Elevated Inflammatory Markers Research Articles

Abdominal pain accompanied by elevated serum inflammatory markers and biliary enzymes for diagnosing immune checkpoint inhibitor-induced sclerosing cholangitis.

Immune-related sclerosing cholangitis (irSC) is relatively rare and its clinical characteristics are not well known. In this study, we aimed to summarize the clinical features of irSC. Clinical data were collected retrospectively from 1,393 patients with advanced malignancy treated with immune-checkpoint inhibitors (ICIs) between August 2014 and October 2021. We analyzed patients with immune-related adverse events of liver injury (liver-irAEs) and compared irSC and non-irSC groups. Sixty-seven patients (4.8%) had a liver-irAE (≥ grade 3) during the follow-up period (median, 262 days). Among these, irSC was observed in eight patients (11.9%). All patients in the irSC group were treated with anti-PD-1/PD-L1 antibodies. Compared with the non-irSC group, the irSC group showed mainly non-hepatocellular liver injury (87.5 % vs 50.8 %, P = 0.065), and had elevated serum inflammatory markers (e.g., CRP and NLR) and biliary enzymes (e.g., GGTP and ALP) at the onset of liver-irAEs. Furthermore, most patients with irSC had abdominal pain. In the non-irSC group, the liver injury of 23 patients improved only with the discontinuation of ICIs, and 22 patients improved with medication including prednisolone (PSL). Conversely, almost all patients (n=7) in the irSC group were treated with PSL, but only two patients experienced an improvement in liver injury. We found that irSC is characterized by a non-hepatocellular type of liver injury with abdominal pain and a high inflammatory response and is refractory to treatment. Further examination by imaging is recommended to detect intractable irSC in cases with these characteristics.

Extension of Lung Damage at Chest Computed Tomography in Severely Ill COVID-19 Patients Treated with Interleukin-6 Receptor Blockers Correlates with Inflammatory Cytokines Production and Prognosis.

Elevated inflammatory markers are associated with severe coronavirus disease 2019 (COVID-19), and some patients benefit from Interleukin (IL)-6 pathway inhibitors. Different chest computed tomography (CT) scoring systems have shown a prognostic value in COVID-19, but not specifically in anti-IL-6-treated patients at high risk of respiratory failure. We aimed to explore the relationship between baseline CT findings and inflammatory conditions and to evaluate the prognostic value of chest CT scores and laboratory findings in COVID-19 patients specifically treated with anti-IL-6. Baseline CT lung involvement was assessed in 51 hospitalized COVID-19 patients naive to glucocorticoids and other immunosuppressants using four CT scoring systems. CT data were correlated with systemic inflammation and 30-day prognosis after anti-IL-6 treatment. All the considered CT scores showed a negative correlation with pulmonary function and a positive one with C-reactive protein (CRP), IL-6, IL-8, and Tumor Necrosis Factor α (TNF-α) serum levels. All the performed scores were prognostic factors, but the disease extension assessed by the six-lung-zone CT score (S24) was the only independently associated with intensive care unit (ICU) admission (p = 0.04). In conclusion, CT involvement correlates with laboratory inflammation markers and is an independent prognostic factor in COVID-19 patients representing a further tool to implement prognostic stratification in hospitalized patients.

Single-Versus Multiple-Dose Antimicrobial Prophylaxis in Peroral Endoscopic Myotomy: A Randomized Controlled Study (SMAPP Trial).

Infections are uncommon after peroral endoscopic myotomy (POEM) procedure. However, prophylactic antibiotics are routinely administered for variable duration during peri-operative period. In this study, we aimed to determine the difference in the rate of infections between single (SD-A) and multiple doses (MD-A) antibiotic prophylaxis groups. The study was a prospective, randomized, non-inferiority trial conducted at a single tertiary care centre from Dec 2018 to Feb 2020. Eligible patients undergoing POEM were randomized into SD-A and MD-A groups. SD-A group received one dose of antibiotic (IIIrd gen cephalosporin) within 30-min of POEM. In the MD-A group, the same antibiotic was administered for a total of three days. Primary aim of the study was to determine the incidence of infections in the two groups. Secondary outcomes included incidence of fever (> 100 °F), inflammatory markers [erythrocyte sedimentation rate (ESR), c-reactive protein(CRP)], serum procalcitonin and adverse events related to antibiotics. (NCT03784365). 114 patients were randomized to SD-A (57) and MD-A (57) antibiotic groups. Mean post-POEM CRP (0.8 ± 0.9 vs 1.5 ± 1.6), ESR (15.8 ± 7.8 20.6 ± 11.7) and procalcitonin (0.05 ± 0.04 0.29 ± 0.58) were significantly higher after POEM (p = 0.001). Post-POEM inflammatory markers (ESR, CRP and procalcitonin) were similar in both the groups. Fever on day-0 (10.5% vs 14%) and day-1 (1.7% vs 3.5%) was detected in similar proportion of patients. Post-POEM infections were recorded in 3.5% (1.7% vs 5.3%, p = 0.618). Single dose of antibiotic is non-inferior to multiple dose antibiotic prophylaxis. Elevation of inflammatory markers and fever after POEM represents inflammation and does not predict infection after POEM.

