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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 Introduction: The COVID-19 pandemic has generated an inexorable cost to governments and a high mortality in general terms, the vaccination process is the only effective strategy to reduce morbidity and mortality in general, however, such administration is not without risks. Case presentation: Female patient of the seventh decade who is vaccinated against COVID-19 and 4 days after the second dose of vaccine against COVID-19 begins to present purpuric lesions that begin in the lower limbs and progressively ascend to the trunk associated with intense arthralgias, abdominal pain and nausea, presents macroscopic rectal bleeding, is admitted finding platelet counts lower than 10 thousand platelets, the diagnosis of a Henoch Scholein purpura associated with a vaccine against COVID-19 was confirmed no requiring specific immunosuppressive therapy with resolution at 21 days. The triggering mechanisms are being studied and described as similar to immunological thrombocytopenia due to heparins. Antibodies against platelet factor 4 have been reported so far. The test known as PIFPA (PF4-induced flow cytometry-based platelet activation) is a cytometric test with high sensitivity and specificity, only available in specialized laboratories, being described for the moment as the only test that allows the detection of immunological thrombocytopenic phenomena secondary to vaccination against COVID-19. Discussion(s): The present case constitutes the appearance of a Henoch Scholein Purpura, a rare pathology with a wide repertoire of triggering events, with infections and vaccine reactions among the main triggers. The present vaccine reaction is rare, being the specific anecdotal, until now there are very few descriptions in the literature about this type of vaccine reaction, which is why it is decided to publish it, mentioning the most recent scientific evidence available on this area. It is noteworthy that these are rare reactions that should not make us underestimate continuing with vaccination campaigns as the best strategy to prevent the advance of this pandemic.
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The novel Coronavirus disease-2019 (COVID-19), which emerged in December 2019 and caused an unexplained viral pneumonia, rapidly spread worldwide within a few months. A pandemic was declared by the World Health Organization in March 2020. Several cutaneous manifestations of the disease among patients with COVID-19 have been reported. Thus far, the most frequently reported cutaneous findings are morbiliform rash, urticarial lesions, purpuric lesions, oral vesicles, and pityriasis rosea. This report presents a case of lichen planus secondary to COVID-19 and its histopathological findings, which is rarely reported in the literature. Copyright © 2022 by Turkish Society of Dermatology and Venereology.
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SESSION TITLE: Critical Systemic Disease Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Granulomatosis with polyangiitis (GPA) is a necrotizing granulomatous vasculitis affecting small-to-medium sized blood vessels. GPA is highly associated with antineutrophil cytoplasmic antibodies (ANCAs) and often triggered by environmental factors such as medications and infectious agents. Tracheobronchial stenosis and diffuse alveolar hemorrhage are serious complications of GPA. CASE PRESENTATION: A 35-year-old Caucasian male with a history of chronic sinusitis requiring balloon sinuplasty and recent tympanostomy had presented multiple times to the emergency room due to dyspnea and cough with pinkish sputum production. This was associated with sore throat and fever, which were attributed to his COVID-19 infection and treated with supportive care. Due to persistent drainage through his tympanostomy he was prescribed levofloxacin by his ENT specialist. After the second dose of levofloxacin, he developed Raynaud's phenomenon, diffuse purpuric lesions and swelling over his lower extremity, eyelids, and elbows. Four days later he developed worsening hemoptysis and dyspnea for which he was admitted for further evaluation. Laboratory findings were remarkable for peripheral eosinophilia, elevated ESR 19mm/hr, CRP 9.2mg/dl, c-ANCA 1:320 titer, positive proteinase-3 antibodies and normal p-ANCA titers. Urinalysis with microscopic hematuria. Chest CT scan showed ground glass opacity, consolidative infiltrate with subpleural sparing and minimal left bronchial stenosis. Bronchoscopy suggestive of diffuse alveolar hemorrhage. Limited lung biopsy showed ulcer and granulation tissue with