Course Of Steroid Therapy Research Articles

Corticosteroid burst therapy in patients with acute heart failure: Design of the CORTAHF pilot study.

Inflammation has emerged as a potential key pathophysiological mechanism in heart failure (HF) in general and acute HF (AHF) specifically, with inflammatory biomarkers shown to be highly predictive of adverse outcomes in these patients. The CORTAHF study builds on both these data and the fact that steroid burst therapy has been shown to be effective in the treatment of respiratory diseases and COVID-19. Our hypothesis is that in patients with AHF and elevated C-reactive protein (CRP) levels without symptoms or signs of infection, a 7-day course of steroid therapy will lead to reduced inflammation and short-term improvement in quality of life and a reduced risk of worsening HF (WHF) events. The study, which is currently ongoing, will include 100 patients with AHF ages 18-85, regardless of ejection fraction, screened within 12h of presentation. Patients will be included who have NT-proBNP>1500pg/mL and CRP>20mg/L at screening. Exclusion criteria include haemodynamic instability and symptoms and signs of infection. After signed consent, eligible patients will be randomized according to a central randomization scheme stratified by centre 1:1 to either treatment once daily for 7days with 40mg prednisone orally or to standard care. Patients will be assessed at study day 2, day 4 or at discharge if earlier, and at days 7 and 31 at the hospital; and at day 91 through a telephone follow-up. The primary endpoint is the change in CRP level from baseline to day 7, estimated from a mixed model for repeated measures (MMRM) including all measured timepoints, in patients without a major protocol violation. Secondary endpoints include the time to the first event of WHF adverse event, readmission for HF, or death through day 91; and changes to day 7 in EQ-5D visual analogue scale score and utility index. Additional clinical and laboratory measures will be assessed. The results of the study will add to the knowledge of the role of inflammation in AHF and potentially inform the design of larger studies with possibly longer duration of anti-inflammatory therapies in AHF.

Immune Thrombocytopenic Purpura: An uncommon manifestation of Hepatitis A with acute liver failure


 
 
 
 
 
 
 
 
 
 
 Hepatitis A Virus (HAV) infection is a benign, self-limited gastrointestinal infection of children. Autoimmune hematological manifestation is very rare in children. Here, we report an 11-year-old male child having HAV infection with acute liver failure, complicated with persistent thrombocytopenia and haematuria during the course of illness and eventually diagnosed as a case of HAV infection associated with immune thrombocytopenic purpura. The child was treated successfully with a short course of steroid therapy.
 
 
 
 
 
 
 
 
 
 
 
 
 

Anti-Ro/SSA Antibodies Blocking Calcium Channels as a Potentially Reversible Cause of Atrioventricular Block in Adults

BackgroundIn ∼50% of severe atrioventricular blocks (AVBs) occurring in adults <50 years, the underlying etiology remains unknown. Preliminary evidence from case reports suggests that autoimmunity, specifically the presence of circulating anti-Ro/SSA antibodies in the patient (acquired form), in the patient’s mother (late-progressive congenital form), or in both (mixed form), could be involved in a fraction of idiopathic AVBs in adults by possibly targeting the L-type calcium channel (Cav1.2) and inhibiting the related current (ICaL). ObjectivesThe purpose of this study was to evaluate whether anti-Ro/SSA antibodies are causally implicated in the development of isolated AVBs in adults. MethodsThirty-four consecutive patients with isolated AVB of unknown origin and 17 available mothers were prospectively enrolled in a cross-sectional study. Anti-Ro/SSA antibodies were assessed by fluoroenzyme-immunoassay, immuno-Western blotting, and line-blot immunoassay. Purified immunoglobulin-G (IgG) from anti-Ro/SSA-positive and anti-Ro/SSA-negative subjects were tested on ICaL and Cav1.2 expression using tSA201 and HEK293 cells, respectively. Moreover, in 13 AVB patients, the impact of a short course of steroid therapy on AV conduction was evaluated. ResultsAnti-Ro/SSA antibodies, particularly anti-Ro/SSA-52kD, were found in 53% of AVB-patients and/or in their mothers, most commonly an acquired or mixed form (two-thirds of cases) without history of autoimmune diseases. Purified IgG from anti-Ro/SSA-positive but not anti-Ro/SSA-negative AVB patients acutely inhibited ICaL and chronically down-regulated Cav1.2 expression. Moreover, anti-Ro/SSA-positive sera showed high reactivity with peptides corresponding to the Cav1.2 channel pore-forming region. Finally, steroid therapy rapidly improved AV conduction in AVB-patients with circulating anti-Ro/SSA antibodies but not in those without. ConclusionsOur study points to anti-Ro/SSA antibodies as a novel, epidemiologically relevant and potentially reversible cause of isolated AVB in adults, via an autoimmune-mediated functional interference with the L-type calcium channels. These findings have significant impact on antiarrhythmic therapies by avoiding or delaying pacemaker implantation.