Hemobilia in the setting of cystic artery pseudoaneurysm secondary to type I Mirizzi syndrome

Hemobilia is an uncommon diagnosis and is often not suspected in the absence of recent hepatobiliary intervention or trauma. Hemobilia in the setting of cystic artery pseudoaneurysm secondary to type I Mirizzi syndrome is a rare occurrence. We report the case of a 61-year-old male who presented with epigastric pain and vomiting. Blood tests demonstrated hyperbilirubinemia with elevated inflammatory markers. Magnetic resonance cholangiopancreatography revealed type I Mirizzi syndrome in the presence of a 21 mm cystic duct stone. During endoscopic retrograde cholangiopancreatography, hemobilia was identified. Subsequent triple phase computed tomography imaging identified a 12 mm cystic artery pseudoaneurysm. Angiography with successful coiling of the cystic artery was accomplished. Cholecystectomy was performed, confirming type I Mirizzi syndrome. This case demonstrates the importance of considering ruptured pseudoaneurysm in patients presenting with evidence of upper gastrointestinal bleeding in the setting of biliary stone disease. Transarterial embolization, followed by surgical management, is effective in both the diagnosis and management of ruptured cystic artery pseudoaneurysm with associated hemobilia.

Clinical Profile, Follow-up, and Role of Neuroimaging in Pediatric Guillain-Barré Syndrome in the COVID Era: An Ambispective Study.

Background: To define the varied presentations of Guillain-Barré syndrome in children in the COVID era and 6 months' follow-up outcome. Methods: Ambispective study of 15 months' duration involving children with Guillain-Barré syndrome aged 1 month to 18 years at a tertiary care pediatric hospital. They were categorized into groups A and B based on COVID-19 serology testing. Hughes Disability Scale was used for disability assessment. Modified Rankin scale was used for improvement assessment in follow-up. Results: Of 19 children with Guillain-Barré syndrome, 9 (47%) were females and 10 (53%) were males. Groups A and B had children with negative (8) and positive serology (11), respectively. The most common presentation in both groups was motor weakness. Post-COVID pediatric Guillain-Barré syndrome presented with variants of Guillain-Barré syndrome rather than the classical form (P = .03). In group B, patients with elevated inflammatory markers had poor response to intravenous immunoglobulin, and 5 of 11 patients had good response to pulse steroids, probably depicting an inflammation-predominant pathology. Conclusion: Post-COVID Guillain-Barré syndrome in children presented with Guillain-Barré syndrome variants rather than the classic form. Neuroimaging is of great value in both confirming Guillain-Barré syndrome diagnosis and excluding differentials. Patients with elevated inflammatory markers and residual weakness may be given a pulse steroid trial.

Chronic granulomatous disease identified in the evaluation of atypical Kawasaki disease in an infant

An 8-week-old full-term male was admitted after 5 days of fever and cough. He was previously admitted at 3 weeks of age for a Klebsiella pneumoniae urinary tract infection (UTI) and treated with 10 days of antibiotics. Blood and cerebrospinal fluid cultures, serum inflammatory markers, and respiratory viral testing obtained at that time were negative. During the current admission, urine cultures grew Klebsiella oxytoca and he was again treated for a UTI.His fevers persisted and on day 8 of illness he met criteria for atypical Kawasaki disease with elevated inflammatory markers, elevated liver enzymes, thrombocytosis, leukocytosis, and anemia. Prior to initiating IVIG, the patient underwent abdominal ultrasound to rule out occult infection, revealing multiple liver and spleen abscesses. Aspirated fluid grew Serratia marcescens and he was started on cefepime. Additional imaging of the chest, abdomen, and pelvis revealed pulmonary nodules. Evaluation of these nodules demonstrated no additional mycobacterial, fungal, or bacterial infections.Chronic granulomatous disease (CGD) was suspected based on the patient’s age, multi-organ abscesses with Serratia marcescens, and parental consanguinity (first cousins). Neutrophil oxidative burst testing showed absent ROS production. Genetic testing demonstrated a homozygous pathogenic variant in NCF2 (exon 3 deletion), confirming the diagnosis of autosomal-recessive CGD. He received high-dose methylprednisolone with a prolonged taper to promote antibiotic penetration of his CGD-associated liver abscesses. Repeat imaging showed interval improvement and the patient began prophylactic itraconazole and trimethoprim-sulfamethoxazole.Familial testing revealed heterozygous carrier status of the same NCF2 variant in both parents and the patient’s two sisters. At 10 months of age, the patient underwent a 10/10 matched sibling bone marrow transplant. Chimerism studies showed rapid neutrophil engraftment with delayed T cell engraftment. As of follow up at 12 months of age, he has appropriate post-transplant weight gain, no infectious complications, and no evidence of GVHD.Initial presentation in patients with CGD and liver/spleen abscesses can be insidious with isolated fever and elevated inflammatory markers. Such patients can readily meet criteria for atypical Kawasaki disease, highlighting the importance of maintaining a broad differential diagnosis for fever of unknown origin with a high index of suspicion for primary immunodeficiency.

