Tapering Course Of Prednisone Research Articles

SAT440 DRESS/DHIS-associated Thyroiditis And Hypophysitis

Abstract Disclosure: I.R. Ranasinghe: None. M.S. Elston: None. V. Boyle: None. Introduction: Drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms (DRESS/DIHS) is a severe life-threatening adverse reaction to specific drugs, including cephalosporin antibiotics (1). It is characterised by rash, fever, eosinophilia, lymphadenopathy, and inflammation of internal organs. Endocrine complications in the form of thyroid disease and Type 1 Diabetes have been reported following DRESS/DIHS (2). We report a case of thyroiditis and hypophysitis following cephalosporin-associated DRESS/DIHS. Case: A 21-year-old male farmer suffered a tractor crash accident resulting in hospitalization for bilateral compound distal femur fractures. He had no past medical history of note. One month later, he developed a maculopapular rash involving his limbs, mouth ulcers, fever, liver function derangement and eosinophilia. Punch biopsy was consistent with DRESS/DHIS. A 2- week tapering course of prednisone was initiated at 40mg daily in conjunction with a topical corticosteroid for 9 days with resolution of rash. Review of medication charts identified the most likely causative agent as cefazolin. An Endocrine consult was requested a month later due to new hypercalcemia. Investigations revealed new onset thyrotoxicosis and a decreasing morning cortisol over the following week despite having stopped all steroids one month earlier, normal ACTH, mildly elevated prolactin and secondary hypogonadism. Short Synacthen test showed suboptimal response. TRAb were negative and technetium thyroid scanning demonstrated a thyroiditis. MRI pituitary was unremarkable. He was commenced on hydrocortisone replacement for symptomatic cortisol deficiency. Biochemical abnormalities gradually normalized and his hydrocortisone ceased with symptomatic resolution. Endocrine involvement, particularly pancreas and thyroid has previously been reported in cases of DHIS/DRESS (3) (4). In this case, DHIS/DRESS-associated hypophysitis with thyroiditis may explain the clinical findings of pituitary dysfunction affecting multiple pituitary axes and the gradual recovery to normal pituitary function.

SAT479 A Case of Thyroiditis Cause by Cabozantinib

Abstract Disclosure: S. Bulchandani: None. N. Janicic-Kahric: None. Introduction: Thyroiditis is an inflammatory disease of the thyroid; the cause can be autoimmune, infectious or drug induced. Patients can have an initial phase of hyperthyroidism (thyrotoxicosis) attributed to the release of preformed thyroid hormone from damaged thyroid cells. This can be followed by hypothyroidism, when the thyroid stores are depleted, and then eventual restoration of normal thyroid function. Some patients may develop permanent hypothyroidism.1 We report a case of thyroiditis caused by cabozantinib. CASE REPORT: 39-year-old female presented with abdominal pain, vomiting and palpitations. Past medical history was significant for metastatic clear cell renal carcinoma. Eight weeks before the presentation, she had started on cabozantinib 60 mg daily as part of therapy for her renal carcinoma. On presentation, the patient’s temperature was 36.6 Celsius, heart rate was 118 beats/minute, blood pressure was 114/84 mm Hg and oxygen saturation was 100% on room air. Laboratory evaluation was notable for white blood cell count of 12.3 k/uL, Hemoglobin of 16.5g/dl, Platelet count of 573 k/uL bicarbonate level of 13 mmol/L, anion gap 24 mmol/L, Total bilirubin of 0.6 mg/dl, Aspartate aminotransferase of 36 units/L, Alanine aminotransferase of 30 units/L, Alkaline phosphatase of 121 units/L. Thyroid function tests revealed thyroid stimulating hormone (TSH) which was low at 0.045 uIU/ml and free thyroxine level (Free T4) which was elevated at 4.29 ng/dl. Thyroid function tests performed eight weeks prior to presentation showed TSH of 6.9 uIU/ml, attributed to immunotherapy that the patient received 1 month prior. She was admitted and received intravenous fluids. Prednisone at 40 mg orally daily was initiated. Labs demonstrated a decrease in Free T4 level. She was discharged on a tapering course of prednisone. Free T4 one week later was normal at 1.35ng/dl. Repeat laboratory evaluation three weeks later revealed that the patient had developed hypothyroidism with TSH level of 8.7 uIU/ml and she was started on 50 micrograms of levothyroxine. Cabozantinib was discontinued. Discussion: Tyrosine Kinase inhibitor therapy can result in clinically significant thyroid dysfunction. Cabozantinib treatment can result in thyroid dysfunction varying from subclinical hypothyroidism to symptomatic thyrotoxicosis. Early detection and close follow-up are essential to provide adequate management2 Presentation Date: Saturday, June 17, 2023

