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SESSION TITLE: TB and TB-Involved Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Patients who are HIV positive have a high risk of co-infection with tuberculosis (TB). Screening tests for HIV identify antibodies that are present during the seroconversion, or window phase. Here we present a case of reactivation TB during the seroconversion phase of HIV with an initially negative QuantiFERON test. CASE PRESENTATION: A previously healthy 24-year-old female presented with a productive cough. She was found to have leukopenia and apical consolidation on chest CT and was treated for community-acquired pneumonia with mild improvement of symptoms. Her QuantiFERON, COVID-19, and HIV antibody screen were negative;however, her reflex HIV antigen was positive. She re-presented a month later with a worsening cough, drenching night sweats, weight loss, vomiting, and dysphonia. Her chest CT noted a right apical cavitary lesion and bilateral upper lobe micronodules with endobronchial spreading. Her QuantiFERON and HIV antibody were now both positive. She was started on rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE) therapy and on raltegravir and emtricitabine/tenofovir. DISCUSSION: Above we describe a case of reactivation TB during the seroconversion phase of HIV with a negative QuantiFERON. Primary TB presents in the middle lobes without signs of structural damage whereas secondary TB typically involves the apices and presents with cavitation. Secondary TB is typically due to reactivation or reinfection in immunosuppressed patients. Although we believe this case is due to reactivation due to radiographic findings, her initial QuantiFERON was negative. However, studies have shown that QuantiFERON may have uncertain results in latent TB infections in patients with underlying HIV (1). Reliable testing for latent TB in HIV-positive individuals is necessary as HIV increases the risk of developing active TB and TB increases the risk of transitioning from HIV to AIDS (2). CONCLUSIONS: TB is one of the top 10 causes of death worldwide and HIV is a common coinfection. To the best of our knowledge, this is the first published report of reactivation TB during the seroconversion phase of HIV with an initially negative QuantiFERON. Overall, more research must be done to identify the risk of infections during the seroconversion phase and physicians must be able to identify radiographic findings concerning for TB in patients with underlying HIV. Reference #1: Elisa Petruccioli, Teresa Chiacchio, Elisa Petruccioli, et al. Effect of HIV-infection on QuantiFERON-plus accuracy in patients with active tuberculosis and latent infection, Journal of Infection, 2020;80(5): 536-546. https://doi.org/10.1016/j.jinf.2020.02.009. Reference #2: Bruchfeld, Judith et al. "Tuberculosis and HIV Coinfection.” Cold Spring Harbor perspectives in medicine vol. 5,7 a017871. 26 Feb. 2015, doi:10.1101/cshperspect.a017871 Reference #3: Johnson JL, Okwera A, Hom DL, et al. Duration of efficacy of treatment of latent tuberculosis infection in HIV-infected adults. AIDS. 2001;15(16):2137-2147. doi:10.1097/00002030-200111090-00009 World Health Organization. Tuberculosis [Internet]. 2021 [cited 2022 Mar. 15];Available from: https://www.who.int/news-room/fact-sheets/detail/tuberculosis DISCLOSURES: No relevant relationships by Loor Alshawa No relevant relationships by Angela Binkowski No relevant relationships by Sara Qutubuddin
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BACKGROUND AND AIMS: In the COVID 19 pandemic era, anti SARS-CoV-2 vaccination showed high efficacy at preventing the infection and its most severe complications. The aim of this report is to describe an unusual double glomerulopathy related to anti SARS-CoV-2 vaccination and the good results obtained with the immunosoppressive treatment. METHOD: An 80-year-old caucasian woman developed a nephrotic syndrome, progressive renal insufficiency and microhematuria. The patient presented a medical history of thrombocytopenic purpura treated and resolved by steroids in 2013, hypothyroidism, hypertension, ischaemic heart disease treated with surgical bypass in 2019 and pacemaker in 2020 for atrial ventricular block. Due to pandemic COVID 19 status, she received two doses of the Pfizer BioNTech mRNA COVID-19 vaccine in March 2021. Two weeks after the second dose her weight increased of 23 kg. The family physician added furosemide to her therapy for generalized edema with no diuretic effect. In April, creatinine was 1.38 mg/dL (versus 0.8 mg/dL 1 year before);urinalysis showed proteinuria (300 mg/dL) and microscopic hematuria;serum total cholesterol level was 218 mg/dL and triglycerides 178 mg/dL;then it was suggested to increase the doses of furosemide. In May 2021, creatinine resulted 2 mg/dL, serum albumin 2 g/dL, and urinalysis confirmed proteinuria and microscopic