Lifting the Lid on CAPS: Uncovering Genetic Anticipation in Cryopyrin-Associated Periodic Syndrome

Cryopyrin-associated periodic syndrome (CAPS) is a spectrum of autoinflammatory conditions comprising three subtypes: familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome (MWS), and neonatal onset multisystem inflammatory disease (NOMID).1 Symptoms include urticaria, fever, arthralgias, conjunctival injection, and headaches, which can occur spontaneously or during periods of cold/stress.2 Complications include permanent sensorineural hearing loss (SNHL), chronic aseptic meningitis, systemic amyloidosis, developmental delay, seizures, and chronic arthropathy.3 CAPS is treated with inhibition of interleukin (IL)-1 which can reduce symptoms and prevent progression of complications including hearing loss, CNS inflammation, and renal disease from amyloidosis.3,4.Here, we present a five-year-old boy who developed unexplained arthralgias, SNHL, increased intracranial pressure, atrophic retinal nerve fiber layer, and painful urticaria. Laboratory testing showed elevated inflammatory markers and neutrophil count. Genetic testing showed a heterozygous variant in the NLRP3 gene that was previously reported in a patient with NOMID. Interestingly, his mother had similar history of arthralgia, aseptic meningitis, SNHL, and recurrent aphthous ulcers, while his maternal grandmother had a history of SNHL and arthralgia. The mother and grandmother had similar elevations in inflammatory markers and neutrophils. Both were found to have the same variant in NLRP3 as the index patient and were diagnosed with CAPS/NOMID. The histories suggested a degree of genetic anticipation, for the child’s symptoms were most severe, while his mother had moderate symptoms and his grandmother was relatively mildly affected. Notably, neither the mother nor grandmother had signs of kidney disease to suggest amyloidosis. All three family members were started on canakinumab injections. The child’s arthralgias and mother’s symptoms improved, and flares have decreased in frequency. The grandmother has not yet received therapy long enough to assess for improved symptoms.CAPS is a group of autoinflammatory disorders with autosomal dominant inheritance, quality-of-life-limiting symptoms, and potential life-long complications. CAPS should be suspected and screened for in relatives of affected individuals. This familial case demonstrates a pattern of increased severity of CAPS symptoms with each subsequent generation from grandmother to grandchild suggestive of genetic anticipation. Early diagnosis and initiation of anti-IL-1 therapy is important to prevent progression and complications.

Abstract 581: Impact Of Iron Deficiency Anemia On Venous Thromboembolic Diseases: A National Inpatient Sample Analysis

Introduction: Iron deficiency anemia has been associated with venous thromboembolic diseases however, there is paucity of data on the subject. We sought to assess this association using a national database. Methods: The National inpatient sample database 2018-2020 was queried to identify adult patients (age>18 yrs) with iron deficiency anemia (IDA). Baseline risk factors and occurrence of venous thromboembolic diseases were compared between patients with and without IDA. Multivariate regression analysis was performed to assess the impact of IDA on VTE. Results: A total of 6417659 patients with IDA were identified with a mean age of 61 years. Patients with IDA had a higher prevalence of diabetes mellitus, hyperlipidemia, tobacco abuse and obesity while they had a lower prevalence of hypertension. The occurrence of acute deep vein thrombosis (DVT), chronic DVT, acute pulmonary embolism (PE) and chronic PE was higher in patients with IDA than patients without (Table1). Multivariate regression analysis revealed a higher odds of developing acute DVT and acute PE in adult patients with IDA (Table 2). Conclusion: In sync with findings from a few other population studies, this analysis also reveals an association between IDA and VTE. Reactive thrombocytosis and elevated inflammatory markers have been proposed as few contributing factors. However, further research is warranted to prove these findings to aid prevent and treat VTE effectively.

