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BackgroundFlare of Rheumatoid Arthritis (RA) following COVID-19 vaccination has been reported with a low occurrence observed in those patients with disease remission. However, no local data is available in our multi-ethnic Malaysian population.ObjectivesTo evaluate the prevalence of RA flare in Malaysian patients following COVID-19 vaccination and its associated risk factors.MethodsThis was a cross-sectional study assessing RA flare based on patient-reported disease flare through self-administered questionnaires and physician-reported flare. Patient self-reported disease flare was defined as ‘a sudden worsening of rheumatology condition or arthritis within 1 month post-vaccination' while physician-reported flare was defined as ‘an increment of disease activity score 28-joint documented within 3 months post-vaccination‘ from either a scheduled or unscheduled clinic visit. A total of 186 RA patients attended the rheumatology clinic in Hospital Putrajaya from May to July 2022 who completed the primary COVID-19 vaccination under the Malaysian National Vaccination Programme were recruited. Demographic data, disease parameters including serology for rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACPA), cessation of disease modifying anti-rheumatic drugs (DMARDs) around vaccination, type of vaccines and adverse events were examined using descriptive and univariate analyses.ResultsMajority (93%) of RA patients enrolled were female with a mean age of 58 years old (standard deviation, SD 12.2) and mean disease duration was 12 years (SD 7.7). More than half were seropositive (66% RF, 63% ACPA) with 47.4% had double seropositivity (RF and ACPA positive). All patients received DMARDs with the majority (71%) were on methotrexate (MTX), 21.5% were on leflunomide, 17.7% on other DMARDs, with a small proportion (14%) of patients were receiving prednisolone. Only 4.8% of patients were on biologics or targeted synthetic disease modifying anti-rheumatic drugs. Half of the patients were in remission prior to vaccination. 62% of patients received Pfizer-BioNTech vaccine as the primary vaccine, followed by Sinovac-CoronaVac (24.6%) and Oxford-AstraZeneca (13.4%) vaccines. A booster dose had been administered to 80% of patients, of which 88.7% was Pfizer-BioNTech vaccine. MTX therapy were discontinued in 39.4% of patients (n=52) post-vaccination for a week duration. The prevalence of RA flare was only 12.9% (n=24) in which 14 were self-reported and 10 were physician-reported flares (4 severe flare, 6 mild-moderate flare). Flare rates were higher during the first and second dose of vaccination with 29.2% respectively, and only 12.5% were reported after booster vaccination. Common vaccine adverse effects were fever (16.8%), myalgia (8.6%) and arthralgia (6.4%). There were no significant differences in the occurrence of flare post-vaccination between age, gender, disease activity prior to vaccination, types of vaccine, usage of MTX and prednisolone, and discontinuation of MTX post-vaccination. Although seropositivity did not exhibit statistically significant flare rate post vaccination, sub-analysis revealed four times higher rate of flare in those who has double positivity compared to seronegative RA patients (12% vs 4%).ConclusionPrevelance of RA flare post-COVID-19 vaccination in Malaysian RA population is low. No significant associated risk factors were identified although double seropositivity appeared to have higher number of flares.References[1]Bixio, R., Bertelle, D., Masia, M., Pistillo, F., Carletto, A. and Rossini, M. (2021), Incidence of Disease Flare After BNT162b2 Coronavirus Disease 2019 Vaccination in Patients With Rheumatoid Arthritis in Remission. ACR Open Rheumatology, 3: 832-833.[2]Li X, Tong X, Yeung WWY, Kuan P, Yum SHH, Chui CSL, Lai FTT, Wan EYF, Wong CKH, Chan EWY, Lau CS, Wong ICK. Two-dose COVID-19 vaccination and possible arthritis flare among patients with rheumatoid arthritis in Hong Kong. Ann Rheum Dis. 2022 Apr;81(4):564-568.Acknowledgements:NIL.Disclosure of InterestsNone Declared.
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BackgroundConsideration is needed when using Janus kinase (JAK) inhibitors to treat RA in pts aged ≥65 years or those with cardiovascular (CV) risk factors. The JAK1 preferential inhibitor FIL was generally well tolerated in clinical trials[1];safety has not been determined in a real-world setting.ObjectivesTo report baseline characteristics and up to 6-month safety data from the first 480 pts treated with FIL in the FILOSOPHY study (NCT04871919), and in two mutually exclusive subgroups based on age and CV risk.MethodsFILOSOPHY is an ongoing, phase 4, non-interventional, European study of pts with RA who have been prescribed FIL for the first time and in accordance with the product label in daily practice. Baseline characteristics and the incidence of select adverse events (AEs) are assessed in pts aged ≥65 years and/or with ≥1 CV risk factor (Table 1), and in those aged <65 years with no CV risk factors.ResultsAs of the end of June 2022, 480 pts had been treated: 441 received FIL 200 mg and 39 received FIL 100 mg. Of the 480 pts, 148 (30.8%) were aged ≥65 years;332 (69.2%) were aged <65 years. In total, 86 (17.9%) were former smokers, 81 (16.9%) were current smokers and 203 (42.3%) were non-smokers (data were missing for 110 pts [22.9%]). In addition to smoking, the most frequent CV risk factors included a history of hypertension (32.3%), a history of dyslipidemia (10.2%) and a family history of myocardial infarction (8.5%;Table 1).23 pts (4.8%) discontinued treatment due to AEs. Of the 354 pts aged ≥65 years or with ≥1 CV risk factor, infections affected 64 pts (18.1%), 34 (9.6%) had COVID-19, 2 (0.6%) had herpes zoster, and cardiac disorders (angina pectoris, atrial fibrillation, palpitations and tachycardia) affected 5 pts (1.4%);no cases of malignancies were observed. In the subgroup aged <65 years and with no CV risk factors (n=126), infections occurred in 18 pts (14.3%) (9 [7.1%] had COVID-19;3 [2.4%] had herpes zoster) and malignancies (myeloproliferative neoplasm) affected 1 pt (0.8%);no pts had cardiac disorders. There were no cases of deep vein thrombosis or pulmonary embolism in either subgroup.ConclusionIn this interim analysis of FILOSOPHY, no unexpected safety signals emerged at up to 6 months. Although infections and cardiac disorders affected a numerically greater proportion of pts aged ≥65 years or with ≥1 CV risk vs those aged <65 years with no CV risk, longer follow-up on a broader cohort is necessary to further characterize the safety of FIL in different groups of pts with RA.Reference[1]Winthrop K, et al. Ann Rheum Dis 2022;81:184–92Table 1.Baseline characteristics and CV risk factorsBaseline demographics/CV risk factorsAll FIL-treated pts (N=480)≥65 years or with ≥1 CV risk factor (n=354)<65 years and no CV risk factor (n=126)*Female sex, n (%)351 (73.1)252 (71.2)99 (78.6)Age, years, mean (SD)57.6 (11.5)60.4 (10.8)49.6 (9.6)Rheumatoid factor positive, n (%)†228 (47.5)167 (47.2)61 (48.4)Anti-citrullinated protein antibody positive, n (%)‡243 (50.6)176 (49.7)67 (53. 