abundant eosinophils, but no granulomatous inflammation noted. Pulse dose steroids and Rituximab were initiated, and rapid clinical improvement was noted. Patient was discharged on prednisone taper and Pneumocystis jiroveci prophylaxis. DISCUSSION: We believe that GPA may have been triggered by recent COVID-19 infection and levofloxacin use. Mild peripheral blood and tissue eosinophilia (<12%) has been described in GPA, however it is a rare finding. GPA and eosinophilic granulomatosis with polyangiitis (EGPA) are both ANCA vasculitis that involve lungs and kidneys. GPA presents with sinusitis, alveolar hemorrhage and high titers of PR-3 antibodies. EGPA presents with a history of atopic, asthma and high titers of myeloperoxidase-ANCA along with abundant peripheral eosinophils. Our patient best fits the diagnostic criteria for GPA with eosinophilia variant rather than EGPA. Our patient had no history of asthma or atopic disease and p-ANCA was normal, which also points away from EGPA. CONCLUSIONS: Clinicians should recognize the differential diagnosis for eosinophils in ANCA vasculitis. Early diagnosis of ANCA vasculitis and initiation of appropriate treatment is important to decrease morbidity and mortality. Reference #1: Potter MB, Fincher RK, Finger DR. Eosinophilia in Wegener's Granulomatosis. Chest 116: 1480-1483, 1999 Reference #2: Krupsky, Meir et al. Wegener's Granulomatosis With Peripheral Eosinophilia. CHEST, Volume 104, Issue 4, 1290 - 1292 Reference #3: Kitching AR, Anders HJ, et al. ANCA-associated vasculitis. Nat Rev Dis Primers. 2020 Aug 27;6(1):71. doi: 10.1038/s41572-020-0204-y. PMID: 32855422. DISCLOSURES: No relevant relationships by Afoma King No relevant relationships by Joshuam Ruiz Vega No relevant relationships by Krishna Shah no disclosure on file for Milos Tucakovic;
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Common causes of viral exanthems in Australia include herpesviruses, enteroviruses, parvovirus B19, varicella, measles and rubella viruses and mosquito-borne alphaviruses. The cause can often be diagnosed clinically from the rash distribution and morphology, confirmed only when necessary with serological or PCR tests. Most viral exanthems are self-limiting, requiring supportive care alone.
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SARS-COV-2 infection is often associated with exaggerated immune response, also referred to as a ‘cytokine storm’. There is growing concern that it may be linked to autoimmunity, with many cases of autoimmune diseases either triggered by or related to SARS-COV-2 having been reported, ranging from Guillain-Barre syndrome, Graves’ disease, multiple sclerosis, Kawasaki-like disease. Our patient was a 20-year-old female with a history of hidradenitis who presented with malaise, feet and ankle swelling, asthenia, anorexia, weight loss of 50 Ibs of 4 months. She had COVID pneumonia 7 months prior and was also seen in the ER thrice afterwards for ankle pain and fatigue managed with antibiotics and analgesics. Exam findings included tender bilateral lower extremity edema, diffuse hyperkeratotic and hyperpigmented purpuric rashes and bilateral suppurative axillary swellings. She was admitted for protein-energy malnutrition. Blood work showed WBC 13.5, low Hb 9.3, AST 509, ALT 104, BUN 29, Creatinine 0.9, Protein 7.5, albumin 1.5 (globulin gap of 6). Urine assay showed 3+ proteinuria Hb 3+ with RBC 3-10/hpf, absent nitrite, LE 1+, protein/creatinine ratio was 2949 mg/g. Blood cultures returned negative. US showed trace pericardial effusion and normal kidneys. Infectious workup returned negative for anti-streptolysin O, HIV, hepatitis B and C. Two days after, she developed AMS, fever, tachycardia and neck stiffness concerning for possible meningoencephalitis. CT head was normal. Lumbar puncture was performed. IV vancomycin and piperacillin-tazobactam was started. CSF fluid analysis revealed total protein of 125mg/dl, elevated IgG 79.8, concerning for an underlying inflammatory pathology. EEG was unremarkable. She became oliguric with creatinine and BUN both peaking at 2.6 and 58 respectively. Renal ultrasound revealed medical renal disease. Urine microscopy showed granular cast and no dysmorphic RBCs. ANA, anti-smith SSA, SSB, DS-DNA, RF, smooth muscle, anti-histone, anti-centromere, JO-1 and RNP antibodies were markedly elevated. She was unstable for CT trocar biopsy of the kidney. She subsequently went into cardiac arrest multiple times about a week into admission, before eventually expiring. Though causation was not established in our patient, SARS-COV-2 infection causing exaggerated immune response may unmask SLE or be associated with SLE.