Abstract #1385480: Goiter and Abdominal Mass: A Rare Presentation of Riedel’s Thyroiditis

Riedel’s thyroiditis (RT), also known as fibrous thyroiditis, is a rare inflammatory autoimmune disease that is often associated with various forms of systemic fibrosis such as sclerosing mesenteritis (SM). A 38-year-old female with a past medical history of hypertension presented with a painful growing goiter and a mesenteric mass, which was complicated by biliary obstruction and hydronephrosis. Physical exam showed tenderness on the abdomen and a diffusely enlarged firm thyroid gland, with no palpable nodules. Initial labs revealed C-reactive protein of 115 mg/L, TSH 180 mIU/L; Free T4: 0.79 ng/dL, positive Thyroid Peroxidase (>1051 IU/mL); normal IgG1 and IgG4. CT abdomen/pelvis demonstrated a mesenteric mass that encased multiple mesenteric vessels and the right ureter without bowel obstruction. Thyroid ultrasound showed an enlarged heterogeneous thyroid without a discrete nodule consistent with autoimmune thyroiditis. Thyroid fine needle aspiration (FNA) was non-diagnostic. Thyroid biopsy showed mostly fibrosis with scattered lymphoplasmacytic aggregates, with no evidence of carcinoma, lymphoma, IgG4-related disease, and no Hürthle cell presence. Interestingly, the mesenteric mass biopsy revealed the same pattern. Peripheral flow cytometry and infectious workup were negative. Diagnosis of RT and SM were made. The patient was treated with steroids and improved clinically. The hallmark of RT is the extension of fibrosis beyond the thyroid. This patient exhibited common features of RT such as neck pressure, and pain; female gender, elevated inflammatory markers, nondiagnostic FNA (scant cellularity due to fibrosis), and a positive steroid response. Moreover, intense infiltrative fibrosis mixed with lymphocytes and plasma cells instead of an extensive lymphocytic infiltrate with the germinal center formation on histology supports Riedel’s thyroiditis rather than Hashimoto's. Similarly, SM is a rare, non-neoplastic inflammatory and fibrotic disease that affects the integrity of mesenteric vessels causing common bile duct and ureter obstruction. Negative flow cytometry, the presence of sclerosis, and the absence of bowel/liver lesions involvement make other common causes of a mesenteric mass (lymphoma, desmoid tumor, carcinoid) less likely, supporting the diagnosis of SM. The concurrent timing of her thyroid enlargement and the mesenteric mass as well as the similarity in histology (dense fibrosis with patchy lymphoplasmacytic aggregates) suggests an association between RT and SM. Overall, the case highlights the challenges in diagnosing RT given its extreme rarity and emphasizes the importance of early treatment to prevent systemic involvement.

Peripheral inflammation is associated with impairments of inhibitory behavioral control and visual sensorimotor function in psychotic disorders.

Elevated markers of peripheral inflammation are common in psychosis spectrum disorders and have been associated with brain anatomy, pathology, and physiology as well as clinical outcomes. Preliminary evidence suggests a link between inflammatory cytokines and C-reactive protein (CRP) with generalized cognitive impairments in a subgroup of individuals with psychosis. Whether these patients with elevated peripheral inflammation demonstrate deficits in specific cognitive domains remains unclear. To examine this, seventeen neuropsychological and sensorimotor tasks and thirteen peripheral inflammatory and microvascular markers were quantified in a subset of B-SNIP consortium participants (129 psychosis, 55 healthy controls). Principal component analysis was conducted across the inflammatory markers, resulting in five inflammation factors. Three discrete latent cognitive domains (Visual Sensorimotor, General Cognitive Ability, and Inhibitory Behavioral Control) were characterized based on the neurobehavioral battery and examined in association with inflammation factors. Hierarchical clustering analysis identified cognition-sensitive high/low inflammation subgroups. Among persons with psychotic disorders but not healthy controls, higher inflammation scores had significant associations with impairments of Inhibitory Control (R2=0.100, p-value=2.69e-4, q-value=0.004) and suggestive associations with Visual Sensorimotor function (R2=0.039, p-value=0.024, q-value=0.180), but not with General Cognitive Ability (R2=0.015, p-value=0.162). Greater deficits in Inhibitory Control were observed in the high inflammation patient subgroup, which represented 30.2% of persons with psychotic disorders, as compared to the low inflammation psychosis subgroup. These findings indicate that inflammation dysregulation may differentially impact specific neurobehavioral domains across psychotic disorders, particularly performance on tasks requiring ongoing behavioral monitoring and control.