2)Body mass index, kg/m2, mean (SD)27.6 (5.7) n=43728.0 (5.4) n=33126.3 (6.4) n=106RA disease duration, years, mean (SD)10.4 (9.4) n=47810.5 (9.5) n=35310.0 (8.8) n=125Tender joint count 28, mean (SD)8.6 (6.9) n=4578.7 (7.1) n=3408.3 (6.3) n=117Swollen joint count 28, mean (SD)5.6 (5.2) n=4525.7 (5.4) n=3365.4 (4.4) n=116Former smoker, n (%)§86 (17.9)86 (24.3)0Current smoker, n (%)§81 (16.9)81 (22.9)0Non-smoker, n (%)§203 (42.3)130 (36.7)73 (57.9)Family history of myocardial infarction, n (%)41 (8.5)41 (11.6)0Medical history of: n (%) CV disease33 (6.9)33 (9.3)0 Diabetes35 (7.3)35 (9.9)0 Dyslipidemia49 (10.2)49 (13.8)0 Hypertension155 (32.3)155 (43.8)0 Ischemic CNS vascular disorders11 (2.3)11 (3.1)0 Peripheral vascular disease17 (3.5)17 (4.8)0*Includes 53 pts with missing smoking status data who were aged <65 years with no other CV risk factors.†Missing/unknown in 154 pts;‡Missing in 153 pts;§Smoking status data missing in 110 pts (22.9%).AcknowledgementsWe thank the physicia s and patients who participated in this study. The study was funded by Galapagos NV, Mechelen, Belgium. Publication coordination was provided by Fabien Debailleul, PhD, of Galapagos NV. Medical writing support was provided by Debbie Sherwood, BSc, CMPP (Aspire Scientific, Bollington, UK), and funded by Galapagos NV.Disclosure of InterestsPatrick Verschueren Speakers bureau: AbbVie, Eli Lilly, Galapagos, Roularta, Consultant of: Celltrion, Eli Lilly, Galapagos, Gilead, Nordic Pharma, Sidekick Health, Grant/research support from: Galapagos, Pfizer, Jérôme Avouac Speakers bureau: AbbVie, AstraZeneca, BMS, Eli Lilly, Galapagos, MSD, Novartis, Pfizer, Sandoz, Sanofi, Consultant of: AbbVie, Fresenius Kabi, Galapagos, Sanofi, Grant/research support from: BMS, Fresenius Kabi, Novartis, Pfizer, Karen Bevers Grant/research support from: Galapagos, Susana Romero-Yuste Speakers bureau: AbbVie, Biogen, BMS, Lilly, Pfizer, Consultant of: Sanofi, Lilly, Grant/research support from: Lilly, MSD, Roberto Caporali Speakers bureau: AbbVie, Amgen, BMS, Celltrion, Eli Lilly, Galapagos, Janssen, MSD, Novartis, Pfizer, Sandoz, UCB, Consultant of: AbbVie, Amgen, BMS, Celltrion, Eli Lilly, Fresenius Kabi, Galapagos, Janssen, MSD, Novartis, Pfizer, Roche, Sandoz, UCB, Thomas Debray Consultant of: Biogen, Galapagos, Gilead, Francesco De Leonardis Employee of: Galapagos, James Galloway Speakers bureau: AbbVie, Biogen, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, Roche, UCB, Consultant of: AbbVie, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, Grant/research support from: AstraZeneca, Celgene, Gilead, Janssen, Medicago, Novavax, Pfizer, Monia Zignani Shareholder of: Galapagos, Employee of: Galapagos, Gerd Rüdiger Burmester Speakers bureau: AbbVie, Amgen, BMS, Chugai, Galapagos, Lilly, Pfizer, Sanofi, Consultant of: AbbVie, Amgen, BMS, Galapagos, Lilly, Pfizer, Sanofi.
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BackgroundComplete peripheral B cell depletion has been considered as a relevant indicator of short-term response to rituximab (RTX) in rheumatoid arthritis (RA) [1,2]. However, no information is available to validate this observation in RA patients long-term treated with RTX.ObjectivesTo determine whether sustained complete B cell (BC) depletion is associated with a better clinical response in RA patients long-term treated with RTX.MethodsRetrospective routine care study conducted in the Rheumatology department of Cochin hospital. We included consecutive patients fulfilling the ACR/EULAR 2010 classification criteria for RA hospitalized in 2021 for a new RTX infusion. All recruited patients had received at least 3 prior RTX infusions and had disease activity assessment (DAS28 and DAS28-CRP) and CD19 counts (Aquios, Beckman Coulter) available during each of the 4 last infusion visits. The primary endpoint was the course of DAS28 and DAS28-CRP, calculated the day of the last 4 infusion visits according to sustained complete (mean CD19 counts <18/µL) or incomplete (mean CD19 counts ≥18/µL) BC depletion. Secondary endpoints were the frequency of end-of-dose effect and patient self-reported RA flares at each infusion visit, as well as the course of pain/fatigue VAS, CRP and gammaglobulin levels according to complete or incomplete B cell depletion.ResultsWe included 126 patients (105 women, 83%) with a mean age of 64±12 years and a mean disease duration of 22± 5 years. Only 43 patients (34%) had maintained complete BC depletion during the last 4 infusions (mean CD19 counts 13±4/µL) (Figure 1A-B). Patients with incomplete BC depletion (n=83, mean CD19 counts: 77±73/µL, p<0.001) did not differ from those who maintained complete BC depletion in terms of age, gender, disease duration, structural damages and concomitant treatment.Patients with incomplete BC depletion had a higher frequency of rheumatoid factor (92% vs. 77%, p=0.018) and ACPA (84% vs. 72%, p=0.11);these patients had received RTX for a longer period (99±57 months vs. 69±47 months, p=0.003), with significantly higher number of infusions (14±7 vs. 12±6 infusions, p=0.037) and increased cumulative dose (10±6 g vs. 8±5 g, p=0.10) compared to patients with sustained complete BC depletion. On the other hand, their interval between 2 infusions was significantly longer (8±3 months vs. 6±1 months, p<0.001).The course of DAS28 and DAS28-CRP during the last 4 infusions was not different between the 2 groups (Figures 1C-D). The mean DAS28 and DAS28-CRP calculated at the time of last 4 infusion visits did not differ between patients with incomplete or sustained complete BC depletion (DAS28: 2.71±1.06 vs. 3.01±1.10, p=0.33 and DAS28-CRP: 2.53±0.88 vs. 2.88±0.84, p=0.095). The frequency of an end-of-dose effect and self-reported flares was similar between the 2 groups, as well as the evaluation of pain VAS, asthenia VAS, CRP and gammaglobulin levels (Figures 1E-H).ConclusionMaintaining complete BC depletion is not a therapeutic target to achieve in RA patients in long-term maintenance therapy with RTX. These results show that it is possible to space out RTX infusions to 8 months without loss of clinical benefit, which remains identical to that of patients treated every 6 months with sustained BC depletion. This result may have clinical implications during the COVID-19 pandemic since the antibody response to SARS-CoV-2 vaccination is preferentially obtained in patients with detectable B cells [3].References[1]Vital EM et al. Arthritis Rheum 2011;63:603–8.[2]Dass S et al. Arthritis Rheum 2008;58(10):2993–2999.[3]Avouac et al, Rheumatology 2022Figure 1.Course of mean (±SD) CD19, DAS28, DAS28-CRP, pain and fatigue VAS, CRP and gammaglobulins at the last 4 RTX infusion visits according to sustained complete or incomplete B cell depletion (CBCD and IBCD respectively).[Figure omitted. See PDF]Acknowledgements:NIL.Disclosure of InterestsNone Declared.