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CASE: 58 year old woman presents with 1 month of dyspnea and productive cough. She also reported loss of smell and hematuria for 1 week. History was notable for hypertension, COPD, substance abuse, specifically crack cocaine, and unstable housing. On admission she was tachypneic and hypoxic, requiring supplemental O2. Exam revealed bilateral crackles, elevated JVP, and mild lower extremity edema, but no skin changes or rashes. Laboratory studies showed an elevated creatine of 7.9. CT chest imaging showed extensive bilateral ground glass opacities with increased septal lines. Infectious work-up, including SARSCoV-2 PCR, was negative. Dialysis was initiated for new renal failure. To determine the etiology of the renal failure, autoimmune studies were obtained and showed a positive ANA and p-ANCA (1:640) and a negative MPO and PR3. Kidney biopsy was consistent with levamisole-induced vasculitis (LIV) from cocaine use. Treatment with steroids was initiated. She was discharged on steroid therapy and outpatient hemodialysis. She had repeated admissions for volume overload due to missed dialysis, and she developed heart failure within the year. She was unable to make appointments to start outpatient rituximab therapy. IMPACT/DISCUSSION: Levamisole-induced vasculitis (LIV) is a complication of use of cocaine adulterated with levamisole. Levamisole is an antihelminthic medication with well known immunomodulatory effects. Increasingly used as a cocaine adulterant, it is believed to be a component of over 80% of cocaine samples in the US. Its use is thought to be driven by levamisole's synergistic effect on the dopaminergic effects of cocaine. Levamisole-induced vasculitis is a p-ANCA associated vasculitis associated with long-term use of cocaine mixed with levamisole. It has been reported with both inhaled cocaine and smoking crack cocaine. Levamisole is thought to induce production of autoantibodies including p-ANCA, ANA, and lupus anticoagulant leading to immune complex deposition and secondary hypercoagulability. The most commonly reported presentation is cutaneous purpuric lesions, most notably the ear, tip of the nose, and malar eminence. LIV can occur without skin involvement and renal and pulmonary involvement including nephritis, renal failure, and hypersensitivity pneumonitis, has been reported. LIV with significant organ involvement is often treated with steroids. Additional immunosuppressive therapies including rituximab, cyclophosphamide, and plasmapheresis have been reported in severe cases. CONCLUSION: This case illustrates a rare presentation of LIV marked by with renal failure and absence of skin lesions. While the health effects of cocaine are well known, the adverse effects of agents used to cut cocaine are less readily considered. LIV should be considered in a patient with substance use disorder presenting with new vasculitis. As this case illustrates, factors like unstable housing and ongoing substance use disorder can complicate management.
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A 58-year-old man known to dermatology services, established on guselkumab for psoriasis and methotrexate for psoriatic arthritis, attended with an acute onset purpuric rash distributed over both his lower limbs, one day after his third dose of SARS-CoV-2 Pfizer-BioNTech vaccine (booster). He had received his initial vaccinations 6 months prior with no reported reactions. He denied any previous SARS-CoV-2 infection or recent symptoms suggestive of COVID-19. There had been no new recent medications and no systemic symptoms were reported. Examination revealed a nonblanching, palpable, purpuric rash distributed over both lower limbs, clinically in keeping with cutaneous vasculitis. Baseline observations were satisfactory including blood pressure and temperature. Bedside investigations included a urinalysis which revealed no proteinuria or haematuria. Punch biopsies were taken and were consistent with a leucocytoclastic vasculitis (LCV). He was managed symptomatically with potent topical steroids with good clinical response. LCV is classified as a cutaneous, small vessel vasculitis, exclusively characterized by deposition of immune complexes in the dermal capillaries and venules (Baigrie D, Bansal P, Goyal A, Crane JS. Leukocytoclastic vasculitis. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing, 2021). LCV following both first and second SARS-CoV-2 vaccinations has been documented in recent literature with a few reports following a third booster dose, and in particular within an immunocompromised population. This particular case has raised questions regarding delayed immune response following SARS-CoV-2 vaccine in this subgroup. The pathophysiology of SARS-CoV-2 vaccine-induced LCV has not been extensively researched;however, it is felt to be caused by offtarget immune activation after the vaccination (Dicks AB, Gray BH. Images in vascular medicine: leukocytoclastic vasculitis after COVID-19 vaccine booster. Vasc Med 2022;27: 100-1).