Pediatric Autoimmune Pancreatitis: A Single-Center Retrospective Case Series.

Autoimmune pancreatitis (AIP) is a rare form of a chronic, immune-mediated, inflammatory pancreatic condition. There is limited data regarding presentation and outcome in the pediatric population. We described a single-center case series of 4 pediatric patients with AIP to better understand the presentation, symptoms, and outcomes of this rare condition. Data collected included demographics, serology markers, symptoms at presentation, imaging, additional organ involvement, histology, treatment methods, and outcomes. The diagnosis of AIP was made by a combination of serology, pancreatic imaging, histology, extrapancreatic manifestations, and steroid response. All patients were diagnosed with type 2 AIP. Abdominal pain, emesis, and obstructive jaundice were the most common symptoms at presentation. Autoimmune markers were negative. Cross-sectional abdominal imaging showed diffuse/focal pancreatic gland enlargement and common bile duct stricture universally and main pancreatic duct irregularity in half of the patients. Biopsies showed lymphoplasmacytic infiltration with associated pancreatic fibrosis and atrophy. Treatment with an 8-week tapering course of prednisone showed prompt response with resolution of symptoms and normalization of laboratory test results. Our case series shows that AIP in children is a rare entity with a distinct clinical presentation, classical radiographic and histological features with good long-term prognosis.

Treatment With Cytarabine at Initiation of Therapy With Cyclosporine and Glucocorticoids for Dogs With Meningoencephalomyelitis of Unknown Origin Is Not Associated With Improved Outcomes.

Meningoencephalomyelitis of unknown origin (MUO) is a common disorder of dogs that results in significant morbidity and mortality. The ideal treatment regimen is not known but a second immunosuppressive agent is often utilized in combination with glucocorticoids to increase efficacy and reduce side effects. Recently, a benefit to using a cytosine arabinoside (CA) constant rate infusion (CRI) at the time of diagnosis has been demonstrated. Here, a retrospective study was performed to determine if administration of CA at the time of diagnosis would alter prognosis in dogs receiving cyclosporine and prednisone for treatment of MUO. Medical records of 51 client-owned dogs diagnosed with MUO at one institution were reviewed (2009-2019). All dogs were treated with cyclosporine and a tapering course of prednisone. Twenty-one dogs received a single initial 200 mg/m2 treatment with CA either as a CRI or subcutaneously. Significantly more patients in the CA treatment group were obtunded on presentation but all other baseline parameters were similar between groups. No differences in success (defined as sustained improvement on neurological exam with owner perceived good quality of life), relapse, or death were identified at 1-, 3-, 6-, 9-, 12-, 18-, or 36-month time points. These results do not support treatment with CA (either as a CRI or subcutaneously) at the time of diagnosis in dogs treated with cyclosporine and prednisone.

