolate was started. Conclusions. SARS-CoV-2 may induce mechanisms for escaping the innate immunity surveillance and causing autoimmune diseases, but more clinical and functional studies are needed to demonstrate this possible association.
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A 50-year-old male patient with agitated depression and hyperlipemia received oral amoxicillin and clavulanate potassium 0.5 g once daily and 2 lopinavir and ritonavir tablets twice daily for novel coronavirus infection, based on previous drugs including quetiapine, clonazepam, and atorvastatin calcium. After 3 days, lopinavir and ritonavir was changed to oral arbidol 200 mg, thrice daily due to suspicious drug interaction. After taking arbidol for 3 days, the patient developed red papules on the whole body. Considering that it might be related to amoxicillin and clavulanate potassium, the drug was stopped and loratadine was given. But the rashes were aggravated. Considering that the drug eruption was caused by arbidol, arbidol was discontinued and the rashes subsided in a large area the next day. Then vitamin C injection, calcium gluconate injection, and ribavirin were added. After 5 days, the rashes subsided completely. After 17 days, the patient recovered from pneumonia.Copyright © 2020 by the Chinese Medical Association.
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Background. Viruses are thought to play a role in triggering juvenile idiopathic inflammatory myopathies (JIIM), which include juvenile dermatomyositis (JDM), juvenile polymyositis (JPM), and overlap myositis. There is growing evidence that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can trigger autoimmune diseases in genetically susceptible individuals, including idiopathic inflammatory myopathies (IIM). Studies have shown similarities between SARS-CoV-2 infection and anti-melanoma differentiation-associated gene 5 (MDA5) antibody-related dermatomyositis, suggesting possible shared underlying autoimmune and/or inflammatory mechanisms. To date, there are few studies describing individual cases of JIIM following SARS-CoV-2 infection, and, to our knowledge, none have explored the effects of SARS-CoV-2 on the clinical presentation of JIIM. In this study, we aim to investigate the impact of SARS-CoV-2 on JIIM by comparing the onset of new JIIM cases, as well as clinical and laboratory characteristics at disease onset, in patients diagnosed before and after onset of the Coronavirus Disease 2019 pandemic (COVID 19). Methods. Patients diagnosed with JIIM prior to age 19 at The Children's Hospital at Montefiore were eligible for study inclusion. Demographic, clinical, and laboratory data, as well as evidence of exposure to SARS-CoV-2, were collected retrospectively by manual chart review. Patients were grouped into pre-COVID 19 (defined as prior to January 1, 2020) and post-COVID 19 (defined as January 1, 2020, or later). Descriptive statistics were used to summarize each variable. Given the small sample size, non-parametric testing was performed using Fischer's exact test and Wilcoxon rank sum test. Results. Forty-four patients were included in the analysis (Table I). Thirty-four patients (77.3%) were diagnosed pre-COVID 19 and ten patients (22.7%) were diagnosed post-COVID 19. Of the ten patients diagnosed post-COVID 19, five (50%) had known exposure to or infection with SARS-CoV-2. Patients diagnosed with JIIM post-COVID 19 were more likely to be of non-Hispanic Black or Asian descent (p=0.041), develop disease at an older age (p=0.009), and present with non-classic cutaneous manifestations (as opposed to classic findings of Gottron's papules/sign or Heliotrope rash) (p=0.031), despite similar frequencies of JDM versus overlap myositis. While presence of muscle weakness did not differ between the groups, patients diagnosed post-COVID 19 tended to have more severe weakness, though results were not statistically significant. Interestingly, despite delays to diagnosis reported during the pandemic, there was no difference between time from symptom onset to diagnosis. Conclusion. This is the first study to explore the effects of SARS-CoV-2 on the clinical presentation of JIIM. In our center, we found that patients diagnosed with JIIM after COVID-19 were more likely to be racial minorities, older at onset, and present with non-classic cutaneous manifestations. While there were no significant differences in myositis specific or associated antibodies, patients diagnosed post-COVID 19 did not have complete autoantibody investigation performed at the time of this study. Clinicians should consider JIIM even in the absence of classic cutaneous manifestations, particularly in the post-COVID 19 era. Patients should be followed longitudinally to explore long-term impacts of SARS-CoV-2 on JIIM. Further investigation is warranted to identify the mechanisms by which SARS-CoV-2 impacts JIIM and how these differ from the effects of other viruses.