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Background/Aims In December 2019, a new type of novel coronavirus (COVID-19) was identified in Wuhan, China. The likelihood of developing an autoimmune and/or rheumatic diseases in COVID-19 survivors is high and a serious matter. The acute SARS-CoV-2 infection may unmask previously undiagnosed rheumatic conditions. We aimed to study rheumatic autoimmune disease manifestations diseases following COVID-19 infection survival. Methods The study was an observational case series study. The data collection was carried out in Iraqi Kurdistan region between the 1st of July 2021 and 20th of March 2022. Seventy-five patients were included: the patients who previously had confirmed COVID-19 infection who developed symptoms of rheumatic autoimmune diseases post COVID-19 cure. The study was conducted via a rigorous evaluation by two rheumatologists. Patients were investigated by (ESR (mm/h) and CRP (mg/L), some autoimmune screen panel for suspecting rheumatological disease patients were sent for ANA, anti-CCP (U/ML) and rheumatoid factor (IU/M) L. Then, patients were diagnosed according to the classification criteria for suspected autoimmune diseases and those with exacerbation were evaluated clinically and by laboratory;rheumatoid arthritis by DAS28, systemic lupus erythematosus by C3, C4. Results A total of seventy-five participants post-COVID-19 infection were enrolled in this study. Age of the participants was 47.15 +/-16.18 SD, more of the participants were female (69) out of 75. For most of the patients the ESR were high with p value of 0.012, which was statistically significant. ANA was high titre in SLE patients which was (3.05+/-2.4) and in antiphospholipid syndrome p-value was significant at 0.042, Anti-CCP were positive in RA patients and in those with exacerbation of RA (44+/-10, 31.7+/-5.7 respectively), DAS28 was (4.95+/-0.59) moderate and high disease activity in patients with exacerbations. C3, C4 were low in patients with exacerbation of SLE (0.47+/-0.22, 0.03+/-0.01, respectively). Most of the patients developed symptoms post-COVID-19 between 4-10 weeks (37 participants). Conclusion Rheumatic autoimmune diseases presenting post-COVID-19 survival most commonly were systemic lupus erythematous followed by rheumatoid arthritis. and previous autoimmune diseases presented with exacerbation. (Table Presented).
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Objectives: Chronic Inflammatory Immune-mediated Diseases (CIMD) can cause pain and severe discomfort to the patient, leading to significant reductions in his/her quality of life. Vaccination against COVID-19 has proven to be an efficient method in preventing cases and serious repercussions. However, there is insufficient evidence on the safety of these vaccines in the CIMD population. Objective(s): To assess disease activity in adolescent patients with CIMD after vaccination against SARS-CoV-2. Method(s): Observational, longitudinal, ambidirectional study with follow-up of groups of adolescent patients with CIMDwho received the vaccine provided by the National Immunization Program -Pfizer/BioNTech. Sociodemographic and clinical disease activity data were collected before and after each vaccine dose. Data were stored through an online platform (REDCap). This study is associated to the SAFER Project from the Brazilian Society of Rheumatology and was approved by the local Research Ethics Committee. Result(s): Nineteen adolescents aged between 12 and 17 years were included, all of whom met the inclusion/exclusion criteria. Of the total, 31.6% have Juvenile Idiopathic Arthritis (JIA)-14.33 +/- 2.25 years of age, whose subtypes included persistent oligoarticular JIA (16.7%), Polyarticular Rheumatoid Factor (RF) negative (33.3%), Polyarticular RF positive (16.7%) and Systemic (33.3%);68.4% have Systemic Lupus Erythematosus (SLE) -14.77 +/- 1.96 years of age. Regarding JIA patients, at inclusion, the mean disease activity assessed by the physician was 3 +/- 3.83 and 3.25 +/- 3.77 as assessed by the patient. After the 1st dose, the mean activity assessed by the physician was 2.8 +/- 3.9 and after the 2nd dose it was 3 +/- 4.24. Themean activity after the first dose as assessed by the patient was 3.2 +/- 3.96, and after the 2nd dose it was 2.8 +/- 3.11. In the SLE patients, at inclusion, the mean degree of disease activity was 1.92 +/- 1.83 and of the SLEDAI-2 K was 4.67 +/- 5.14. After the 1st dose, the mean disease activity was 1.11 +/- 1.96, and after the 2nd dose, it was 2.25 +/- 2.76. After the 1st dose, the SLEDAI-2 K was 1.11 +/- 1.76, and after the 2nd dose it was 4.25 +/- 5.28. No reports of worsening of disease activity after the vaccine were found. Conclusion(s): The vaccination proved not to contribute to worsening of clinical activity of rheumatic diseases in adolescents, without significant changes in SLE assessment indices and in the personal and medical assessment of JIA patients.
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Case report Erythema nodosum (EN) is considered a delayed type IV hypersensitivity reaction, triggered by exposure to an antigen, which diagnostic workout is usually challenging. Several conditions have been described as possible causes for EN, including infections, sarcoidosis, pregnancy, neoplasic and inflammatory diseases. Rarely, vaccines such as tetanus, diphtheria, BCG, hepatitis B, human papillomavirus, malaria, rabies, smallpox, typhoid, and cholera have been associated with subsequent EN. We present a 31-year- old leucodermic female with suppurative adenitis, who developed painful erythematous nodules on the pretibial area of the lower limbs. Ten days prior to presentation she had received the first dose of the COVID-19 mRNA-1273 vaccine. Fever, lymphadenopathy, fatigue, weight loss, arthritis, cough, diarrhoea, other organ-specifc symptoms and close contact with tuberculosis were excluded. She was under oral contraception for several years, that was not discontinued. Pregnancy was excluded. No positive signs were detected on physical examination besides the referred nodules. Laboratory tests revealed a normal complete blood count, erythrocyte sedimentation rate, C-reactive protein, antistreptolysin O titer, renal and hepatic tests. Interferon-gamma release assay was negative. Circulating rheumatoid factor was normal, anti-nuclear, anti-double stranded DNA and anti-neutrophil cytoplasmatic antibodies were negative. Angiotensin converting enzyme and protein electrophoresis were normal. Hepatitis B and C, HIV 1/2 and syphilis serologic profiles were negative. Urinalysis and fecal calprotectin were unremarkable. The patient was treated with naproxen and topic betamethasone dipropionate. Violaceous involution was reported, with complete resolution of the EN lesions over the following month. In the literature, there are rare reports of EN following SARS-COV2 infection and also after COVID-19 vaccination. To our knowledge this is the second report of EN after the COVID-19 mRNA-1273 vaccine. This case highlights the importance of clinical awareness for the possible association of COVID-19 vaccination and EN, adding to the already extensive list of causes included in the etiological investigation of these patients.