Reversible Complete Heart Block in a Pregnant Woman Responding to Steroids: A rare Case Report

Background: Complete heart block (CHB) is the total absence of conduction from atria to ventricles with an escape rhythm most commonly arising from the AVN or His bundle. CHB in pregnancy is very rare, and most reported cases are due to congenital variety, where the pre-existing CHB from birth is either detected incidentally or presented with symptoms during pregnancy. Pregnancy is associated with various physiological changes, such as a pro-inflammatory, hypercoagulable state with possible oedema of the heart's conduction system, which may rarely give rise to CHB. There are no clear guidelines to manage CHB complicating pregnancy. Case Presentation:: An asymptomatic 27-year-old lady with G2P1L1, 39 weeks of gestation with breech presentation, was referred for delivery given the low maternal heart rate of 40 bpm. Per abdominal examination revealed a term size uterus with active contractions and a fetal heart rate of 140bpm. An ECG revealed a CHB with an escape rate of 40 bpm. Other routine investigations were normal, with negative serological evaluation for hepatitis B, C, and HIV. ANA and Anti-Ro ⁄ SSA antibodies. She underwent an emergency LSCS under spinal anaesthesia with a backup temporary pacemaker (TPM). She received a short course of empirical steroid therapy for three days as there were no obvious secondary causes for CHB, which reverted to sinus rhythm after 48 hours. Discussion: CHB complicating pregnancy with or without symptoms may require definitive therapy in the form of permanent pacemaker implantation. However, the insertion of a TPM for managing pregnancy is controversial as opinion in the literature is divided. There are no reports of CHB occurring in pregnancy without congenital or other known acquired causes. In the reported case, the CHB reverted to sinus rhythm with a short course of IV steroid therapy without any subsequent need for a PPM implantation. Conclusion: Congenital CHB remains the most common cause of rarely seen CHB complicating pregnancy. Through the conduction system oedema and inflammation, physiological changes in gestation may rarely cause CHB during pregnancy. In the absence of congenital CHB and other demonstrable acquired causes, a short course of steroid therapy may reverse the CHB avoiding PPM implantation as shown in the reported case.

A Case of Post-Fever Retinitis in a Patient with Positive Lyme Borreliosis Serology

Background: Lyme Borreliosis accounts for less than 1% of all uveitis cases. The challenge in diagnosing Lyme-associated uveitis in a seropositive patient is determining whether the serology status is causative or incidental. We describe a case that illustrates this challenge: a post-fever retinitis in a patient with persistent positive Lyme serology. Case Presentation: A patient presented to the eye clinic with complaints of blur and foreign body sensation in his right eye after getting sawdust in his eye. Further lab workup was only remarkable for Lyme IgG and IgM and the patient was subsequently diagnosed with a post-fever retinitis. Management and Outcomes: The patient was treated with oral prednisone, and a subsequent IOP spike was managed with topical ocular hypotensive drops until the course of steroid therapy was completed. The uveitis resolved over seven weeks. Conclusions: Post-fever retinitis is a diagnosis of exclusion, and diagnosis can be challenging in the presence of positive serology for other known causes of uveitis. This case highlights the importance of detailed case history and clinical findings in determining alternative causes of uveitis in patients with positive LB serology. CE Notification: This article is available as a COPE accredited CE course. You may take this course for 1-hour credit. Read the article and take the qualifying test to earn your credit. Click here to Enroll (https://www.crojournal.com/a-case-of-post-fever-retinitis-in-a-patient-with-positive-lyme-borreliosis-serology) Please check COPE course expiry date prior to enrollment. The COPE course test must be taken before the course expiry date.