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Case report Introduction: Vaccines have been recognized as agents associated with development of different forms of vasculitis. We describe the case of a leukocytoclastic vasculitis which developed after immunization with inactivated COVID-19 vaccine. Case presentation: A 68-years old female patient presented with painful purpuric papules and plaques, and areas of necrosis, dominantly localized on her feet (Figure 1), developing 12 days after she received first dose of inactivated COVID-19 vaccine (BBIBP Cor-V). There were no other symptoms except mild fatigue and low-grade temperature of 37.3degreeC. Skin biopsy showed damaged vessel wall with perivascular, neutrophilic inflammatory infiltrate, leucocytoclasia and erythrocytes extravasation (Figure 2). Thorough work-up, including broad immunoserological and virological analysis didn't reveal any other potential trigger. Three months before vaccination the patient recovered from COVID-19 pneumonia. After the four weeks course of prednisone (initially 20 mg/day) with tapering a complete resolution of skin changes was achieved. The patient was followed for one year with no relapses. Conclusion(s): COVID-19 immunization should be considered as a potential trigger for development of cutaneous vasculitis.
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We present a literature review of dermatology features in historical pandemics. A pandemic is an epidemic occurring worldwide, or over a very wide area, crossing international boundaries and affecting a large number of people. Smallpox was the first documented pandemic, around 10 000 BC, spread by the inhalation of airborne droplets. A few days after an initial high fever, headache and fatigue, a mucocutaneous maculopapular eruption appeared, which then developed pustules and erosions. The last outbreak occurred in the USA in 1949. Smallpox was eradicated in 1980, following a vaccination programme. Mycobacterium tuberculosis is the causative agent of tuberculosis (TB), an ongoing global pandemic. The earliest documentations were 3300 years ago. In 2020, the World Health Organization (WHO) provisionally estimated 1.5 million deaths globally. Most commonly affecting the lungs, cutaneous TB may present with inflammatory papules, plaques, suppurative nodules and chronic ulcers. Requiring long, complex antibiotic regimens, multidrug resistant TB is an increasing problem. Now extremely rare, yet still with recent outbreaks in 2021 in Madagascar, bubonic plague arrived in Europe in 1346 causing 75-200 million deaths. It is caused by the bacterium Yersinia pestis, transmitted through fleas that have fed on infected rodents. Clinical features include papules, pustules, ulcers and eschars, tender lymphadenopathy and systemic symptoms, and it responds to antibiotics. Syphilis, caused by the bacterium Treponema pallidum, is sexually transmitted. The first known outbreak was during warfare in 1494-5 in Naples, Italy. In 2020, the WHO estimated that, globally, seven million people had new infections. Primary syphilis typically produces a painless, genital ulcer (or chancre). Secondary syphilis presents with a nonitchy, maculopapular erythema over the trunk, palms and soles. Early recognition and antibiotic treatment usually lead to good outcomes. Estimated by the WHO to affect 37.7 million people in 2020, HIV is thought to have mutated from simian immunodeficiency virus by the 1960s in sub-Saharan Africa, spreading to the Caribbean and USA by the late 1960s. Initial symptoms include a fever, headache and lymphadenopathy. Dermatological features are common, including opportunistic cutaneous infections, nonspecific exanthemas, seborrhoeic dermatitis and Kaposi sarcoma. Advances in antiretroviral therapies mean people with HIV can have an excellent prognosis, although the WHO estimated in 2020 that more than 200 000 people with HIV died from concomitant TB. Since 2019, COVID-19 has had a considerable global impact on healthcare. With more than 300 million cases and 5.5 million deaths to date, some services have been overwhelmed owing to large case numbers, variable vaccine uptake, workplace changes to reduce transmission and staff shortages. Cutaneous features include perniosis, urticarial, purpuric, vesicular or maculopapular eruptions. Pandemics throughout history have been repeatedly shown to present with an element of skin involvement. We can utilize this to promote education and early recognition of these features, to facilitate diagnosis and raise awareness of the potential complications of serious diseases.