A Case of a Relapsing Remitting Macrophage Activating Syndrome After Covid-19 Vaccine In a Teenager with UNC13D Heterozygous Variant of Uncertain Significance

IntroductionMacrophage activation syndrome (MAS) is a severe hyper inflammatory condition caused by the over-activation and proliferation of T cells, NK cells and macrophages. It is often associated with complications of rheumatic/immune diseases. We present a case of a 15-year-old female who experiences recurrent episodes of MAS without any known definitive underlying etiology. Case PresentationA 15-year-old previously healthy female developed fatigue, fevers, myalgia, chest pain, splenomegaly and lymphadenopathy 10 days after receiving her first Pfizer COVID-19 vaccine. Her symptoms recurred 10 days after receiving the second dose. Her myocarditis, MIS-C, and infectious work up was negative except for positive EBV IgG. Laboratory studies revealed anemia, hypertriglyceridemia, hypofibrinogenemia, and hyperferritinemia. She initially responded to decadron; however, her symptoms recurred with steroid taper. Bone marrow biopsy revealed hemophagocytosis. Whole exome sequencing (WES) revealed a heterozygous variant of uncertain significance in UNC13D c.962C>A (p.Thr321Asn). She had multiple re-admissions with significantly elevated inflammatory markers, including extremely high IL2-R, IL-18 and CXCL9. Each episode was complicated by an acute viral infection. She responds to high dose steroids, anti-IL-1, and JAK inhibitors. Nonetheless, it has been difficult to wean decadron without triggering a flare. She continues to require increasing doses of baricitinib. DiscussionMAS may be seen as a complication of rheumatic diseases, as well as inborn errors of immunity. However, none of these conditions have been diagnosed in this patient despite extensive testing, including WES. The degree of her immune dysregulation has been very severe making her disease process unpredictable and extremely difficult to control. She has frequent flares precipitated by viral infections or attempts at adjusting her immunomodulators. Weaning her medications has been challenging as she continues to require increasing doses of baricitinib and corticosteroids. The UNC13D gene is associated with autosomal recessive familial hemophagocytic lymphohistiocytosis type 3 (FHL3). Our patient is heterozygous for an UNC13D variant of uncertain significance. Additional genetic inquiries with whole genome sequencing to help elucidate the underlying etiology of her severe condition is being conducted. We hypothesize she developed MAS due to a combination of genetic predisposition, prior EBV infection, and immune stress associated with the COVID-19 vaccine. [Display omitted] [Display omitted] [Display omitted]

HbA1c, And Blood Glucose, Changes When Treating Periodontal Disease with the Perio Protect Method™

Periodontal disease is a chronic wound resulting in host elevated local and systemic inflammatory markers in response to the microorganisms of the periodontal biofilm. Separately from its importance as an oral ailment, chronic periodontitis has gained relevance since it can develop into a systemic condition characterized by hyper-inflammation, disruption of the innate and adaptive immune system, and other system-wide alterations. There is compelling evidence that inflammation and chronic infection play an essential role in the development of inflammatory markers and of type 2 diabetes. Studies in humans suggest that circulating inflammatory marker levels may predict type 2 diabetes years in advance of the onset of the disease. Local and systemic expression of inflammatory cytokines, such as TNF-alpha and IL-6, increase in individuals with periodontitis. TNF-alpha and IL-6 impair intracellular insulin signaling, which may lead to insulin resistance and are significantly associated with cardiovascular events and stroke. This case study demonstrates treating periodontal disease with a direct medication delivery method (Perio Protect Method™) manages the patient’s periodontal disease and lowers daily blood glucose and HbA1c levels.

REcovery and SURvival of patients with moderate to severe acute REspiratory distress syndrome (ARDS) due to COVID-19: a multicenter, single-arm, Phase IV itolizumab Trial: RESURRECT

ABSTRACT Background Itolizumab, an anti-CD6 monoclonal antibody, down-regulates COVID-19-mediated inflammation and the acute effects of cytokine release syndrome. This study aimed to evaluate the safety and efficacy of itolizumab in hospitalized COVID-19 patients with PaO2/FiO2 ratio (PFR) ≤200 requiring oxygen therapy. Research design and methods This multicenter, single-arm, Phase 4 study enrolled 300 hospitalized adults with SARS-CoV-2 infection, PFR ≤200, oxygen saturation ≤94%, and ≥1 elevated inflammatory markers from 17 COVID-19 specific tertiary Indian hospitals. Patients received 1.6 mg/kg of itolizumab infusion, were assessed for 1 month, and followed-up to Day 90. Primary outcome measures included incidence of severe acute infusion-related reactions (IRRs) (≥Grade-3) and mortality rate at 1 month. Results Incidence of severe acute IRRs was 1.3% and mortality rate at 1 month was 6.7% (n = 20/300). Mortality rate at Day 90 was 8.0% (n = 24/300). By Day 7, most patients had stable/improved SpO2 without increasing FiO2 and by Day 30, 91.7% patients were off oxygen therapy. Overall, 63 and 10 patients, respectively, reported 123 and 11 treatment-emergent adverse events up to Days 30 and 90. No deaths were attributable to itolizumab. Patient-reported outcomes showed gradual and significant improvement for all five dimensions on EQ-5D-5L. Conclusion Itolizumab demonstrated acceptable safety with a favorable prognosis in hospitalized COVID-19 patients. Clinical trial registration CTRI/2020/09/027941 (Clinical Trials Registry of India).