Clinical Course and Impact of Immune Checkpoint Inhibitor Colitis Resembling Microscopic Colitis.

Microscopic colitis (MC) is suspected to result from increased immune activity in gut mucosa. Immune checkpoint inhibitors (ICIs) treat cancer by activating the immune system, and further investigation is needed regarding their role in the development of MC. A retrospective case series investigated cases of endoscopically and histologically confirmed MC developing after administration of ICIs. Clinical notes and medication administration records were reviewed for demographics, symptom duration, and treatment response. Nineteen cases of de novo MC were identified, with 95% of cases requiring steroid treatment, 53% presenting with hospitalization, and colitis-related mortality in 1 individual. Symptom onset occurred a median of 160 days after initiation of ICI therapy and 53 days after their most recent dose of therapy. Patients had a median of 125 days of symptoms, and ICI therapy was held in 70% of individuals due for treatment. MC can develop after ICI administration, and presents with severe symptoms, often requiring hospitalization and steroid treatment. In certain individuals this can require a prolonged treatment course of steroid therapy or immunomodulators. Individuals developing diarrhea after ICI therapy warrant thorough workup including endoscopy and rapid treatment initiation given the disease severity observed in this series.

Steroid-induced diabetic ketoacidosis - case report

Background: Diabetic ketoacidosis (DKA) is an acute complication of diabetes, a severe metabolic disorder that requires urgent treatment. The aim of this article is to present a case of steroid-induced diabetes with complications. Case Presentation: A young 25-year-old man without any co-morbid, presented to the emergency department with fever, vomiting, coughing, and buttock pain which started 3 days before. On the right gluteus, there was a hematoma approx. 10 × 5 cm with fluctuation. The patient had hyperglycemia (9.1 mmol/l), associated with high anion-gap metabolic acidosis, acute kidney injury (AKI), grossly elevated muscle enzymes, hyperkalemia, hyperphosphatemia, hypoalbuminemia, hypocalcemia and hypomagnesemia, and deranged liver function tests. The urine dipstick was grossly cola-colored and biochemically was positive for glucose, ketones, and proteins. Abscess drainage was performed, and Streptococcus pyogenes was isolated on culture and sensitivity. The patient was treated for DKA, complicated by an AKI and infection. Diabetes is confirmed based on glycosylated hemoglobin. Conclusion: The risk of ketoacidosis and hyperglycemia should be considered in the course of steroid therapy, even without a diagnosis of diabetes, in patients who abuse steroids or have risk factors for diabetes and obesity.