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Autoantibodies against melanoma differentiation-associated protein 5 (MDA5) associated with dermatomyositis have recently been described in Asians with rapidly progressive respiratory disease. Here we report the case of a middle-aged white woman with anti-MDA5 antibody-associated amyopathic dermatomyositis with interstitial lung disease (ILD), which is stable with minimal immune suppression. A 55-year-old woman was referred to a virtual dermatology clinic during the COVID-19 pandemic suspected of having widespread eczema involving the chest, face, arm and hands on the background of atopy. On direct questioning, she admitted to having constitutional symptoms, exertional dyspnoea, joint pain and symptoms of proximal muscle weakness. On clinical suspicion of possible connective tissue disorder, she was urgently reviewed in the hospital, where she was found to have a photodistributed rash involving cutaneous ulceration and violaceous plaques. Hand examination showed mechanic's hand mimicking hand eczema, ragged nail cuticles and acute tenosynovitis in the left index finger. Her upper and lower limb muscle power was normal and respiratory examination revealed bi-basal fine end-expiratory crepitation. Her repeated biochemical, haematological and muscle enzymes remained normal. Skin biopsy taken from photosensitive rash over the wrist showed hypergranulosis, Civatte body formation, colloid bodies and dyskeratotic keratinocytes, in keeping with severe lichenoid eruption. Superficial dermis showed patchy red-cell extravasation, perivascular chronic infiltration, dermal oedema and serum on the surface, in keeping with ulceration secondary to severe inflammatory processes. There were no eosinophils and eccrine coils were free of inflammation, raising the suspicion of a drug eruption. Her antinuclear antibody and double-stranded DNA were repeatedly negative. Myositisspecific antibody panel was performed owing to a high clinical suspicion of photosensitive dermatoses, both clinically and histologically. Histology revealed positive anti-MDA5 antibodies;repeated positive testing confirmed this. Although lung function was normal, computed tomography revealed evidence of ILD. We made a diagnosis of anti-MDA5 antibodyassociated amyopathic dermatomyositis with ILD. Her malignancy screening was negative. The patient was started on lowdose prednisolone and hydroxychloroquine 200 mg twice daily, with topical steroid applications, which resulted in remarkable clinical improvement. Anti-MDA5 associated dermatomyositis has characteristic cutaneous lesions consisting of skin ulceration and tender palmar papules, mechanic's hands, inflammatory arthritis and rapidly progressive ILD, which is frequently fatal. Although our patient had ILD, she was relatively stable on minimal immunosuppression. It is important for clinicians to have an increased awareness of this disease as it could have a highly variable clinical presentation in the white population.
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Seborrhoeic keratosis is a benign brownish-black skin lesion that is almost always seen in middle-aged and elderly populations. The sudden onset and rapid increase in size and/ or number of seborrhoeic keratoses is called the Leser-Trelat sign, suggesting a paraneoplastic manifestation of internal malignancy. However, eruptive seborrhoeic keratoses are also described in some nonmalignant conditions such as human papillomavirus infection and HIV infection. Herein, we report a case with Leser-Trelat sign in a patient following COVID-19 infection. A 50-year-old man presented to our dermatology clinic complaining of the sudden appearance of multiple warty-like lesions on his back, which had occurred 2 months after recovery from COVID-19 infection. According to his medical history, the patient presented with cough, fever and dyspnoea about 2 months prior to the appearance of his skin lesions. He was referred to a health centre, where a nasopharyngeal swab was taken, and his polymerase chain reaction test for COVID-19 was positive. In addition, bilateral patchy ground-glass infiltration was reported in his high-resolution computed tomography (HRCT) scan, all in favour of COVID- 19 infection. The patient was then treated with acetaminophen, dexamethasone (intramuscular