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Case report Cytomegalovirus (CMV) causes latent asymptomatic infection in most adults worldwide. Immunodeficiency or immune activation can disrupt viral suppression and lead to viral reactivation, occasionally causing a mononucleosis-like illness in otherwise healthy immunocompetent people. A 37-year- old female presented with a 10-day history of fevers, chills, right-sided neck tenderness, rapidly expanding rash, as well as myalgia, arthralgia, and weakness. She had received her first dose of tozinameran (Pfizer-BioNTech COVID-19 mRNA vaccine) 11 days prior to symptom onset. She was admitted to hospital for further investigations, and was seen by an allergy/clinical immunology specialist, with the diagnosis initially felt to be a delayed serum sickness-like reaction to the vaccine. On admission to hospital, the patient was febrile (37.8C) and tachycardic (122 beats/min). Her physical examination was remarkable for right-sided submandibular tenderness, diffuse blanchable, nonpruritic, erythematous, maculopapular rash, and mild facial swelling. There were no effused joints, lymphadenopathy, nor splenomegaly. Bloodwork showed pancytopenia and mild liver transaminase elevation. Blood cultures were negative. Multiple PCR tests for COVID-19 were negative. Monospot and serology for HBV, HIV, and B. burgdorferi were negative. CMV serology was positive, but unavailable until after discharge. ANA and rheumatoid factor were negative. CT head demonstrated nonspecific edema in the right submandibular area without abscess. On outpatient follow-up, the patient reported symptom resolution over two months. Repeat CMV titres two months post hospitalisation showed strongly elevated IgG, which upon consultation with infectious diseases was felt to represent CMV reactivation (Table 1). CMV viral load was negative. Pancytopenia resolved and transaminases normalized. She received her second dose of tozinameran 4 months post first dose with prophylactic valacyclovir 1g once daily for 1 week prior to and 1 week post vaccination as recommended by infectious diseases and remained asymptomatic. This case is the first known description of CMV reactivation secondary to COVID-19 vaccination. It may be underdiagnosed due to nonspecific symptomatology, as CMV seropositivity ranges from 60-100% of all adults. While causality has yet to be established, recognition of this condition may allow appropriate treatment and prophylaxis in order to facilitate safe COVID-19 vaccination in affected individuals. The patient has provided verbal consent through the telephone for the publication of this case report due to the current COVID-19 pandemic, with written consent to follow.
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Myocarditis can lead to myocardial infarction in the absence of coronary artery obstruction. We report a case of probable myocarditis, complicated by myocardial infarction with non-obstructive coronary arteries. A 19-year-old man presented with chest pain typical of myocarditis. He was a smoker but was otherwise well. Electrocardiogram revealed diffuse ST-elevation and echocardiography revealed a thin, akinetic apex. Troponin-T levels on admission were raised leading to an initial diagnosis of myocarditis being made. However, late gadolinium enhancement study on cardiac magnetic resonance imaging demonstrated transmural enhancement typical of ischaemia. Coronary angiogram was normal, leading to a likely diagnosis of myocardial infarction with non-obstructive coronary arteries. It is important to highlight that coronary assessment remains important when working up for myocarditis, as myocardial infarction with non-obstructive coronary arteries can often complicate myocarditis in cases of normal angiography. Another important lesson was on how cardiac magnetic resonance imaging provided vital evidence to support underlying ischaemia despite normal coronary angiogram, leading to a diagnosis of myocardial infarction with non-obstructive coronary arteries. Myocardial infarction with non-obstructive coronary arteries remains a broad 'umbrella' term and cardiac magnetic resonance imaging, as well as more invasive coronary imaging techniques during angiography, can further assist in its diagnosis. Our case provides a reminder that myocardial infarction with non-obstructive coronary arteries, although increasingly recognised, remains under-diagnosed and can often overlap with peri-myocarditis, highlighting the need to employ multi-modality imaging in guiding management.Copyright © The Author(s) 2021.
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Livedoid vasculopathy (LV) is a noninflammatory thrombotic disease caused by occlusion of dermal small vessels associated with systemic autoimmune disorders and coagulopathies. However, LV is often reported as being 'idiopathic', despite extensive investigation. We report a case of severe LV in an otherwise healthy 27-year-old woman, associated with parvovirus infection. The patient presented with a short history of a livedoid rash initially covering her torso, which spread to acral sites. Burning pains in the lower limb caused reduced mobility;systemically, she remained well and stable throughout. Examination revealed generalized acral skin pallor, livedoid patches of violet erythema and purpura with deep serpiginous ulcerations over extensor aspects of upper and lower limbs with a more broken/racemosa nonulcerated livedoid appearance on the trunk. On admission a transaminitisareas continued to ulcerate. Codeine was present with a creatine kinase of 1569 U L.1, but other blood test results were unremarkable including erythrocyte sedimentation rate, complement, cryoglobulins, antinuclear antibodies, antineutrophil cytoplasmic antibodies, extractable nuclear antigen, rheumatoid factor, myositis screen, antiphospholipid screen and thrombophilia screen. Parvovirus IgG and IgM were both positive and tested for, as the patient's young daughter had recently been diagnosed with 'slapped cheek disease'. Magnetic resonance imaging of the thighs showed a diffuse mild myositis;electromyography, nerve-conduction studies, barium swallow and computed tomography of the chest, abdomen and pelvis were all normal. An incisional skin biopsy was performed, which revealed a blood vessel with organizing (Solimani F, Mansour Y, Didona D et al. Development of severe pemphigus vulgaris following SARS-CoV-2 vaccination with BNT162b2. J Eur Acad Dermatol Venereol 2021;35: e649- 51) have been reported. The main proposed mechanisms for AstraZeneca vaccine-induced pemphigus could be a hyperimmune reaction in genetically predisposed individuals, with eventual formation of anti-desmoglein antibodies. An alternative hypothesis is that vaccine components could act as foreign antigens resulting in a cross-reaction with pemphigus antigens. The close association of COVID-19 vaccination with the acute onset of pemphigus in our patient, as well as exacerbations after subsequent vaccine administration, is more than coincidental. Considering the recent pandemic with COVID-19 and the widespread administration of the COVID-19 vaccine, continued observation and documentation of true adverse events is essential.