Does Elevated Inflammatory Markers Predict Functional Outcomes in Hospitalized Patients with COVID-19 and Acute stroke? (P14-5.007)

<h3>Objective:</h3> To determine if elevated inflammatory markers are associated with worse functional outcomes in SARS-CoV-2 positive patients presenting with acute cerebrovascular events. <h3>Background:</h3> The association of acute Coronavirus disease 2019 (COVID-19) with both arterial and venous thromboembolic events is well-established. One of the several proposed mechanisms is excessive inflammatory response. We aim to assess if higher inflammatory markers are associated with worse functional outcomes <h3>Design/Methods:</h3> Medical records of adult patients admitted to our institution between 3/2020 and 8/2021 with positive SARS-COV-2 and acute cerebrovascular events were reviewed (n=29). Demographics, neuroradiological and pertinent lab findings were collected. Functional outcomes were assessed using binarized mRS scores (worse 4–6 vs better 0–3) ascertained on discharge day. A series of logistic regression models were utilized to assess the association of inflammatory markers with stroke outcomes. Variables assessed were; [admission day heart rate, temperature and white blood cell count], binarized maximum procalcitonin ( &gt; 0.1 ng/mL vs &lt;/= 0.1 ng/mL) and maximum ferritin level. All analyses were conducted using SAS software. <h3>Results:</h3> Among 29 patients (mean age 63.6 +/− 13.4 years, 65.5% males), tested parameters of inflammation were not shown to be significantly associated with stroke outcomes in an adjusted logistic regression model. When assessing stroke outcome via binarized modified Rankin stroke scale, binarized maximum procalcitonin level showed 1.95 times the odds of a poor outcome (OR: 1.95, 95% CI: 0.05, 84.3, p-value: 0.73). Additionally, temperature on admission showed 1.59 times the odds of a poor outcome (OR: 1.59, 95% CI: 0.42, 6.07, p-value: 0.17). <h3>Conclusions:</h3> Among patients with acute cerebrovascular events associated with positive SARS-COV-2 result, no significant associations of worse functional outcomes in those with elevated inflammatory markers were observed. A trend of higher mRS scores on discharge in those with elevated procalcitonin and those with fever on admission was noted. Further research is needed to confirm these findings <b>Disclosure:</b> Dr. Elsekaily has nothing to disclose. Dr. Ansari has nothing to disclose. Dr. Sheikh has nothing to disclose. Dr. Ayub has nothing to disclose. Dr. Triay has nothing to disclose. Miss Angelette has nothing to disclose. Ms. Gaudet has nothing to disclose. Dr. Kelley has nothing to disclose.

Preporuke Hrvatskog društva za infektivne bolesti za dijagnostiku i liječenje multisistemskog upalnog sindroma u djece

Multisystem inflammatory syndrome in children is a novel entity first described in April 2020. It is a complication of COVID-19 that appears with a latency of 2-6 weeks and is characterized by fever, multiorgan involvement, and elevated inflammatory markers. Diagnosis is based on certain diagnostic criteria, and in these recommendations we chose the World Health Organization case definition. Patients should be treated with intravenous immunoglobulin and glucocorticoids together with other symptomatic and supportive measures. Follow-up should be at least a year-long, and even longer in case of cardiac complications. The aim of these recommendations is to help clinicians in diagnosing and treating this disease.