injection), salmeterol and a fluticasone inhaler, and his symptoms improved. Two months after recovery from his mild COVID-19 infection, several small asymptomatic pigmented verrucous papules appeared on his back. Physical examination revealed multiple rough, oval-shaped, brownish papules of varying size. Dermatoscopy of the lesions was also performed. Both clinical and dermoscopic findings were in favour of seborrhoeic keratosis. In order to reach a final diagnosis, a skin biopsy was performed, and microscopic examination of the biopsy specimen showed hyperkeratosis and well-defined epidermal hyperplasia composed mainly of the proliferation of benignlooking basaloid cells and fewer squamoid cells and horn cysts and increased melanin, mostly at the dermoepidermal junction. The dermis showed no significant change. Based on the above findings, the patient was diagnosed with eruptive seborrhoeic keratosis. To determine the possible cause of this eruption, the patient was further evaluated. In his past medical history, he was generally healthy before his COVID-19 infection and had no history of comorbidities. The patient underwent a workup to rule out any internal malignancies. Laboratory tests revealed normal results and included a complete blood count, liver and kidney function tests, electrolytes, prostate-specific antigen and urine analysis. Gastrointestinal endoscopy and colonoscopy ruled out any gastrointestinal malignancy. Chest X-ray and HRCT revealed no malignant lesion. In addition, the patient's abdominopelvic sonography was normal. The patient had no family history of similar skin lesions and gave no history of any chronic inflammatory skin diseases or viral conditions. Therefore, the appearance of the Leser-Trelat sign after COVID- 19 infection was a possibility in this patient. The role of transforming growth factor-alpha and tumour necrosis-alpha in eruptive seborrhoeic keratoses, as well as in COVID-19 infection, can be a common area of interest to explore in the aetiology of this entity.
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Introduction: Coronavirus disease 2019 (COVID-19) pandemic is ongoing and new variants of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV- 2) are emerging. There is an urgent need for COVID-19 vaccines to control disease outbreaks by herd immunity. Vaccines can trigger immunity as many vaccine-related immunological adverse events have been described. Case Presentation: A case of a 32 years old Filipino female with no known co-morbidity who presented with rashes on bilateral lower extremities one day after receiving her second dose of CoronaVac-Sinovac vaccine. These were non-pruritic nor painful, which appeared to be initially well-defined round erythematous macules, papules, and plaques, mostly raised. It was associated with colicky abdominal pain and inflammatory arthritis affecting the both knees and ankles. She has no vices but known to have allergy with seafood. There were multiple well defined erythematous round to irregularly shaped purpuric macules, papules and plaques, non-blanching, flat and raised, on arms near the antecubital fossa, abdomen and lower extremities. She underwent skin biopsy and direct immunofluorescence showed interface dermatitis with leukocytoclastic vasculitis and IgA +1 vessel wall, and fibrinogen +2 vessel wall, respectively. There was microscopic hematuria and proteinuria. The Urine protein creatinine ratio was normal at 0.193 gm/gm. She was managed as a case of IgA vasculitis and was given moderate dose of steroid (0.5mg per kilogram per day prednisone equivalent) and omeprazole. She was discharged improved with resolution of rashes evident during follow up at the out-patient consultation. Conclusion(s): We report a case of an adult Filipina developing IgA vasculitis following CoronaVac COVID-19 vaccination. She responded well following initiation of steroid therapy. Autoimmune phenomenon following immunization is possible through different mechanisms. These include molecular mimicry, a hyper-stimulated inflammatory state, and autoimmune syndromes induced by adjuvants. While no strategies have been found to prevent autoimmunity following vaccination, it should be emphasized that vaccine recipients should seek medical care for any untoward events following receipt of any immunization.