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The novel coronavirus disease 2019 (COVID-19) has given rise to a global pandemic, as well as a multitude of long-term sequelae that continue to perplex physicians around the world, including in the United States. Among the most common and impactful long-haul symptoms experienced by survivors is COVID-19 fatigue. This review will use long COVID-19, post-acute COVID-19 syndrome (PCS), and PostAcute Sequelae of COVID-19 (PASC) as synonymous terms to refer to the chronic symptomatology;chronic fatigue associated with PASC will be referred to as COVID-19 fatigue. While the knowledge and research on the exact pathophysiological mechanisms involved in the disease is still limited, parallels have been drawn between fatigue as a component of long COVID-19 and myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS). Current studies suggest applying principles of pathophysiology, diagnosis, and treatment similar to those for ME/CFS in order to aid in managing chronic fatigue in COVID-19 survivors, particularly in the primary care setting. The osteopathic family physician can use the proposed pharmacologic agents, along with osteopathic manipulative treatment (OMT), as therapeutic modalities that can be tailored to each patient's unique case. Nevertheless, research on proven successful treatments is still scarce. For that reason, it is essential that COVID-19 fatigue is recognized early, especially since its longitudinal impacts may be debilitating for many. This review of the available literature on COVID-19 fatigue aims to help provide quality care and lessen the disease burden experienced by patients.Copyright © 2023 by the American College of Osteopathic Family Physicians. All rights reserved.
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AIM: Coronavirus disease 2019 (COVID-19) has been proposed as triggering autoimmunity. The aim of this study was to evaluate the presence and clinical significance of autoantibodies in patients with COVID-19. METHODS: We retrospectively collected data from 245 patients who were hospitalized for COVID-19. All patients were tested for the presence of antinuclear antibody (ANA), rheumatoid factor (RF), anti-citrullinated peptide antibody (ACPA), and anti-cytoplasmic neutrophil antibody (ANCA). Risk factors for death and critical COVID-19, defined as the need for invasive mechanical ventilation or extracorporeal membrane oxygenation, were analyzed. RESULTS: Ninety (36.7%) patients tested positive for ANA, and 51 (20.8%) patients tested positive for RF. Three patients each (1.2%) tested positive for ACPA and ANCA. RF-positive patients had higher rates of invasive mechanical ventilation and death than RF-negative patients (70.6% vs 28.4%, P < 0.001 and 45.1% vs 18.6%, P < 0.001, respectively). Underlying lung disease, kidney disease, heart disease, quick COVID severity index (qCSI), and lactate dehydrogenase (LDH) were associated with in-hospital death. RF (odds ratio [OR] 7.31, 95% CI 2.50-21.37, P < 0.001), qCSI (OR 1.42, 95% CI 1.19-1.69, P < 0.001), and LDH (OR 1.004, 95% CI 1.002-1.005, P < 0.001) were associated with critical COVID-19. Combination of RF, qCSI, and LDH showed good prognostic value (area under the curve = 0.903, P < 0.001) for critical COVID-19. CONCLUSIONS: ANA and RF were frequently detected in COVID-19 patients. RF could be a risk factor for critical COVID-19. The results of this study suggest immune dysfunction contributes to the complications of COVID-19.
Subject(s)
Arthritis, Rheumatoid , COVID-19 , Humans , Rheumatoid Factor , Retrospective Studies , Antibodies, Antineutrophil Cytoplasmic , Hospital Mortality , Autoantibodies , Antibodies, AntinuclearABSTRACT
Background and Aim: Since the emergence of COVID-19, tele-rheumatology care has presented as an appealing alternative way for accessing health care. The efficacy of tele-care needs to be evaluated in our setting. This study aimed at assessing the agreement between the tele-visit and the face-to- face clinic-based visit. Methodology: We prospectively recruited patients with rheumatoid arthritis;who were following up in the out-patient department clinics between December 2021 and May 2022. Each patient underwent disease activity assessment by means of disease activity score 28-c- reactive protein (DAS28-CRP) and disease activity score28-erythrocyte sedimentation rate (DAS28-ESR). Within two weeks from the face-to- face visit, we virtually assessed their disease activity, through a telephone-based interview, by applying Routine Assessment of Patient Index Data 3 (RAPID3) score, collecting data on demographics and inquiring about satisfaction with the tele-visit. Disease activity scores were categorized into remission or low disease activity, and moderate to high disease activity. Result(s): In our study, 78 patients were recruited and completed the two-points interview. A total of 62(79.49%) of the participants were female;mean age of 54.73 +/- 13.71 years. Seropositivity for rheumatoid factor and/or anti-citrullinated peptide was found in 51(83.61%) participants. 27% of patients with RAPID3 had remission or low disease activity. While this was 71% and 33% for DAS28-CRP and DAS28-ESR, respectively. Moderate to high disease activity percentage of 73%, 29% and 67% were found in RAPID3, DAS28-CRP and DAS28-ESR, respectively. Furthermore, the correlations of RAPID 3 were relatively moderate but significant with DAS28-CRP (r = 0.6, P-value < 0.001) and DAS28-ESR (r = 0.4, P-value = 0.001), respectively. Satisfaction rates with the tele-visit were at odds with other reported publications. Conclusion(s): Tele-rheumatology assessment of disease activity for patients with rheumatoid arthritis appears to be feasible in our setting. Further studies should aim at assessing patients' satisfaction and the recently implemented video-based tele-clinics.
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Background: Rheumatoid Arthritis (RA) flare post-COVID- 19 vaccination has been reported and poses a great concern among patients. This study aims to evaluate the prevalence of RA flare post COVID-19 vaccination and its associated risk factors. Method(s): This was a cross-sectional questionnaire-based study assessing RA flare based on patient self-report disease flare or documented physician assessment (physician-reported flare). The study was conducted from May to July 2022 in Hospital Putrajaya and recruited RA patients who received at least one dose of COVID-19 vaccine under the Malaysian National Vaccination Programme. Patient self-reported disease flare was defined as 'a sudden worsening of rheumatology condition or arthritis within 1 month post-vaccination' while physician-reported flare was defined as 'an increment of disease activity score 28-joint (DAS28 CRP/ESR) documented within 3 months post-vaccination' from either a scheduled or unscheduled clinic visit. Demographic data, vaccination history and disease parameters were retrieved from electronic medical records. Statistical analysis included descriptive and univariate analyses were performed using SPSS. Result(s): A total of 186 patients were enrolled. Majority (93%) were female with the mean age of 58 years old (standard deviation, SD 12.2). Most patients were seropositive (66% Rheumatoid factor, 63% anti-citrullinated peptide antibodies) with mean disease duration of 12 years (SD 7.7). Majority were on methotrexate (MTX) (71%), 21.5% were on leflunomide and only 4.8% were on biologics or targeted synthetic disease modifying anti-rheumatic drugs. A small proportion of patients were on steroids (14%). Half of the patients were in remission prior to vaccination. All patients completed 2 doses of vaccination in which 62% received Pfizer-BioNTech vaccine followed by Sinovac (coronaVac) vaccine (24.6%) and Oxford-AstraZaneca vaccine (13.4%). Only 80% received booster dose, of which 88.7% was Pfizer-BioNTech vaccine. A total of 52 patients who were on MTX therapy discontinued the drug post-vaccination for a week duration. The prevalence of flare was only 12.9% (n: 24) in which 14 were self-reported and 10 were physician-reported flares (4 severe flare, 6 mild-moderate flare). Majority of flares occurred during the first and second dose of vaccination with 29.2% respectively, and only 12.5% were reported after booster vaccination. There were no significant differences in the occurrence of flare post-vaccination between age, gender, disease activity prior to vaccination, types of vaccine, usage of MTX and steroids, and discontinuation of MTX post-vaccination. Conclusion(s): Prevelance of RA flare post-COVID- 19 vaccination is low and there were no significant associated risk factors identified in this study.