A 74 year old man with a rash, facial droop and multifocal intracranial stenosis (P9-10.006)

<h3>Objective:</h3> NA <h3>Background:</h3> Although atherosclerosis is the most common cause of intracranial stenosis, the differential diagnosis includes infectious and inflammatory causes. We report a case of a Varicella Zoster Virus (VZV) induced vasculitis. <h3>Design/Methods:</h3> The study is a case report. <h3>Results:</h3> A 74 year old man presented with an episode of loss of consciousness. CT angiography showed stenotic distal internal carotid arteries (ICA), severe stenosis of the left M1 segment, and moderate stenosis of the right M1 segment of the middle cerebral arteries (MCA) (Figure 1A–B). CT perfusion showed delayed perfusion to the left MCA territory (Figure 1C). MRI brain revealed a punctate right frontal infarct (Figure 2A). He was transferred to our hospital for superficial temporal artery - middle cerebral artery (STA-MCA) bypass. However, neurologic exam was notable for right facial droop involving right forehead and incomplete eye closure. MRI of the brain with vessel wall imaging showed thin enhancement of the bilateral ophthalmic and supraclinoid ICA’s and left M1 enhancement (Figure 2BC). A rash was found behind the right ear with crusted vesicles as well as bilateral cranial nerve 6 palsies. Cerebrospinal fluid had 47 nucleated cells/uL with 37 red blood cells/uL. Glucose was 75 mg/dL and total protein was 57 mg/dL. CSF VZV IgG returned positive at 819.0 and CSF VZV IgM was negative at 0.25. Thus, the diagnosis was VZV vasculitis. He was treated with intravenous acyclovir and transitioned to oral valacyclovir for a 14 day course. <h3>Conclusions:</h3> Even though intracranial atherosclerotic disease is the most common cause of vasculopathy, infectious or inflammatory vasculitis should be considered on the differential. Before considering bypass surgery or other invasive neurosurgical procedures, ensure reversible causes of vasculopathy have been ruled out. The presence of cranial neuropathies, rash, and/or elevated inflammatory markers should be red flags for vasculitis in patients presenting with stroke. <b>Disclosure:</b> Dr. Aghajan has nothing to disclose. Dr. Bilodeau has nothing to disclose. Dr. Izzy has received publishing royalties from a publication relating to health care.

A teenager with adenoviral myocarditis mimicking hypertrophic cardiomyopathy.

A 14-year-old previously healthy female presented with chest pain and dyspnoea for 2 days in the setting of a recent upper respiratory infection. She had elevated inflammatory markers and troponin, resulting in the diagnosis of acute myocarditis. Transthoracic echocardiography demonstrated mild systolic dysfunction and a moderate pericardial effusion. Additionally, her echocardiogram showed concentric left ventricular hypertrophy raising concern for hypertrophic cardiomyopathy. She was treated with intravenous immunoglobulin. Serial echocardiograms revealed rapid resolution of her ventricular hypertrophy. Cardiac magnetic resonance confirmed the diagnosis of myocarditis.

A Curious Case of Cocaine-Induced Hypokalemic Periodic Paralysis Mimicking Guillain-Barre Syndrome (P10-5.003)

<h3>Objective:</h3> To describe a rare cause of progressive ascending paralysis resembling Guillain-Barre Syndrome (GBS). <h3>Background:</h3> Cocaine inhibits the reuptake of monoamines at the synaptic cleft to prolong sympathetic output. This adrenergic hyperresponsiveness mimics thyrotoxicosis as it replicates sodium/potassium ATPase hyperactivity, causing a cellular influx of potassium (hypokalemia), hyperpolarization, and sodium channel inactivation that presents as sudden, painless muscle weakness and paralysis. <h3>Design/Methods:</h3> Consent obtained from patient. <h3>Results:</h3> A 30-year-old female with no past medical history was evaluated in the ED for acute lower extremity weakness that ascended to the upper extremities within &lt; 12 hours. Labs were significant for hypokalemia at 1.6, elevated inflammatory markers, elevated Free T4 at 2.58, and low TSH at &lt; 0.015. Urine drug screen was positive for cannabis and cocaine. Serum toxicology was negative. MRI of the T-spine and L-spine were unremarkable. Lumbar puncture was unremarkable. Cranial nerves were intact. Strength was 1/5 throughout, including at the neck. Flaccid tone. Lower extremity reflexes were 2+. Negative Babinski. Positive Hoffman bilaterally. Preserved sensation. The patient was admitted to the ICU, intubated for impending respiratory distress, and treated with IVIg. MRI of the C-spine was unremarkable. Further labs demonstrated elevated Free T3 at 7.13 and positive anti-TPO antibodies, significant for Grave’s disease. Urine labs were substantial for distal RTA. Anti-SSA and SSB antibodies were positive, indicating likely Sjogren’s syndrome (SS). Ganglioside panel was negative. Potassium was aggressively repleted. By day 1, the patient was moving all four extremities, and IVIg was discontinued. By day 2, she was successfully extubated. She was ambulating without difficulty on discharge. <h3>Conclusions:</h3> Secondary hypokalemic periodic paralysis may mimic Guillain Barre syndrome (GBS), a life-threatening demyelinating neuropathy that presents as rapidly progressive, symmetric, ascending paralysis or paresthesia with loss of reflexes. In our case, cocaine was the most plausible trigger for hypokalemia. <b>Disclosure:</b> Dr. Baumann has nothing to disclose. Dr. Rizvi has nothing to disclose. Ms. Alayon has nothing to disclose. Mr. Kendall has nothing to disclose. Dr. Shaffer has nothing to disclose. Dr. Mouhanna has nothing to disclose. Dr. Kenniff has nothing to disclose.