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Purpose: To report a case of a 51-year- old male who developed dermatomyositis following the second dose of coronavirus disease (COVID-19) vaccine. Method(s): Case report Result: Case: We report a case of 51-year- old male who developed erythematous maculopapular rash on the upper anterior chest and upper back along with symmetric proximal muscle weakness two months after receiving his second dose of CoronaVac vaccine. His symptoms were followed by edema in the periorbital area which later involved the upper and lower extremities. He had dysphagia and weight loss. He had no known family history of autoimmune diseases. Physical examination revealed macular erythema over the lower anterior neck and upper back. Heliotrope rash and hyperkeratotic pink scaly papules on bilateral lateral second digits (mechanic's hands) were seen. Symmetric proximal muscle weakness in the upper and lower extremities was objectified. Blood tests showed elevated muscle enzymes (total CK: 3899 U/L, CK MB mass: 15.4 ng/mL, LDH: 683, AST: 232 U/L, ALT: 66 IU/L) elevated ESR (36) and normal CRP. Anti Jo 1 and anti U1 RNP were negative. Work up for systemic infection, thyroid function and malignancy were unremarkable. Diagnosis: Diagnosis of dermatomyositis was made based on clinical history and physical exam findings of symmetric proximal weakness, presence of heliotrope rash, V sign and shawl sign. Laboratory tests revealed elevated total CK, CK MB mass, LDH, AST, ALT and ESR consistent with an inflammatory myositis. Intervention(s): Hydrocortisone 1 mg/kg/day was started. Azathioprine was commenced on the 3rd hospital day. Ethical consideration: Informed consent for both written and photographic content was secured and patient confidentiality was observed. Conclusion(s): This case highlights the possible association between COVID 19 vaccine and this rare autoimmune disease. We hypothesize that among patients with genetic predisposition, the possibility of vaccines triggering and unmasking an autoimmune event is possible. (Figure Presented).
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Background Generally, the diagnosis of OCD can be considered after a history of exposure to the suspected material and a thorough physical examination. Meanwhile, vital information about it is often overlooked during the initial consultation. Objective Evaluating the epidemiological profile of OCD cases in health workers due to the COVID-19 pandemic and evaluating complaints, manifestations and causative materials of OCD cases in health workers at the isolation ward of Dr. Soetomo Surabaya Hospital during the Covid-19 pandemic. Methods Purposive sampling was used to design research samples from accessible populations that matched the inclusion requirements while those who met exclusion criteria were included as research samples. Results Majority OCD patients are women and the most common age range is between 22-35 years old. The occupation most affected by OCD while working at isolation ward during the pandemic is nurses. The most common complaint is itching followed by redness of the skin which appears most frequently on the hands. The most prominent clinical manifestations are desquamation followed by erythema-like skin lesions. Medical gloves are the sort of personal protection equipment that causes OCD the most, followed by hand hygiene activities. High risk factors for OCD include a family history of atopic illnesses, history of asthma and an early history of atopic dermatitis. Conclusion The use of PPE can cause several effects on the skin such as physical trauma to the skin, acne, contact dermatitis, urticaria, and aggravate previous skin diseases. The most common skin disorders are erythema, papules, scales, fissures, erosions, ulcers, vesicles and wheals. Complaints of contact dermatitis can be reduced and prevented by taking preventive measures in the form of using moisturizers on areas that are often exposed. Copyright © 2023 Pakistan Association of Dermatologists. All rights reserved.
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Case 1 was an 81-year-old man undergoing treatment for the nummular eczema of the lower leg. The day after being administered the first dose of a COVID-19 vaccine, the patient developed generalized pruritus, multiple serous papules, and erythema on the trunk, upper extremities, and palms, as well as worsening of pre-existing eczema on the lower legs. The serum TARC level of the patient was 1,383 pg/mL. After taking oral antihistamines and topical steroids for two weeks, the erythema faded, papules crusted, and serum TARC level normalized. Case 2 was a 22-year-old woman who had been treated with topical steroids for contact dermatitis by poultices on the ankles. On the same day as she received the second dose of COVID-19 vaccine, erythema with pruritus on the dorsum of the feet appeared and gradually expanded to papules and edematous erythema on the face, extremities, and trunk. The serum TARC level of the patient was 2,090 pg/mL. After taking 15 mg/day oral prednisolone and topical steroids for 10 days, overall erythema became hyperpigmented, and the erythema on the dorsum of the hands and fingers persisted for approximately 2 weeks and then became pigmented. Serum TARC level normalized after the skin rash reformed. Case 3 was a 74-year-old woman with a history of asthma. She received SBT/ABPC therapy for acute cholangitis for one week. Ten days after treatment, she received the first COVID-19 vaccination dose. Two days after vaccination, the patient became aware of pruritus on the extremities ipsilateral to the vaccination site, and small erythematous patches appeared all over the body in a disseminated pattern. Her serum TARC level was 3,862 pg/mL. After taking oral antihistamines and topical steroids for 3 weeks, the erythema completely faded, and the serum TARC level normalized. The DLST showed positive by SBT/ABPC, but the result of drug challenge test was negative. There have been no previous case reports of rash with a high TARC level after vaccination. In the future, it is necessary to accumulate patients with a high TARC level by vaccination and analyze the clinical and pathological trends including immunological mechanisms. Copyright © 2022 Osaka University Medical School. All rights reserved.