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Case report - Introduction: This is the case of an adolescent referred to rheumatology following 5 years of back pain. After years of trying a number of treatments without much success, the cause was found to be a previously undiagnosed urological pathology. The case highlights awareness of non-rheumatological causes and incidental findings which can redirect a patient towards more appropriate treatment and reduce the potential for long-term adverse health issues and anxiety. Case report - Case description: B was referred age 16 to rheumatology with a 5-year history of lower back pain. She had previously seen paediatricians with symptoms initially attributed to constipation due to intermittent straining and hard stool. However, constipation remedies had not relieved the pain which progressed gradually to a more persistent dull ache with impact on daily activities. Various analgesics (including paracetamol and non-steroidal anti-inflammatories), exercises and acupuncture had not helped. There was no history of recurrent urinary tract infections or symptom correlation with fluid intake, menstruation or bowel habit. No inflammatory features or connective tissue disease symptoms were noted and family history was unremarkable Clinical examination was normal apart from mild tenderness in the lumbar region. Rheumatoid factor was borderline positive (15 iu/mL) with the rest of blood tests normal including renal function, inflammatory markers (CRP, ESR), anti CCP and ANA. She had minimal microscopic haematuria without proteinuria. MRI spine in 2015 was normal. In view of her young age and symptoms affecting daily activities, STIR sequence spinal MRI was requested. This excluded any new or old inflammatory changes but incidentally identified a dilated left pelvi-calyceal system. Renal ultrasound confirmed a grossly hydronephrotic left kidney with hydroureter and minimal renal tissue suggesting longstanding obstruction. No calculi were seen. The patient was referred to urologists. Further investigations (including MRI abdomen) confirmed similar findings and a distal ureteric stricture. A MAG 3 renogram showed a normal right kidney but only 12% functioning of the left kidney. Urologists have advised surgery (removal of left kidney and ureter) which may relieve symptoms or a conservative non-surgical approach (continue analgesia, physiotherapy and monitoring). The patient and her family are relieved to have a possible cause identified and are considering the surgical option due to ongoing flank discomfort. Case report - Discussion: This was an interesting finding of hydroureter and hydronephrosis causing longstanding back pain presenting to rheumatologists. Until completion of the spondyloarthropathy protocol MRI (STIR images), aetiology had been unclear. Hydronephrosis and hydroureter has no specific age or racial predilection. Signs and symptoms may depend on whether obstruction is acute/chronic. Chronic cases may be asymptomatic or present as a dull discomfort (like this case). Some cases may only present in adulthood with pain precipitated by fluid intake. Blood tests may show impaired kidney function. Post-mortem studies suggest 50% of people have at least one renal abnormality (e.g., renal cysts, duplex ureters) with autopsy series incidence of hydronephrosis reported as 3.1%. Causes include anatomical abnormalities such as vesico-ureteric reflux, urethral strictures (usually present in childhood), calculi, benign prostatic hyperplasia, or intrapelvic neoplasms, pregnancy and infections (e.g., TB). Sudden onset unilateral renomegaly was reported in one case of primary Sjogren's with lymphocytic interstitial nephritis and positive Sjogren's autoantibodies. Our patient has no clinical or serological evidence of connective tissue disease. Minor pelvi-calyceal distension can occur as a normal finding in wellhydrated patients and pregnancy. However, significant hydronephrosis requires assessment to determine cause as it may affect long term renal function. Imaging via computed tomography, ultrasound and urograms can help guide further management. In this case the preceding cause and duration of pathology is unknown. Sterile, giant hydronephrosis treatment options include observation and ureteric stent or nephrostomy in patients unfit for surgery. Nephrectomy is advised for pain and recurrent infection in a non-functioning kidney. Complications may include bowel perforation, vascular injury and urine leakage. Both open and minimally invasive procedures have good reported outcomes. The COVID-19 pandemic and exams have affected timing of any elective procedures and the patient understands surgery may or may not offer complete symptom resolution. Case report - Key learning points: . Non-inflammatory causes of back pain should always be considered in cases of persistent back pain, particularly in young people to ascertain if there is a treatable cause . Hydronephrosis cases can be asymptomatic or present with vague, intermittent, non-specific abdominal symptoms with normal physical examination with or without haematuria. This can cause diagnostic uncertainty and delay referral to urology and appropriate renal investigations . Assessment of renal function (including MAG 3 renogram) is important to guide further management . Surgical interventions (pyeloplasty/nephrectomy) may ease symptoms long term but there is no guarantee of a successful outcome and operative risks need to be considered too . Left undiagnosed, potentially this patient could have had further disruption to daily activities and both physical and mental well being.
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Objective: To present a case of seronegative oligo-arthritis following COVID-19 infection. Background(s): COVID-19 infection caused by SARS-CoV- 2 may induce autoimmune phenomena. Although musculoskeletal symptoms are usual in COVID-19 infections, clinical arthritis with signs of inflammation are relatively uncommon. Our case highlights the occurrence of reactive arthritis following a COVID-19 infection. Case: A 37 year old woman developed sore throat, rashes, erythema and painful swelling of the 3rd distal interphalangeal joint of the hand and 1st metatarsophalangeal joint of the right foot following COVID-19 exposure. Nasopharyngeal swab test for SARS-CoV- 2 infection was positive. She had completed COVID-19 (inactivated Sinovac) vaccine 2 months earlier. There was a history of undifferentiated inflammatory arthritis 2 years earlier which had resolved with few months of methotrexate and non-steroidal anti-inflammatory drugs (NSAIDs). Work-up disclosed normal complete blood count and erythrocyte sedimentation rate (ESR), slightly elevated C-reactive protein;rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCP) were negative. She took NSAID for arthritis and anti-histamine for rashes and completed home-based quarantine. Symptoms resolved over the subsequent 2 to 3 weeks without sequelae. Conclusion(s): This case illustrates an autoimmune reaction to COVID-19 infection in the form of reactive arthritis (ReA). Although the clinical presentation, pathomechanisms, and management are likely similar to those described for ReA, we explore additional insights into other mechanisms and manifestations unique to post COVID-19 infections, and the increased susceptibility of this patient with prior history of undifferentiated inflammatory arthritis.