Arterial hypertension in children with nephrotic syndrome

The review presents materials on the prevalence of NS in children, variants of its course: steroid-sensitive (SSNS) and steroidresistant (SRNS) steroid-dependent (SSNS). Minimal change nephrotic syndrome minimal changes (NSMC) is the most common glomerular disorder. Although NSMC has an excellent prognosis with a low risk of progression to t-CRF, its recurrent nature requires children to receive frequent courses of steroid therapy and other medications, many of which are known to affect blood pressure (BP). The interrelation of NS in children with arterial hypertension (AH) is shown. Prevalence of hypertension in children with SCNS, SRNS, SZNS is given. The regulation of hypertension in children is mandatory in the treatment of NS, due to the fact that hypertension is not established in a timely manner, is insufficiently controlled and is often masked. Vascular dysregulation, fluid overload, increased cardiac output and peripheral vascular resistance, alone or in combination, can lead to hypertension in CKD. The use of modern methods to monitor and control blood pressure is critical for improving hypertension management and preventing target organ damage in children. 24-hour blood pressure measurements are an important tool in determining the prognosis and treatment of children with HC. Many comorbidities increase the risk of cardiovascular disease, including obesity, left ventricular hypertrophy (LVH), increased arterial stiffness (increased BMI, endothelial dysfunction), impaired glucose metabolism, and hyperlipidemia. The pathophysiological aspects of hypertension in children with NS are considered. The pathophysiology of hypertension in NS is complex, with many renal and extrarenal factors. Renal factors include sodium retention, fibrosis / decreased GFR, and progression of kidney disease, and a direct link between albuminuria and blood pressure has recently been described. Other factors include drug side effects, comorbidities and genetic predisposition. Sodium metabolism plays an important role in the development of edema and blood pressure regulation in NS. There are two main hypotheses for sodium retention in NS, the hypothesis of underfilling and overfilling. The role of the epithelial sodium channel (ENC), atrial natriuretic peptide (ANP), nitric oxide (NO), steroid hormones and other drugs in sodium retention and the pathogenesis of hypertension is also considered. In children with NS, hypertension leads to target organs damage (TOD): left ventricular hypertrophy (LVH), damage to the organ of vision, cognitive impairment and more rapid progression of chronic kidney disease. Salt restriction and RAAS inhibition are considered integral parts of the treatment of children with proteinuria, and both are known to have blood pressure lowering effects. The RAAS blockade has a renoprotective effect in patients with glomerular damage. Studies have found greater reductions in proteinuria with ACE / ARB combination therapy. This renoprotective effect is explained by both a decrease in blood pressure and mechanisms independent of blood pressure. Lifestyle modifications, weight control, healthy eating, reduced sodium intake, supportive exercise, and basic drug therapy using angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), diuretics can slow the progression of NS in children.

Acquired hypofibrinogenemia in patients with leukemia during steroid therapy

Acquired hypofibrinogenemia is observed in patients with severe liver disease, disseminated intravascular coagulation, and high-volume perioperative fluid replacement. In lymphoblastic leukemia, hypofibrinogenemia is most frequently caused by the administration of L-asparaginase. Here we report the cases of two patients with acquired hypofibrinogenemia that occurred during steroid-containing chemotherapy treatment against lymphoblastic blast crisis of chronic myeloid leukemia in the first case and acute lymphoblastic leukemia in the second case. Administration of steroids repeatedly and promptly caused hypofibrinogenemia, irrespective of the products (prednisolone, dexamethasone, or methylprednisolone) or routes (oral or intravenous) that were used. Monitoring of the fibrinogen levels, especially during the first course of steroid therapy, would be useful for early diagnosis.

The benefits or harms of systemic corticosteroids for community-acquired pneumonia in adults: аn overview of reviews

Background: The problem of reducing mortality in patients with community-acquired pneumonia remains extremely important despite the progress in the development of antibiotics. There is a certain consensus on the etiological treatment of typical and atypical variants of the disease, however, the efficacy of corticosteroids as a means of pathogenetic therapy for many years has remained a subject of discussion, in spite of the large number of studies conducted and several dozen reviews of them.&#x0D; The aim of our study is to summarize more than one systematic review of randomized controlled trials to assess the evidence for the effect of adjuvant systemic CS in adults with CAP on mortality, symptom dynamics, risk of complications, and harmful side effects.&#x0D; Methods: From July to September 2020, we searched for systematic reviews in the PubMed, Embase, CENTRAL databases in accordance with the recommendations of the Cochrane Guidelines for Systematic Reviews 6 version up to 2020. The methodological level of the selected reviews was assessed using the АMSTAR-2 form.&#x0D; Results: 12 systematic reviews were selected that were performed in different countries from 2012 to 2018, covering 24 clinical trials with 2,791 participants. Comparison and generalization of review data confirms that additional prescription of CS led to a decrease in mortality in severe CAP, and with any severity of CAP - to a decrease in the risk of treatment failure in the first 57 days from its onset, acceleration of the onset of signs of clinical improvement, and a decrease in the risk of development respiratory failure and transfer to artificial lung ventilation, reducing the length of hospital stay and treatment in the intensive care unit. Short courses of steroid therapy did not increase the risk of harmful plug events, with the exception of hyperglycemia, which was easily controlled.&#x0D; Our analysis has also shown that there is a feasibility of bridging the gap between existing regulations and the evidence base for current systematic reviews of RCTs on the use of CS in CAP.