hematuria;proteinuria was 10 g/day. Abdomen ultrasound showed normal liver, kidneys and spleen, not ascites. Lower limb eco-Doppler showed right superficial femoral artery stenosis of 60% and absence of venous thrombosis. The physical examination evidenced anasarca. The patients were admitted to the nephrology unit;hepatitis B surface antigen, hepatitis C antibody and human immunodeficiency virus antigen and antibody were negative. Both complement C3 and C4 levels resulted within the normal range. Cryoglobulins were absent. Urinary Bence Jones, antinuclear antibody (ANA), anti-extractable nuclear antigen (ENA), anti-double stranded DNA (nDNA) antibodies were negative. Antineutrophil cytoplasm antibodies (ANCA) were 1:2560 with Perinuclear pattern and anti-MPO positivity (716 UA/mL);anti-proteinase-3 antibodies (PR3) were negative. Antiphosholipase A2 receptor antibody (PLA2R Ab) was positive with high titre. A kidney biopsy was performed showing a double nephropathy: a focal segmental glomerulosclerosis (FSGS) with some collapsing features, superimposed on membranous glomerulonephritis (Fig. 1). RESULTS: We started the Ponticelli regimen (alternate months steroids and cyclophosphamide). After the first month of therapy, blood tests revealed creatinine 1.7 mg/dL, haemoglobin 11.7 g/dL;serum albumin 2.7 g/dL and urinalysis without microscopic haematuria. At the third month of therapy, the patient developed atrial fibrillation and started anticoagulation;blood tests were as follows: creatinine 1.1 mg/dL, serum albumin 3.0 g/dL, Ab anti-MPO 7 UA/mL and PLA2R Ab was absent. A left ocular, frontal and parietal herpes zoster induced a short discontinuation of therapy and responded well to Acyclovir;then we concluded the fourth month of therapy. At the fifth month, a SARS CoV 2 RT PCR unexpectedly resulted positive;the patient remained asymptomatic, but we stopped definitively the therapy. One month later, blood tests showed: creatinine 1 mg/dL, serum albumin 4 g/dL, proteinuria 0.7 g/die, MPO 2 UA/mL and PLA2R Ab absent. CONCLUSION: To our knowledge, this is the first case of nephrotic sindrome secondary to a De novo MN and FSGS, associated with positive MPO antibody, following Pfizer-BioNTech mRNA vaccination COVID 19;the patient responded well to immunosoppression going in remission and regaining renal function. (Figure Presented).
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Background: COVID-19 clinical manifestations range from asymptomatic to severe disease. Prior immune responses to human coronaviruses may affect individual responses to SARS-CoV-2. We surveyed coronavirus responses pre-pandemic in individuals from Kenya, Nigeria, Tanzania, Uganda and Thailand;81% were people living with HIV. Methods: Specimens were screened for SARS-CoV-2 Spike S2 subunit IgG responses. Selected samples were tested using a bead-based immunoassay that profiled the specificity, isotype and subclass of antibody responses to coronavirus, flavivirus and HIV antigens. Wilcoxon rank sum tests were performed to compare responses across antigens and participant group. Results: We screened 1,875 samples (one per individual) collected between 2013 and October 2019: 1,630 samples were from Africa (87%) and 245 from Thailand. 6.99% of participants (n=131, 116 from Africa (89%) and 15 from Thailand) showed responses above the naïve signal threshold and were further tested. Using a signal to noise ratio of >10 as a cut-off value, 44, 27 and 42 samples showed IgG responses to the Spike protein of SARS-CoV-2, SARS-CoV-1 and MERS-CoV respectively, while 7, 9 and 4 samples showed responses to Nucleocapsid for these same antigens. Some individuals had higher responses than those seen in SARS-CoV-2 convalescent individuals. We found a strikingly different pattern of reactivity in Africa compared to Thailand (Figure 1). Antibody responses were significantly higher in the African participants compared to Thai participants across antigens corresponding to SARS-CoV-2 (p<0.001), SARS-CoV-1 (p<0.001) and MERS-CoV (p<0.01). Similar patterns were seen for IgG subclasses, IgA and IgM. The difference was less pronounced for the four endemic coronaviruses, nonetheless anti-Spike responses were significantly higher in African participants for HKU1 and OC43 (p≤0.018). In addition, mapping responses to 21 flavivirus antigens showed the highest reactivity in Thailand and in Nigeria. Conclusion: Our serosurvey of pre-pandemic samples showed that there were significantly higher antibody responses against coronaviruses, including SARS-CoV-2, in Africa than in Thailand. Profiling flavivirus responses showed that the difference between the two regions was not due to a higher background reactivity across African samples. Further analysis is needed to explain pre-pandemic SARS-CoV-2-like antibody responses among African participants and explore implications for geographic diversity in disease severity.