RELAPSING CRYPTOGENIC ORGANIZING PNEUMONIA

SESSION TITLE: Wednesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Organizing pneumonia is a form of Interstitial lung disease. It has equal prevalence in men and women. Adults 40-60 years are most commonly affected. It can be idiopathic, called cryptogenic organizing pneumonia(COP), or secondary to other factors; secondary organizing pneumonia. CASE PRESENTATION: 77-year-old female with history of hypertension, CHF, COPD presented with 3 weeks of dyspnea. She was hospitalized 3 weeks prior and treated for CAP.CXR at that time demonstrated b/l upper lobe consolidations. She was discharged on 4L O2 and PO cefpodoxime. Pt reported subjective improvement, however she was not back to her baseline. CT chest revealed patchy consolidation in the b/l upper lobes, and multiple nodular opacities in lower lobes. On initial evaluation patient was afebrile, hypoxic, with PaO2:91 on non-rebreather saturating at 95%. WBC count of 8.9. Bronchoscopy was performed. BAL revealed WBC: 693, lymphocytes: 35%, cultures: negative. BAL analysis was supportive of a diagnosis of COP. Biopsy not done due to high FiO2 requirements and unstable condition. Patient was started on prednisone 40 mg x 4 weeks followed by 20 mg x 4 weeks. Patient was lost to follow up, and steroids stopped by PCP. 3 months later she was re hospitalized for hypoxia. CXR showed worsening opacities and she required 5 L O2 via NC. A tapering course of Prednisone was started. Patient seen on follow up at 3 months with resolution of symptoms. DISCUSSION: COP has an insidious onset. Risk factors include infections, connective tissue disease, malignancies, chronic recurrent aspiration, radiation, cocaine etc. The radiographic appearance of COP is variable. On chest CT scan patchy consolidation, is seen in 90% of patients. Nodules and irregular linear opacities or ground-glass attenuation may be seen. Diagnosis is made on history, Imaging, PFTs, Bronchoscopy with BAL and biopsy findings. PFTs may show obstructive vs restrictive defect. DLCO is usually decreased. Typical BAL findings include increases in lymphocytes (20 to 40 percent), neutrophils (5 to 10 percent), and eosinophils (5 to 25 percent). Foamy macrophages, mast cells, and a decreased CD4/CD8 T cell ratio may be seen. BAL neutrophilia (>10%) tends to correlate with relapse. Transbronchial/surgical lung biopsy provides a definitive diagnosis. Patients with minimal symptoms can be monitored without therapy as spontaneous remission may occur. For patients with severe disease: Long term course of steroids: 0.75-1 mg/kg/day for 4-8 weeks then 0.5 mg/kg/day for 4-8 weeks. Most patients respond to therapy with recovery usually occurring in two-thirds of patients. Approximately one-third of patients experience persistent symptoms, abnormalities on pulmonary function testing, and radiographic disease. CONCLUSIONS: Close monitoring is essential to ensure response and completion of therapy, as early discontinuation of steroids may result in recurrence of symptoms. Reference #1: 1. Cordier, J. F. "Cryptogenic organising pneumonia." European Respiratory Journal 28, no. 2 (2006): 422-446. Reference #2: 2. Drakopanagiotakis, Fotios, Koralia Paschalaki, Muhanned Abu-Hijleh, Bassam Aswad, Napoleon Karagianidis, Emmanouil Kastanakis, Sidney S. Braman, and Vlasis Polychronopoulos. "Cryptogenic and secondary organizing pneumonia: clinical presentation, radiographic findings, treatment response, and prognosis." Chest 139, no. 4 (2011): 893-900 Reference #3: 3. Epler, Gary R. "Bronchiolitis obliterans organizing pneumonia: definition and clinical features." Chest 102, no. 1 (1992): 2-6. DISCLOSURES: No relevant relationships by Siddique Chaudhary, source=Web Response No relevant relationships by Bhavna Sharma, source=Web Response No relevant relationships by Paul Kristan Valestra, source=Web Response

P067 AORTITIS IN ASSOCIATION WITH CROHN’S DISEASE: HOW FAR CAN CROHN’S DISEASE HIT?