Vitamin D level in nephrotic syndrome, Factors of impact?

Introduction Nephrotic syndrome (NS) usually responds to steroid therapy; however, the majority of children relapse, resulting in prolonged and repeated courses of steroid therapy. Vitamin D is a vital component of bone metabolism and calcium homeostasis. Maintenance of adequate levels of vitamin D is recommended to maintain good bone health and other organ systems of NS patients. The study aimed to assess serum 25 (OH) D levels in children with NS, compare its level with healthy age and sex-matched controls and compare its level in different types of NS. Patients and Methods It was a cross-sectional study for measuring 25(OH) D levels in 60 patients with NS and 60 apparently healthy children, to be compared as controls. Nephrotic patients were classified as steroid sensitive (20 cases) steroid dependent (20cases), and steroid resistant (20 cases). Serum 25-hydroxyvitamin [25(OH) D] was measured using Enzyme Linked Immune Sorbent Assay (ELISA) technique. Results Serum 25(OH) D was significantly lower in NS patients than control group (p<0.001).Steroid resistant nephrotic syndrome (SRNS) patient group showed the highest drop than the other 2 groups (p<0.001). There was significant negative correlation between vitamin D level and number of relapses, 24 hours urinary proteins and serum cholesterol. Conclusion It is recommended that NS patients especially on long term steroid therapy should undergo regular follow up of vitamin D level and early prophylactic supplementation with calcium and vitamin D should be advised.

Acceleration of interstitial lung disease induced by raltitrexed

Raltitrexed is a folate analogue, which selectively inhibits thymidylate synthase, used in the treatment of colorectal carcinoma. Common side effects include asthenia and gastrointestinal and haematological toxicities. We present the case of a 74-year-old gentleman with incidental mild interstitial lung disease on preoperative staging CT Chest who developed acute breathlessness whilst undergoing adjuvant raltitrexed treatment for a completely excised colorectal adenocarcinoma. Discontinuation of raltitrexed and a course of steroid therapy resulted in resolution of symptoms, mirrored by an improvement in lung function tests. The clinical pattern of rapid progression with steroid response highlights the potential for significant acceleration of interstitial lung disease by raltitrexed.

EOSINOPHILIA AND DYSPNEA: NOT ALWAYS AN ASTHMA EXACERBATION

SESSION TITLE: Tuesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Eosinophilia is a common laboratory finding in patients diagnosed with asthma, however combined with dyspnea and a chronic cough, other diagnoses can be overlooked.. Chronic eosinophilic pneumonia is characterized by a chronic and progressive course similar to worsening asthma with the addition of specific pathologic findings. Here we present a case of a patient with known asthma who presented with progressively worsening cough, shortness of breath and eosinophilia. CASE PRESENTATION: A 46-year-old male with a history of asthma presented to the emergency department (ED) with worsening shortness of breath at both rest and exertion for two months. The patient had associated wheezing, thick yellow sputum and rhinorrhea. At presentation he also noted a two-week history of night sweats with a ten pound weight loss. Prior to presentation the patient underwent a chest x-ray and was treated for two weeks with antibiotics. for presumed pneumonia. The patient then underwent a repeat chest x-ray and was subsequently referred for chest CT. In the ED the patient was noted to have leukocytosis of 34 K/uL with 23.2 K/uL eosinophils (68.2%) Chest X-Ray demonstrated patchy air-space opacities with a predominantly mid to upper lung zone distribution. The patient was started on methylprednisolone, ceftriaxone, and azithromycin for community acquired pneumonia and was seen by the pulmonary and infectious disease consultants. The patient was tested for angiotensin converting enzyme, P-ANCA, Aspergillus, HIV, and tuberculosis, all of which were negative. The patient clinically improved and antibiotic therapy was discontinued. Three days after admission a repeat CXR, showed improved bilateral pulmonary parenchymal abnormalities. The patient’s eosinophilia resolved within three days and the patient continued to clinically improve with a tapering course of steroid therapy. DISCUSSION: Chronic eosinophilic pneumonia (CEP)is characterized by chronic and progressive clinical features and specific pathological findings. The onset of CEP is generally insidious, either subacute or chronic. Accordingly, the symptoms often appear several months before the diagnosis is made. The diagnosis of CEP is based on the association of respiratory symptoms, alveolar or blood eosinophilia, a non-segmental pulmonary infiltration with peripheral predominance involving mainly the upper lobes on chest imaging and the exclusion of other eosinophilic lung diseases. Corticosteroid treatment results in rapid resolution of symptoms, radiologic opacities and peripheral eosinophilia as occurred in our case. CONCLUSIONS: This case demonstrates the need for physicians to broaden their differential diagnoses when considering the etiology of eosinophilia in patients with a history of asthma. Reference #1: https://www.uptodate.com/contents/chronic-eosinophilic-pneumonia?search=chronic%20eosinophilic%20pneumonia&source=search_result&selectedTitle=1∼37&usage_type=default&display_rank=1 DISCLOSURES: No relevant relationships by Jang Chadha, source=Web Response No relevant relationships by Yelenis Fuertes Yanes, source=Web Response No relevant relationships by Nida Hameedi, source=Web Response