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Purpose of Study: Report a rare case of onset of seronegative, juvenile dermatomyositis likely potentiated by Covid-19 infection Methods Used: Case analysis and literature research Summary of Results: A 7 year-old previously healthy male presented with 3 weeks of progressive, bilateral upper and lower extremity weakness, difficulty swallowing, voice changes, periorbital edema, and rash. Recent history was notable for diagnoses of COVID-19 one month prior to presentation and streptococcal pharyngitis 2 months prior to presentation. Notably, there is a family history of systemic lupus erythematosus. On examination, the patient demonstrated bilateral periorbital swelling with purple discoloration of the upper eyelids, a violaceous, pruritic, macular rash on his upper extremities and on his abdomen. Musculoskeletal exam was significant for severe axial (strength 2/5) and proximal (strength 3/5) muscleweakness with notable inability to sit unsupported or maintain head control. His neurologic exam was nonfocal;however, diffuse hyporeflexia in both upper and lower extremities were elicited. Initial screening labs were notable for mild transaminitis;positive ANA (1:80 in speckled pattern), negative ANCA, negative dsDNA/Anti- Sm, elevated aldolase of 10.3, CK 464, and LDH 665;normal thyroid studies and normal inflammatory markers. MRI with and without contrast of the spine indicated diffuse myositis of all muscle groups. Due to concern for autoimmune mediated myositis, Rheumatology was involved early in the patient's course. Empiric treatment was initiated early in the patient's presentation with IVIG, steroids, methotrexate, and plaquenil leading to gradual improvement in symptoms. Subsequent muscle biopsy was consistent with juvenile dermatomyositis (JDM). Conclusion(s): JDM is rare, occurring in 1 to 15 per million children. It classically presents with proximal myopathy and dermatologic findings of Gattron's papules, a heliotrope and malar rash. Its pathophysiology is not yet well defined but is thought to be a humoral mediated autoimmune disease. Muscle biopsies characteristically show perifascicular and perivascular infiltration. Early diagnosis and treatment with steroids, immune modulators, and physical therapy is critical to limit muscle atrophy. Viral infections are known triggers of rheumatologic diseases broadly;however, the more pronounced type 1 interferon response associated with COVID-19, which is known to be a driving pathway of JDM, may be a risk factor for severe, recalcitrant disease. Future research is needed to better identify involved pathophysiology and target future treatment efforts. Additionally, more education and case reports could focus on dermatologic presentations of individuals with pigmented skin. Copyright © 2023 Southern Society for Clinical Investigation.
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Background: Amyopathic dermatomyositis is a rare autoimmune skin disease with similar cutaneous manifestations as classic dermatomyositis (CDM), but with absent or subclinical muscle involvement i.e. Clinically Amyopathic Dermatomyositis (CADM). Inciting agents including vaccines have been linked to CADM. We describe a case of new-onset CADM associated with COVID-19 vaccine. Objective(s): To illustrate the occurrence of new-onset CADM in a 27-year- old male following COVID-19 immunization. Case Summary: A previously well 27-year- old male developed joint and muscle aches accompanied by scattered erythematous patches on the face and both upper and lower extremities, a week after receiving first dose of viral vector SARS-CoV- 2 vaccine. He took an anti-histamine and paracetamol with some relief of pains and slight clearing of the rashes. He proceeded to receive a second dose of the same vaccine 2 months later. A few days following the second dose, there was exacerbation of the skin lesions and was referred to Rheumatology clinics. Physical exam disclosed an ambulatory well-built male with normal vital signs and no objective muscle weakness. Skin involvement included facial rash, and the characteristic Heliotrope rash, Gottron's papules, and Holster sign. Complete blood counts, chemistries and muscle enzymes were within normal. Antinuclear antibody (ANA), erythrocyte sedimentation rate (ESR) and Smith/ribonucleoprotein (Sm/RNP) antibody were positive. He was managed with tapering prednisone and maintained on methotrexate and folic acid with significant improvement at time of this report. Conclusion(s): This is the first reported case of adverse reaction to COVID-19 vaccine that had studied in detail the skin and systemic autoimmune reaction. Development of autoimmune reaction following SARS-CoV- 2 vaccine has been described extensively;however, evidence of autoimmunity following vaccination is still relatively scant. Our case suggests that in predisposed subjects' vaccination could trigger an autoimmune reaction similar to the natural infection.