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Background/Aims There is a growing number of reports of new-onset autoimmune disease or complications of underlying autoimmune disorders following COVID-19 infection and vaccination. Methods We describe two cases of systemic lupus erythematosus (SLE) that developed De novo in two female patients shortly after receiving their COVID-19 vaccinations. Results The first case is a 29-year-old female with no prior medical history. One week following her COVID-19 Pfizer/BioNTech vaccination, she developed widespread pruritus, fatigue, myalgia, arthralgia, fever and night sweats. Blood tests showed pancytopenia and she was referred for an urgent haematology opinion due to lymphoma. Positron Emission Tomography/computed tomography (PET/CT) demonstrated widespread lymphadenopathy. Bone and lymph node biopsy showed reactive changes only. Her symptoms progressed with polyarticular inflammatory arthritis, oral ulceration, Raynaud's, pleuritic chest pain, palmar purpuric rash, and a widespread tender urticarial rash. Further investigations showed low complement C3/C4, anti-double stranded DNA antibody titre (dsDNA) >200 IU/mL, positive Anti-Ro antibody, positive Anti-La antibody, weakly positive anti-RNP antibody and an Anti-C1q antibody >400 units/ml with a urine protein/creatinine ratio (PCR) of 39 mg/mmol. A diagnosis of SLE with urticarial vasculitis was made and she commenced Hydroxychloroquine in addition to weaning prednisolone (60mg). A skin biopsy confirmed lupus vasculitis. Despite high dose prednisolone, urine PCR increased over 2 weeks from 39 to 84 mg/mmol. Renal biopsy demonstrated class 3 lupus nephritis. She was pulsed with 500mg IV methyl prednisolone over 3 days and commenced mycophenolate 1g BD. Within weeks she was in clinical remission. The second case is a 70-year-old female with a past medical history of diverticulosis, uterine fibroids and small hand joint osteoarthritis. She presented with a sudden onset, 6-week history of bilateral symmetrical small and large joint synovitis that developed 8 days following the first dose of the COVID-19 Oxford-AstraZeneca vaccine. Her investigations showed reduced lymphocyte counts (0.9 109/L), raised CRP 26 mg/L and ESR 32 mm/hr. Antinuclear antibodies were weakly positive with a homogenous pattern. DsDNA titre was raised at 175 IU/mL and C4 reduced at 0.14 g/L. There was no proteinuria or any evidence of major internal organ involvement. She was started on a short reducing course of oral prednisolone given the severity of her presenting clinical features. Her symptoms improved, with no recurrence on stopping steroids but she has continued elevation in DsDNA;a conservative management approach is being adopted. Conclusion Both cases met the EULAR/ACR and SLICC classification criteria for SLE. There was a clear temporal association between the onset of SLE symptoms and COVID-19 vaccination. Our cases raise the possible association/causation of SLE following COVID-19 vaccination. Potential mechanisms include immune responses elicited by the COVID-19 vaccination, triggering autoimmunity in genetically predisposed individuals. Further research and data from registries are required.
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Background: Vasculitis is a known, although not commonly observed, manifestation of bacterial endocarditis. It is imperative that diagnosis is made promptly and appropriately treated, as vasculitis can often be painful and uncomfortable for patients. Case: 75-year-old male is admitted to the hospital for Coronavirus Disease 2019 (COVID-19). Several weeks after recovering from his respiratory infection, patient developed a diffuse, purpuric rash that began on his forearms and gradually spread throughout his bilateral upper extremities to his hands and fingers, as well as to his shoulders and lateral chest. Skin biopsy was performed and revealed findings suggestive of leukocytoclastic vasculitis. Blood work revealed Methicillin Resistant Staph Aureus (MRSA) bacteremia, sensitive to Vancomycin. Transthoracic echocardiogram revealed native mitral valve endocarditis. Transesophageal echocardiogram was not performed due to patient's underlying comorbidities and high risk. Decision-making: Patient was diagnosed with leukocytoclastic vasculitis secondary to bacterial endocarditis. Rheumatologic workup, including antineutrophil cytoplasmic antibodies, antinuclear antibodies, serum complement levels, anti-smith antibodies and double stranded deoxyribonucleic acid, was negative. Patient was ultimately discharged on a prolonged course of Vancomycin and his diffuse rash resolved one month later. Conclusion: There are only a few case reports describing the direct association between leukocytoclastic vasculitis and infective endocarditis. It is important to consider the association of vasculitis and endocarditis in order to effectively treat because immunosuppression, particularly with steroids, is the gold standard treatment for vasculitis. Our patient experienced near complete resolution of the rash after completion of antibiotics and no other therapy was deemed necessary.