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Introduction/Background: Primary bone marrow oedema syndrome is an elusive and less well-defined entity. Whether Rheumatologists should consider it as a stand alone diagnosis, is debatable. It possibly would be best described as an MRI feature which could be a finding in a number of diseases which would include the initial phases of Osteonecrosis of the bone, Rheumatoid Arthritis, Spondyloarthritis, Enthesitis related, Post traumatic, OA, Infections and Cancers. The treatment options become constricted due to the paucity of evidence. Rheumatologists need to consider this as an area of unmet need with development of consensus classification criteria and treatment approaches. Description/Method: 27-year-old male, Height 174 cms Weight 90 Kgs BMI 29 Kg/m2, became symptomatic in Jan 2022 with complains of pain in the both hip joints & groin regions, pain became excruciating and he became bed-bound, with early morning stiffness lasting approximately 45 mins. Had received steroids for COVID infection in August 2020. Investigations Hb 13.5gm/dl TLC 7000/mm3 Platelet 400 x 103/mm3 Sr Bil 0.8mg/dl AST 16 IU/L. ALT 24 IU/L Sr Creatininine 1.1mg/dl Blood Sugar Levels, Fasting 89 mg/dl Post Prandial 102 mg/dl ESR 10mm in 1st hour by Wintrobes method CRP Quantitative 29.38mg/L HLA B27 by PCR Negative, RF Negative, ACCP Negative Serum, IgG, Beta2 Glycoprotein 1.44 SGU Serum, IgM, Beta2 Glycoprotein 3.44 SGU Serum, IgG, Cardiolipin antibody 8.4 GPL Serum, IgG, Cardiolipin antibody 17.45 GPL Lupus anticoagulant by DRVVT Negative Sr Cholesterol 211mg/dl HDL 29 mg/dl LDL 156mg/dl TGs 130 mg/dl MRI Hips & SI joints Transient bone marrow oedema/osteopenia of bilateral hip. PET CT Increased metabolic activity in both hip joints Bone Scan (99mTcMDP) Increased vascularity in perfusion phase, increased accumulation in soft tissue in blood pool phase and increased uptake in bilateral Hip joints in skeletal phase scan, suggestive of CRPS Type-I. Management Was initially managed with Tab Etoricoxib 90mg BD, also started on Tab Sulphaslazine and Tab Methotrexate. However, when he had no symptomatic relief he was administered Inj Infliximab on 12 May 2022 and a second dose on 9 June 2022. He had excellent pain relief after the 1st dose, however after 10 days of the administration, he again began experiencing pain especially after walking. He also had pain in the knees on this occasion. He was also administered Inj Zoledronic 4mg on 23 May 2022. He is at present not requiring any NSAIDs over the last 1 month. Discussion/Results: The patient having presented with excruciating and debilitating pain was worked up and evaluation revealed features of bone marrow oedema on MRI which was corroborated with bone scan and PET CT imaging. The acute phase reactant CRP was also significantly elevated. The patient also gave history of early morning stiffness lasting approximately 45 mins. Hence an underlying Inflammatory process such as Spondyloarthritis(Peripheral) with enthesitis was considered. The confounding factors were the pain which worsened on mobilization, HLA B27 negative status, Rheumatoid Factor and ACCP negative status and past history of having received IV Corticosteroids for COVID infection in August 2020. In view of the debilitating pain and aworking diagnosis of Spondyloarthritis, hewas started onNSAIDs alongwith rest, initially, followed by conventional synthetic disease modifying agents in Rheumatic disease followed by biologic synthetic diseasemodifying agent - Inj Infliximab. The thought process was to avoid prolonged NSAID use to prevent the associated side effects. However, since Avascular Necrosis of the Femoral head is a very likely possibility, the patient is planned to be kept under close follow up. Key learning points/Conclusion: Collaborative efforts between the Departments of Nuclear Medicine, Radiology, Orthopaedics and Rheumatology are crucial in the early detection and approach to cases of Bone Marrow oedema. Avascular necrosis of head of Femur is a far more common entity and must be kept in ind even when a diagnosis of Bone Marrow oedema syndrome is being entertained. Diagnosis of Bone Marrow oedema syndrome must be entertained only as a diagnosis of exclusion. Continued follow up and regular imaging must be pursued rigorously in patients diagnosed with Bone Marrow oedema syndromes. There is a requirement to document acute phase reactants such as CRP and ESR in patients diagnosed with Avascular necrosis of bone as this data could help us differentiate AVN from Primary Bone marrow oedema in the early stages.
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SESSION TITLE: Dyspne Mysteries SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: Anti-synthetase (AS) syndrome is characterized by interstitial lung disease (ILD), arthritis, myositis, fever, or Raynaud's phenomenon in the presence of an AS autoantibody (1). At least 70% of patients with AS syndrome develop ILD (2), and it represents the major cause of mortality in these patients with a 10 year survival rate of 73%. In a small cohort study, the anti-PL-12 antibody subtype was found to be strongly associated with ILD (3). CASE PRESENTATION: A 35 year old female with a history of tobacco use disorder presented to the hospital with three months of recurrent subjective fevers, non-productive cough, and dyspnea on exertion. She denied arthralgias, muscle weakness and hemoptysis. She initially presented to her primary care physician with these symptoms and was prescribed amoxicillin for streptococcal pharyngitis. The patient continued to be symptomatic and was treated empirically for COVID-19 pneumonia twice despite two negative COVID-19 tests and without any significant clinical improvement in her respiratory status. On admission, she was febrile, tachycardic, and had a new oxygen requirement with bilateral coarse breath sounds on exam. She had no leukocytosis and her COVID-19 test was negative. CT angiography of the chest showed extensive mixed reticular and airspace opacities with peribronchial predilection and peripheral sparing (figure 1). A bronchial alveolar lavage was notable only for neutrophilia (19%) and eosinophilia (4%). Rheumatological workup revealed elevated rheumatoid factor, positive antinuclear antibody (1:40), weakly positive anti–Sjögren's-syndrome-related antigen A antibody (50 AU/ml), undetectable anti-Jo-1 antibody and positive anti-PL-12 antibody. Pulmonary function testing revealed a TLC of 40% and DLCO of 28%, consistent with a restrictive pattern. Considering the patient's organizing pneumonia, positive antibodies, and findings of "mechanic's hands,” the patient was diagnosed with anti-synthetase syndrome with ILD. She was started on oral prednisone and mycophenolate mofetil. On follow-up, she was noted to have symptomatic improvement and stable hypoxia without clinical signs of disease progression. DISCUSSION: During the coronavirus pandemic, the resemblance of COVID-19 pneumonia to other diseases, in the absence of conscious suspicion for other etiologies, can lead to anchoring and availability bias thereby delaying diagnosis and appropriate treatment. Additionally, anti-synthetase syndrome should be considered in the differential diagnosis of ILD even in the absence of arthritis and myositis, as respiratory symptoms are often the first presenting signs. CONCLUSIONS: Increased responsibility is required of diagnosticians to exercise due diligence and active recognition of COVID availability and anchor bias to avoid missing crucial diagnoses. Reference #1: Cojocaru, Manole, Inimioara Mihaela Cojocaru, and Bogdan Chicos. "New insights into antisynthetase syndrome.” Maedica 11.2 (2016): 130. Reference #2: Marco, Joanna L., and Bridget F. Collins. "Clinical manifestations and treatment of antisynthetase syndrome.” Best Practice & Research Clinical Rheumatology 34.4 (2020): 101503. Reference #3: Kalluri, Meena, et al. "Clinical profile of anti-PL-12 autoantibody: cohort study and review of the literature.” Chest 135.6 (2009): 1550-1556. DISCLOSURES: No relevant relationships by Mario Flores No relevant relationships by David Jackson No relevant relationships by Lisa Saa No relevant relationships by Abu Baker Sheikh