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SESSION TITLE: Severe and Unusual Blastomycosis Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: This is a case of a patient 74-year-old immunosuppressed woman presenting with a one-week history of skin lesions. CASE PRESENTATION: A 74-year-old woman with Crohn's disease (on weekly adalimumab);pulmonary hypertension (RVSP 76 mmHg);OHS/OSA, on home BPAP 17/7 cmH2O;and morbid obesity presented with a one-week history of skin lesions. She was seen by her primary care physician two days prior with skin lesions, shortness of breath, and decreased vision. She was hypoxic during the visit and given doxycycline for empiric treatment of pneumonia. She denied recent travel or exposure to animals. On admission, she was afebrile (36.9C) and saturating 98% on 2 L nasal cannula. She appeared chronically ill with mouth ulcers and an eroded nodule with overlying hemorrhagic crusting and peripheral pustular area above her right eyebrow (figure 1). Throughout her skin, she had multiple erythematous papules, some with overlying vesicles/pustules. Labs were significant for a leukocytosis of 19.3 with left shift, lactate of 3.5, serum creatinine of 1.9 (likely higher than patient's previous baseline of 1.7 with previous history of recurrent AKIs on CKD), elevated inflammatory markers, and normal ALT/AST. Influenza and COVID were negative. A CT chest showed consolidations and numerous pulmonary nodules highly suspicious for an infectious or inflammatory process (figure 2). She was treated empirically with vancomycin, piperacillin-tazobactam, valacyclovir, and amphotericin B, the latter given the concern of blastomycosis. During her hospitalization, she had further respiratory failure requiring intubation and multiorgan failure. Disseminated blastomycosis was confirmed via a skin biopsy which demonstrated pyogranulomatous inflammation with numerous broad-based budding yeasts (figure 3) and supported with a bronchoalveolar lavage (BAL) culture growing the same. Given her continued decline, her medical decision maker decided to transition the patient to hospice care. DISCUSSION: Blastomycosis is a systemic pyogranulomatous infection that is caused from the inhalation of the conidia form of the dimorphic fungus. It can manifest as asymptomatic infection, acute or chronic pneumonia, or extrapulmonary disease. BAL yields a positive diagnosis in 92% of patients and definitive diagnosis requires growth of the organism from a clinical specimen. Without appropriate treatment of amphotericin B or one of the azole antifungals, the disease had a 90% mortality rate. CONCLUSIONS: Prompt recognition of multiorgan failure secondary to blastomycosis is important for early treatment and improved survival in immunocompromised patients Reference #1: 1)Chapman, S W et al. "Endemic blastomycosis in Mississippi: epidemiological and clinical studies.” Seminars in respiratory infections vol. 12,3 (1997): 219-28. Reference #2: 2)Saccente, Michael, and Gail L Woods. "Clinical and laboratory update on blastomycosis.” Clinical microbiology reviews vol. 23,2 (2010): 367-81. doi:10.1128/CMR.00056-09 Reference #3: 3)Chapman, Stanley W et al. "Clinical practice guidelines for the management of blastomycosis: 2008 update by the Infectious Diseases Society of America.” Clinical infectious diseases : an official publication of the Infectious Diseases Society of America vol. 46,12 (2008): 1801-12. doi:10.1086/588300 DISCLOSURES: No relevant relationships by Jennifer Duke No relevant relationships by Ashley Egan