Crohn’s disease (CD) is an inflammatory disorder of unclear etiology that may involve the entire gastrointestinal tract from mouth to the perianal area and may be associated with several extraintestinal manifestations. Venous thromboembolic events represent the most common cardiovascular complication in CD. Other cardiovascular complications are extremely rare and include aortic valvular disease, aortic root dilation, aneurysms and thoracoabdominal aortitis.Case report: A 62-year-old female with a history of ileocolonic CD diagnosed 15 years ago and was on oral mesalamine. She presented with a sudden onset of moderate epigastric pain radiating to the back of one day duration. The pain was associated with nausea and 3-4 episodes of watery diarrhea. She denied fever, chills, night sweats, headache, visual disturbances, chest pain, hemoptysis, or urinary symptoms. She lived in a rural area in northern Michigan, had contact with farm animal and was consuming well water occasionally. On initial evaluation, she was hemodynamically stable and afebrile. Her pulses were symmetrical and normal. A CT of the abdomen and pelvis with contrast (figure 1A) was suggestive of abdominal aortitis and a distal ileitis. Initial workup is shown in table 1. Vascular surgery, rheumatology and infectious diseases services were consulted. An MRA of the abdomen showed a distal abdominal aortic aneurysm with moderate circumferential enhancing wall thickening. There was no evidence of systemic vasculitis, giant cell arteritis, Takayasu arteritis, or sarcoidosis. The decision was to hold on doing a vascular biopsy due to absence of constitutional symptoms. Given her epidemiological risk factors for infection, she was started on empirical antimicrobial treatment pending the results of the rest of the workup (table 1). She was approved to start on steroids after being on antimicrobials for 48 hours with negative blood cultures. The patient’s abdominal pain improved, and she remained afebrile. She was discharged on a 6-week course of antibiotics and a tapering course of prednisone. The rest of her rheumatological and infectious workup was unrevealing (table 1). A follow up MRA of the abdomen (figure 1B) showed an evidence of persistent abdominal aortitis. It was thought that this is due to her CD; she was started on oral prednisone 1 mg/kg with a taper of 10 mg weekly and adalimumab 40 mg subcutaneously every 2 weeks. Her follow up imaging 3 months later showed improvement of aortitis and no evidence of active inflammatory bowel disease. Aortitis in association with CD has been documented in few case reports and could be related to the local inflammation or the autoimmune nature of the disease. Other important causes of large vessel vasculitis must be ruled out, especially Takayasu arteritis, giant cell arteritis, sarcoidosis and infectious vasculitis. Full laboratory workup Full laboratory workup Figure 1: A) CT of the abdomen and pelvis contrast showing a new wall thickening and adjacent fat stranding to abdominal aorta and proximal left common iliac artery that was most compatible with aortitis, in addition to a wall thickening and inflammatory changes adjacent to the distal ileum suggestive of an active CD. B) A follow up MRA of the abdomen showing a persistent mild fusiform dilatation of the infrarenal abdominal aorta just above the level of the bifurcation, with periaortic inflammatory changes seen circumferentially surrounding the distal aorta and extending into the proximal left common iliac artery.

Acinetobacter radioresistens Septicemia Associated With Pneumonia in a Patient With Chronic Obstructive Pulmonary Disease and Hepatitis C