41. A common rheumatology referral of vague constitutional symptoms and raised inflammatory markers

41. A common rheumatology referral of vague constitutional symptoms and raised inflammatory markers

A retrospective longitudinal study on the effect of ultra short course of steroid therapy on clinical and hematologic parameters of secondary hemophagocytic lymphohistiocytosis in children

Background: The aim was to study the effect of ultra-short course of injectable steroid followed by oral steroid therapy for cumulative 14 days on clinical and hematologic parameters of secondary hemophagocytic lymphohistiocytosis in children.Method: A retrospective longitudinal study was conducted by collecting data from case records. Cases diagnosed with secondary hemophagocytic lymphohistiocytosis had been included. The cases with malignancy were excluded. Remaining cases had been given injectable methyprednisolone (30 mg/kg/day) for three days followed by oral prednisolone (1 mg/kg/day) for 11 days. The time to cessation of fever and organomegaly were noted. The changes in mean hematologic parameters, ferritin and triglycerides were noted at the time of suspicion of HLH or MAS, after therapy and on follow up.Results: About 96% of children were afebrile within five days of therapy. There was regression of hepatospleenomegaly in all 100% surviving children by day seven of therapy. Improvement in hemoglobin (mean value 8.1 mg/dl to 8.7 mg/dl) and platelet count (mean value 0.89 lakh to 1.47 lakh) was seen by day seven of therapy. Fall in serum ferritn (mean value 1419 ng/ml to 298 ng/ml) and serum triglycerides (mean value 307 mg/dl to 176 mg/dl) was seen at one-month follow-up. 96% survival was observed. None of the survivors had any recurrence at 6 months follow up.Conclusion: Ultra short course of injectable methyprednisolone for 3 days followed by oral prednisolone for 11 days was successful in 95% survival in our study. This cost-effective regimen, with use of less toxic drugs leading to a shorter hospital stay maybe helpful in resource limited settings.