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SESSION TITLE: Drug-Induced and Associated Critical Care Cases Posters 1 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Interstitial pneumonitis (ILD) is inflammation of lung interstitium leading to scarring and pulmonary fibrosis. Various etiologies include idiopathic, connective tissue disorders, sarcoidosis and drug induced1. Many chemotherapy agents have been implicated in drug related ILD such as bleomycin, taxanes. However, newer chemotherapeutic drugs such as molecular agents such as anti-VEGF, anti-EGFR (panitumumab) could be causative of drug induced ILD. CASE PRESENTATION: A 75-year-old female with stage IV sigmoid colon cancer treated with surgery, adjuvant FOLFOX chemotherapy and Panitumumab. She presented to the emergency department with shortness of breath and hypoxia after known COVID-19 exposure. Initial imaging with chest radiography showed bilateral ground glass opacities. A chest CT pulmonary embolism protocol was negative for pulmonary embolism but showed bilateral ground glass opacities (GGOs) and some interstitial thickening (L>R) not typical of COVID-19 infection. She was treated with remdesivir and dexamethasone, however her oxygen requirements continued to rapidly escalate. A repeat CT chest without contrast showed bilateral asymmetric interstitial thickening and GGOs. Given persistence of CT chest abnormalities, workup for interstitial lung disease was initiated. The results include ANA titer 1:80, otherwise negative ANCA profile, rheumatoid factor, anti-CCP, Scl-70, Sjogren antibodies. Given clinical history and imaging findings, diagnosis of ILD was suspected, and she was started on solumedrol 1 mg/kg. Her oxygen requirements decreased significantly over the next 2 days, and she was discharged home on oral steroid taper and pneumocystis pneumonia prophylaxis. DISCUSSION: Panitumumab is a fully humanized monoclonal antibody against EGFR. Approved by the US Food and Drug Administration in 2006 for advanced or recurrent colorectal cancer exhibiting wild-type KRAS mutation.2 ILD is rarely reported with panitumumab monotherapy, but higher incidence when used as a combination treatment such as with FOLFOX or FOLFIRI. A Japanese post-marketing surveillance study from 2010-2015 showed an ILD incidence of 1.3% but mortality rates of 51.3%.2 EGFR is expressed on basal cells and non-cilia cells of the bronchioles and type II cells of the alveolus. EGFR mediated mechanisms are important in tissue repair.3 Therefore inhibition of this pathway has been postulated to play a role in development of ILD. Another mechanism was decreased surfactant production by type II cells in pre-clinical study.4,5 ILD secondary to Panitumumab can occur at any point during therapy and up to 1 year after administration of drug.6 The role of infectious processes, in this case, COVID-19 pneumonia, could synergistically worsen ILD presentation. CONCLUSIONS: Although the incidence of ILD is low, the mortality rate is high, therefore early recognition and treatment is associated with improved clinical outcomes. Reference #1: Mudawi D, Heyes K, Hastings R, Rivera-Ortega P, Chaudhuri N. An update on interstitial lung disease. Br J Hosp Med (Lond). Jul 2 2021;82(7):1-14. Reference #2: Osawa M, Kudoh S, Sakai F, et al. Clinical features and risk factors of panitumumab-induced interstitial lung disease: a postmarketing all-case surveillance study. Int J Clin Oncol. Dec 2015;20(6):1063-1071. Reference #3: The FASEB Journal - 2000 - Puddicombe - Involvement of the epidermal growth factor receptor in epithelial repair in asthma.pdf. DISCLOSURES: No relevant relationships by Navitha Ramesh No relevant relationships by Uba Udeh
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SESSION TITLE: Unusual Cancer Cases SESSION TYPE: Case Reports PRESENTED ON: 10/19/2022 09:15 am - 10:15 am INTRODUCTION: Cutaneous lesions may present as a clue to an internal malignancy and provide an easily accessible site for tissue confirmation. We present a case of an eyelid metastatic lesion presenting as an initial sign of primary pulmonary malignancy. CASE PRESENTATION: A 67-year-old woman with past medical history of SARS-COVID-2 pneumonia six months ago and reformed smoker (26 pack year) who quit 27 years ago, presented to the primary care physician's office with a chief complaint of a small right upper eyelid margin (base of eyelashes) lesion (Figure 1A), and ongoing nonproductive cough and fatigue since diagnosis of SARS-COVID-2 pneumonia. The eyelid lesion appeared two weeks prior and had quickly grown in size. The lesion was associated with mild itching, but without any associated pain, discharge, or bleeding. She also complained of left elbow and foot pain but denied fever, chills, rigors, hemoptysis, pleurisy, and weight loss. Physical examination was negative for lymphadenopathy. Chest x-ray revealed a hazy left upper lobe opacity. Urine antigen for blastomycoses and histoplasma were negative. Rheumatoid factor, erythrocyte sedimentation rate, C reactive protein, QuantiFERON TB gold and anti-nuclear and cyclic citrullinated peptide antibodies were negative. Computed tomography of chest revealed a left upper lobe 3.7 x 5.4 x 5.6 cm mass, numerous bilateral ground glass opacities, and scattered (less than 5 mm) nodules (Figure 1B). Simultaneously, the patient was evaluated by an ophthalmologist for excision of the eyelid lesion. Histopathological evaluation revealed malignancy compatible with metastatic lung adenocarcinoma (Figure 1C) DISCUSSION: While an uncommon presentation, this case highlights the importance of a through history and examination in a patient presenting with pulmonary symptoms with risk factors for a lung malignancy. While she did have imaging that demonstrated lung masses, the diagnosis of lung cancer came not from invasive sampling of these masses, but rather from excision and histopathological evaluation of an eyelid soft tissue mass. Lung cancer is prone to metastasis, however cutaneous manifestations of lung cancer are relatively rare and are more common in the advanced stages of disease, making cutaneous metastasis a poor prognostic factor. In terms of cutaneous metastases, ocular metastases are one of the rarest locations making this a unique presentation. In a patient presenting with pulmonary masses, any concurrent development of new and/or growing skin lesions should be evaluated to rule out metastasis and potentially yield diagnosis. CONCLUSIONS: In patients presenting with concern for a malignant lung process, a skin exam should be completed, and suspicious skin lesions should be biopsied. Although rare, lung malignancies do metastasize to ocular cutaneous tissues and are a marker of more advanced stage of the malignancy. Reference #1: Hidaka T, Ishii Y, Kitamura S. Clinical features of skin metastasis from lung cancer. Intern Med. 1996;35:459-462. Reference #2: Marcoval J, Penin RM, Llatjos R, Martinez-Ballarin, I. Cutaneous metastasis from lung cancer: retrospective analysis of 30 patients. Australas J Dermatol. 2012;53(4):288-290. Reference #3: Abdeen Y, Amireh S, Patel A, Al-Halawani M, Shaaban H, Miller R. Cutaneous metastasis as a first presentation for lung adenocarcinoma. N Am J Med Sci. 2016;8(5): 222-225. DISCLOSURES: No relevant relationships by Gregory Griepentrog No relevant relationships by Chinmay Jani No relevant relationships by Bailey Ray No relevant relationships by Harpreet Singh No relevant relationships by Amit Taneja No relevant relationships by Kara Young