P025 The knee that gave it away: a case report of melioidosis

Abstract Background/Aims Melioidosis, an infectious disease caused by the Burkholderia pseudomallei is very rare within the UK. This gram-negative bacterium is endemic in Southeast Asia predominately Thailand and Northern Australia which is found within the soil and fresh surface water. We present a challenging case of melioidosis who was diagnosed following a culture of a discharging knee swelling. Methods N/A Results 35-year-old, Caucasian gentleman with no previous past medical history presented with a ten week history of diffuse abdominal pain, weight loss, dry cough, fatigue and night sweats. On examination, he appeared pale and initial bloods showed a CRP of 229 mg/L. His other initial observations and baseline blood tests were normal. Abdominal ultrasound detected free peritoneal fluid and a subsequent CT chest and abdominal showed abnormal thickening of his small bowel, mediastinal and retroperitoneal lymphadenopathy along with bilateral pulmonary nodules. A laparoscopy and laparotomy with peritoneal, intraperitoneal and mesenteric lymph node biopsies were inconclusive. Microscopy and culture (MC&amp;S) as well as acid fast bacilli MC&amp;S were both negative. He continued to have systemic symptoms, as well as elevated inflammatory markers. He underwent a bronchoscopy which showed erythematous and a nodular endobronchial mucosa with white plaques seen within the lower trachea and minor narrowing of the lumen. Endobronchial biopsies showed chronic inflammation with no evidence of any malignant cells. Repeated bloods including retroviral screening, anti-nuclear antibody (ANA) and antinuclear cytoplastic antibodies (ANCA) and serum ACE were normal. At this stage, the clinical picture was suggestive of sarcoidosis, however a subsequent rigid bronchoscopy and biopsy did not evidence of granulomas or vasculitis. The patient started to develop increasing right knee swelling with difficulty in walking. The swelling burst open, and the discharging fluid was sent for MC&amp;S. This was positive for Burkholderia pseudomallei. The gentleman completed a 20-week course of antibiotics with clinical resolution. Conclusion Meliodosis can cause a wide range of clinical manifestations varying from asymptomatic to septicemia, osteomyelitis, abscesses, septic arthritis and encephalomyelitis. Our case had travelled to Thailand around 8 months prior to the onset of symptoms. This highlights the possible long latent period between exposure and clinical presentation. Definite diagnosis is through isolation of Burkholderia pseudomallei in cultures. This proved challenging in our case, as multiple biopsies and cultures from different sites did not grow the bacterium. The diagnosis was confirmed following knee fluid culture. Musculoskeletal involvement of melioidosis is a known presentation and its potential to mimic other conditions, may render a diagnostic challenge especially when it occurs outside an endemic area. The case highlights the need for rheumatologists to have a high level of clinical suspicion for early detection, isolation of the organism and proper disease management. Disclosure A. Maksoud: None. L. Sammut: Other; LS has received funding for educational events and activities - from Lilly, Roche/Chugai.

Clinical Characteristics of Pediatric Patients With Septic Shock Caused by Acute Appendicitis: A Case Series.

This study aimed to explore the clinical characteristics of septic shock in pediatric patients caused by acute appendicitis. This case series included patients with septic shock caused by acute appendicitis in Beijing Children's Hospital between January 2015 and December 2020. Six patients with septic shock caused by acute appendicitis were enrolled. One patient was an infant with extremely low weight; 2 patients were obese. The diagnosis was delayed in 4 patients (the time from onset to diagnosis was 5 days in 3 children and 4 days in 1 child). All patients had abnormally raised inflammatory markers (C-reactive protein 119.17 ± 48.36 mg/L, procalcitonin 129.95 ± 86.09 ng/mL). Severe abdominal infection was found in all patients. There was appendix perforation in 4 patients and diffused peritonitis in 3 patients. Two patients had metabolic diseases (Wilson disease and decreased biotinase activity, respectively). Five patients had an appendectomy and 1 patient received conservative treatment. Five patients were discharged in stable condition, while 1 patient died. Children with delayed diagnosis, abnormal body weight, significant elevation in inflammatory markers, and underlying metabolic disease may be at greater risk of complicated appendicitis and septic shock. Level of Evidence: IV.