CHALLENGING CASE OF RECURRENT PNEUMONIA IN A PATIENT WITH COAL WORKER’S PNEUMOCONIOSIS

SESSION TITLE: Medical Student/Resident Occupational and Environmental Lung Diseases SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Coal worker’s pneumoconiosis (CWP) is a chronic occupational lung disease leading to irreversible lung damage. Severe forms result in progressive massive pulmonary fibrosis (PMF). We will be discussing a case of an elderly male with CWP and recurrent episodes of pneumonia. CASE PRESENTATION: 72-year-old male with past medical history significant for working in the coal mines for about 27 years with a diagnosis of CWP and PMF. PFTs showed mixed obstructive and restrictive defects. He had multiple hospitalizations for sepsis secondary to recurrent pneumonia. His symptoms consisted of productive cough without hemoptysis, chills, pyrexia, worsening dyspnea and hypoxia. CT chest showed severe CWP with PMF, right lower lobe consolidation and a cavitary mass in the left upper lobe. The patient had been diagnosed with ESBL positive E. coli pneumonia and treated with IV Ertapenem for 4 weeks. He was readmitted to the hospital shortly after completing this treatment and was diagnosed with Streptococcus pneumoniae bacteremia and pneumonia, for which he was treated with IV Rocephin. CT guided biopsy of the cavitary mass was negative for malignancy, but the procedure was complicated by pneumothorax requiring chest tube and pleurodesis by general surgery. Bronchoscopy with EBUS was also performed which was again negative for malignancy and AFB, but one BAL sample showed prominent eosinophils. CBC also showed eosinophilia. IgE level was elevated at 1,909; his IgA, IgG, and IgM levels were all within normal limits. Quantiferon TB gold was negative. Patient’s Strongyloides antibodies were elevated at 1.66 and he was diagnosed with Strongyloides stercoralis hyperinfection syndrome. He was treated with one dose of Ivermectin. Patient was followed in the outpatient pulmonology clinic and had no further hospitalizations due to pneumonia. DISCUSSION: Most common risk factors for Strongyloides hyperinfection syndrome includes being in an institutionalized population or living in rural areas. The mode of transmission is through contact with contaminated soil. Activities that increase contact include walking with bare feet, contact with human waste, and occupations that increase contact with soil. Coal miners are at higher risk of infections such as, Strongyloides. Most cases reported are due to chronic immunosuppression secondary to chronic steroid use. Even though our patient was not on chronic steroids, he had received many courses of steroid therapy during his numerous hospitalizations. The chronic changes of PMF can add more challenges and increase the complexity of the clinical presentation and may delay timely diagnosis and treatment of this uncommon cause of recurrent infections. CONCLUSIONS: The workup for recurrent pneumonia in patient's with progressive massive fibrosis should include the evaluation for Strongyloides hyperinfection syndrome in the appropriate clinical context. Reference #1: Arnold, Carrie. "A Scourage Returns: Black Lung in Appalachia." Environmental Health Perspective (2016): A13-A18. Epublished January 1, 2016. Reference #2: Asdamongkol N, Pornsuriyasak P, Sungkanuparph S. "Risk factors for strongyloidiasis hyperinfection and clinical outcomes." The Southeast Asian Journal of Tropical Medicine and Public Health (2006): 875-884. Reference #3: Gourahari Pradhan, M.D.,1 Priyadarhini Behera, M.D.,1 Manoj Kumar Panigrahi, M.D.,corresponding author1 Sourin Bhuniya, M.D.,1 Prasanta Raghab Mohapatra, Jyotirmayee Turuk, and Srujana Mohanty, M.D. et. al. "Pulmonary Strongyloidiasis Masquerading as Exacerbation of Chronic Obstructive Pulmonary Disease." Tuberculosis and Respiratory Disease (2016): 301-311. Epublished October 5, 2016. DISCLOSURES: No relevant relationships by Haytham Adada, source=Web Response No relevant relationships by Mahmoud Amarna, source=Web Response No relevant relationships by Camelia Chirculescu, source=Web Response No relevant relationships by Rabab Elmezayen, source=Web Response No relevant relationships by Sana Yakoob, source=Web Response

Osteocalcin Level in Children with Steroid Dependent/Frequently Relapsing and Steroid Resistant Nephrotic Syndrome

Background: Children with nephrotic syndrome (NS) may be at risk for metabolic bone disease because of biochemical derangement caused by renal disease as well as steroid therapy. Osteocalcin (OC) functions as an inhibitor of bone mineralization. We aimed to evaluate linear growth and bone turnover markers (including serum osteocalcin) in children with steroid-dependant/frequently-relapsing and steroid resistant NS in comparison to a matched control group. Methods: Our study was a cross-sectional study conducted at children’s hospital, Cairo University, Egypt from July 2014 to August 2015. The study included 60 patients, aged 2 - 15 years recruited from outpatient nephrology clinic. Twenty eight age- and sex- matched healthy children were included as a control group. Serum OC was measured by immune-radiometric assay. Results: Serum OC levels were significantly higher in both SDNS/FRNS and SRNS than in control group, with P value 0.02 and 0.01, respectively. There was statistically significant negative correlation between OC and serum calcium. There was a negative correlation between height for age percentile and number of relapses. There were also negative correlations between height for age percentile and steroids, cyclophosphamide and cyclosporine duration of treatment. We found that both of our patients groups (SDNS/FRNS and SRNS) showed lower height for age percentile compared to control group (P = 0.017 and 0.001 respectively). Conclusions: Height as a growth parameter is more affected when recurrent relapses occur with multiple courses of steroid therapy. Use of OC as screening tool is recommended for bone turnover while patients on steroids.