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Introduction: Obesity is highly prevalent among patients with renal transplants. It is associated with increased risk of overall mortality, obesity-related complications such as diabetes, increased renal graft loss rates and shortened graft survival. Roux en Y gastric bypass in contrast to other non malabsorptive procedures, may affect the pharmacokinetics of certain drugs, which is of particular importance for immunosuppressant drugs required by patients post-transplant to avoid graft rejection. Methods: 43-year-old female known case of IgA nephropathy biopsy proven in 2000, progressed to end stage renal disease (ESRD) and was initiated on hemodialysis. She underwent live unrelated renal transplantation. Creatinine was 79 micromole/L and eGFR 85ml/min/1.73 m2. Her maintenance immunosuppression included azathioprine 50 mg daily, cyclosporine 75 mg bid and prednisolone 5 mg daily. She had two successful pregnancies post renal transplantations. She developed post renal transplant diabetes in 2013 and uncontrolled hypertension. She had persistent microscopic hematuria. Her creatinine peaked up to 275 micromol/L, her allograft kidney biopsy showed histopathologic features for mild acute T-cell mediated rejection (probably modified slightly by anti-rejection treatment). Grade 1A by Banff working grading. C4d stain is negative with background of focal proliferative and sclerosing glomerulonephritis with associated IgA deposits, consistent with IgA nephropathy ("M1, E1, S1, T0" Oxford classification). Her rejection was treated with pulse IV steroids, azathioprine was changed to mycophenolate and dose of cyclosporine was increased to 100 mg bid. Her creatinine came down to 105 micromol/L. Her post transplantation course involved purpuric rash, joint pain, abdominal pain, h/o HSP biopsy proven with elevated ESR and CRP most likely this is HSP again associated with medication exposure, possible the fibrate. Results: She lost follow up in our clinic and showed up after 5 years with uremic symptoms and creatinine of 1,063micromol/L and was initiated on hemodialysis in 2019. She had second live unrelated renal transplantation, she received 3 sessions of plasma exchange and IVIG prior to transplantation and was maintained on tacrolimus, mycophenolate and prednisolone. Her creatinine was 88 micromol/L. She had Laparoscopic sleeve gastrectomy and Dermo lipectomy of abdominal wall 2 months following her transplantation and lost 22 kgs since then, her BMI was 32 kg/m2 dropped to 24 kg/m2 in 6 months duration. The patient suffered from recurrent multi drug resistant E.Coli urinary tract infection treated with IV ertapenem and continued on trimethoprim sulpha- methoxazole prophylaxis for 6 months. She is still using insulin in smaller doses and her blood sugar is within acceptable ranges. She recently suffered from covid 19 pneumonia requiring home quarantine during which her creatinine went up to 106 micromol/L but settled down to baseline of 88 micromol/L during further follow up. Conclusions: Limited evidence suggests that bariatric surgery is safe and feasible for selected obese patients post-renal transplant. It is associated with good, if variable, short-term excess weight loss and resolution of co-morbidities. More studies should address long term complications in renal trnasplant patient population. No conflict of interest
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Leukocytoclastic vasculitis (LV) is an inflammation of the small vessels in the dermis characterised by the deposition of immunocomplexes in the involved vessel walls. It commonly manifests as palpable purpura, limited to the skin and predominantly of the lower limb. We report a rare case of necrotising LV (NLV) affecting bilateral breast, manifesting clinical features of necrotising fasciitis (NF), and emphasizes the potential diagnostic challenges that markedly influence the treatment and survival of patients. A 48-year-old female presented with an acute onset left breast skin necrosis and discolouration that rapidly progressed to the contralateral breast with surrounding erythema and oedema of the chest wall yet spared the intermammary cleft. Some non-blanching purpuric rash were also noted on upper abdomen and left lower limb. COVID-19 test was negative. CT scan showed extensive bilateral breast fat stranding and oedema. Patient became clinically septic with a moderately raised CRP and mild acute kidney injury. Radical mastectomies and chest wall excision were performed with intra-operative findings of cloudy fluid and easily peeled away subcutaneous tissue from fascia. Urgent gram stain and culture showed no organisms. Tissue biopsies subsequently showed the diagnosis of NLV. Chest wall defect was then reconstructed with split skin grafts, NLV treated with corticosteroids and patient made an uneventful recovery. This case highlights the incidence of a rare and aggressive manifestation of NLV on the breast that mimics NF, emphasizing the clinical differentiation that may lead to catastrophic results and significant cosmetic defect, if a differential diagnosis cannot be determined at the time.