GR 02.04 Current Standard in Monitoring of Immunotherapy-Related Toxicity

GR 02.04 Current Standard in Monitoring of Immunotherapy-Related Toxicity

Semi-quantitative metabolic values on FDG PET/CT including extracardiac sites of disease as a predictor of treatment course in patients with cardiac sarcoidosis

BackgroundCardiac sarcoidosis is associated with major adverse cardiac events including cardiac arrest, for which anti-inflammatory treatment is indicated. Oral corticosteroid is the mainstay among treatment options; however, adverse effects are a major concern with long-term use. It would be beneficial for providers to predict treatment response and prognosis for proper management strategy of sarcoidosis, though it remains challenging. Fluorine (F)-18 fluorodeoxyglucose (FDG)-positron emission tomography(PET)/computed tomography(CT) has an advantage over anatomical imaging in providing semi-quantitative functional parameters such as standard uptake value (SUV), metabolic volume, and total lesion glycolysis (TLG), which are well-established biomarkers in oncology. However, the relationship between these parameters and treatment response has not been fully investigated in cardiac sarcoidosis. Also, the prognostic value of extracardiac active inflammation noted on FDG-PET/CT in the setting of cardiac sarcoidosis is unclear. The aim of this retrospective study was to investigate the prognostic value of semi-quantitative values of both cardiac and extracardiac disease sites derived from FDG-PET/CT in predicting treatment course in cardiac sarcoidosis.MethodsSixteen consecutive patients with suspected cardiac sarcoidosis, who demonstrated abnormal myocardial activity on cardiac-inflammation FDG-PET/CT encompassing the entire chest/upper abdomen and subsequently underwent corticosteroid therapy for diagnosis of active cardiac sarcoidosis, were included. Semi-quantitative values of hypermetabolic lesions were derived from all visualized organ system and were compared to daily corticosteroid dose at 6 months.Results Of the 16 patients, 81.3% (13/16) of the patients showed extracardiac involvement. The lesion with the greatest SUV was identified in the heart in 11 patients (68.7%), in the liver in 1 patient (6.3%), and in lymph nodes in 4 patients (25%). The maximum SUV across all visualized organ systems including the heart were 8.8 ± 3.1 for the patients with corticosteroid dose ≤ 10 mg and 12.5 ± 3.3 for those with > 10 mg (P = 0.04). Metabolic volume and TLG across all visualized organ systems or any values in the heart alone showed no significant statistical difference between the two groups.ConclusionsMaximum SUV across all involved organ-systems of the chest and upper abdomen, not that of the heart alone, could be a predictor of treatment course of steroid therapy at 6 months in patients with active cardiac sarcoidosis.

Eosinophilic Gastrointestinal Disorder Presenting as Intractable Vomiting and Ascites in a Young Girl

Eosinophilic gastrointestinal disorder (EGID) is a rare disease in children that affects the bowel wall, with eosinophilic infiltration in the absence of any other causes for eosinophilia. The etiology remains unknown, but allergies and immunological imbalance are suspected triggers. We encountered a case of serosal EGID presenting as intractable vomiting and ascites in a 9-year-old girl, after influenza virus infection. Peripheral eosinophilia was not present. The diagnosis was confirmed by biopsy of the bowel wall through laparotomy and endoscopy, and controlled by 2 courses of steroid therapy due to recurring symptoms. Influenza virus infection was assumed to play a role in the onset of EGID through a Th2 response that stimulated eosinophilic infiltration in the GI tract. We therefore report this case along with a literature review.