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Case report-IntroductionBased on initial clinical data, it was suggested that patients with vasculitis who were immunosuppressed, would have a more severe COVID-19 infection. Here we present a case of a young 26-year old lady with granulomatosis with polyangiitis (GPA) on rituximab who developed COVID-19 infection while on active GPA treatment. Her COVID-19 infection confirmed on PCR serology, has been protracted but non-fulminant. She did not require mechanical respiratory support. At the same time her GPA remained active and worsened requiring further immunosuppression after she developed mild pulmonary haemorrhage. She is currently still receiving vasculitis treatment.Case report-Case descriptionA 26-year-old lady with a background history of obstructive sleep apnoea and fibromyalgia was diagnosed with ENT-limited GPA in 2017. She was initially treated with azathioprine then methotrexate, and later switched to Rituximab in 2018 after she developed organ-threatening manifestations with bilateral hearing loss. She was stable on periodic infusions of rituximab at 6 to 9-monthly intervals and did not develop other organ-threatening features.She had been given one dose of rituximab for a flare of her GPA. In between rituximab doses, she was admitted with acute COVID-19 infection with related pneumonia and treated with antibiotics, fluids, and oxygen. Shortly after discharge, she was readmitted with worsening symptoms of non-resolving COVID-19 pneumonia which was evident on chest X-ray and levofloxacin treatment was initiated. Her condition improved and she was discharged. No mechanical respiratory support was required. She had her 2nd dose of rituximab after it had been delayed by about 2 weeks. She had been afebrile after the acute COVID-19 infection and her persistent positive results were explained as related viral shedding over a period of 8 weeks.One week later, she represented to hospital with fever, cough and shortness of breath, and her blood results showed a remarkable rise in inflammatory markers, including a CRP of 242. She was treated for non-resolving COVID-19 pneumonitis with worsening chest X-ray features. After hospital discharge, her GPA continued to flare with persistent epistaxis with nasal crusting. She also had worsening inflammatory arthritis with purpuric rash on her legs. An ENT review confirmed nasal septum perforation, but no renal involvement was found. Additional cyclophosphamide was commenced via the day-case unit. Her SARS-CoV-2 serology was negative prior to commencing cyclophosphamide. She is now SARS-CoV-2 positive after two doses of cyclophosphamide, but she is afebrile and stable.Case report-DiscussionCOVID-19 infection carries a high mortality rate in patients with multiple co-morbidities, but recent literature suggests that patients on immunosuppressants may not actually have fulminant COVID-19 disease. This case illustrates the challenges of treating active vasculitis in the context of ongoing COVID-19 infection. Her vasculitis remained active requiring escalation of immunosuppression with caution, while she was concomitantly fighting SARS-CoV-2 and superadded bacterial infection. A similar case has been published by Guilpain et al of a 52-year-old woman with PR3-ANCA vasculitis on maintenance therapy with rituximab and low-dose prednisone who developed COVID-19 infection. They reported milder evolution of COVID-19 infection in comparison with previous reports.It is now well known that some disease-modifying anti-rheumatic drugs (DMARDs) such as tocilizumab, hydroxychloroquine and tofacitinib could suppress the cytokine profile seen in severe COVID-19 infection. In addition, several case reports have even reported possible protective effect of immunosuppressants against severe complications of COVID-19 in patients with rheumatological and non-rheumatological conditions. Another complexity in this case was monitoring the disease progression, since both COVID-19 and GPA can have similar findings on chest CT scan of ground glass opacity. In order to better understand the role of imm nosuppressants in rheumatological patients with COVID-19 infection, more data is required, currently European League Against Rheumatism (EULAR) is collecting data to monitor and report outcomes of COVID-19 in adult and paediatric population, this will provide invaluable insight for Rheumatologists. Case report-Key learning points This case poses a challenge for Rheumatologists in managing a patient with active vasculitis and concomitant COVID-19 infection due to limited data available literature. It has also stressed the importance of working in a multidisciplinary team when managing such complex patients. Importance of continuous surveillance of patients receiving immunosuppressive therapy is advised due to possible increased risk to SARS-CoV-2.
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Coronavirus disease (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily affects the epithelium of the airways. With the increasing involvement of dermatologist in management of this crisis, cutaneous symptoms gained more and more attention. In this review, we will describe cutaneous symptoms of patients of all ages in association with COVID-19. We will focus on such disorders that are caused by direct action of SARS-CoV-2 on tissues, complement, and coagulation system and on nonspecific eruption of the systemic viral infection. Drug-induced reactions are only mentioned in the differential diagnoses. Although more systematic investigations are warranted, it becomes clear that some symptoms are clinical signs of a milder COVID-19 course, while others are a red flag for a more severe course. Knowledge of the cutaneous manifestations of COVID-19 may help in early diagnosis, triage of patients, and risk stratification.