To the Editor: Acinetobacter radioresistens is a gram-negative coccobacillus, which is ubiquitous in soil and water, but however, is rarely responsible for causing clinically significant infections. We present a case of a 61-year-old white man with chronic obstructive pulmonary disease (COPD) and hepatitis C who developed septicemia because of A. radioresistens in the setting of pneumonia. CASE DESCRIPTION A 61-year-old white man presented to the emergency room with chills, fever, shortness of breath, and right-sided chest pain with mild cough for 3 days. The patient denied any recent travel, sick contacts, occupational hazards/exposures, animal hunting, or slaughtering. His history was significant for oxygen-dependent COPD; multiple, spontaneous right-sided pneumothoraxes due to COPD, which needed talc pleurodesis; gastroesophageal reflux disease; and hepatitis C virus (HCV). His medications included budesonide/formoterol, tiotropium, ginger root, and glucosamine/chondroitin. The patient was a former smoker and quitted smoking cigarettes 3 years ago. He admitted to drinking alcohol once every 1 to 2 weeks. Physical examination showed a temperature of 38.4°C (101.1°F), pulse of 132/min, respiratory rate of 27/min, blood pressure of 163/91 mm Hg, and an oxygen saturation of 92% on 3-L/min oxygen by nasal cannula. He was tachypneic and seemed in moderate respiratory distress with bibasilar lung crackles, prolonged expiratory breath sounds, and occasional generalized wheezing. The rest of the physical examination was unremarkable. Electrocardiogram showed sinus tachycardia. Influenza A/B/H1N1 polymerase chain reaction was negative. Complete blood cell count showed a white blood cell count of 10,600/mm3 (reference, 4000–11000/mm3) with 9000/mm3 neutrophils (reference, 2000–8000/mm3). Arterial blood gas showed a pH of 7.42, Pco2 of 31 mm Hg, and Po2 of 65 mm Hg on 3-L/min oxygen. The rest of the electrolytes were unremarkable. Chest radiograph showed severe emphysematous changes with bilateral basal patchy airspace disease/consolidation. He was empirically started on ceftriaxone and azithromycin for suspected pneumonia and was given intravenous methylprednisolone and albuterol nebulizers for presumptive exacerbation of COPD and was admitted to the hospital. The following day (after 24 hours), his blood cultures turned positive in aerobic bottle for gram-negative coccobacilli (BacT/ALERT System; BioMérieux, Marcy-l'Etoile, France), so he was switched to piperacillin-tazobactam. Nonlactose fermenting growth was seen on MacConkey agar, and whitish colonies of gram-negative coccobacillus were seen on blood and chocolate agars. Next day, bacterium was identified to be A. radioresistens using Vitek 2 automatic bacterial identification system (BioMérieux, Marcy-l'Etoile, France). Because the patient had no known predisposing risk factors for Acinetobacter infections such as open wound, trauma, indwelling line, or multiple recent hospitalizations, testing for human immunodeficiency virus was performed, which came back negative. His HCV viral RNA load was 1.8 million IU/mL (reference, <15), HCV genotype was 3a, and anti-HCV antibody was reactive. On further questioning, the patient revealed that he had been digging dirt a week before presenting to the emergency room, which resulted in few minor scratches/excoriations on his skin. Acinetobacter radioresistens was sensitive to piperacillin/tazobactam, ampicillin/sulbactam, cefepime, ciprofloxacin, levofloxacin, trimethoprim-sulfamethoxazole, imipenem, gentamycin, and tobramycin. The patient was treated with intravenous ampicillin-sulbactam for 14 days. He was also prescribed an oral tapering course of prednisone for his COPD as well. The patient finished a total 14-day course of antibiotics without any difficulty, and his shortness of breath improved significantly. DISCUSSION Acinetobacter radioresistens is a non–spore forming, aerobic gram-negative coccobacillus. Biochemically, it does not ferment lactose and is catalase positive and oxidase negative. Acinetobacter is ubiquitous in soil and water. It has also been found in stool and river water and on vegetables, pillows, and head lice. Its ability to withstand extreme desiccation and radiation exposure (hence the name radioresistens) helps it survive in extreme weather conditions and cause nosocomial infections.1 Acinetobacter radioresistens has previously been shown to cause septicemia in an immunocompromised individual where origin of septicemia was thought to be middle ear/sinus infection.2 Outside the United States, there has been a reported case, similar to ours, where this bacterium caused pneumonia in a patient with COPD.3 There have been reports of nosocomial outbreak of A. radioresistens from hospital pneumatic tube systems as well. Treatment of A. radioresistens infection is with antibiotics, and although the bacterium was pan-sensitive in our case, antibiotic susceptibilities are variable, and there is evidence of carbapenem, fluoroquinolone, and tetracycline resistance in the medical literature.4 Thus, treatment should be guided by local antibiotic susceptibility reports. Duration of treatment may be longer than 2 weeks and depends on patient's clinical response. CONCLUSIONS Acinetobacter radioresistens is a rare but important cause of community-acquired infection (septicemia in our case). This case adds to the growing scientific body of evidence that A. radioresistens, a rare gram-negative coccobacillus, is a true clinical pathogen. Rajanshu Verma, MD, FACP Department of Hospital Medicine Augusta Health Fishersville, VA [email protected]Allison L. Baroco, MD Department of Infectious Diseases Augusta Health Fishersville, VA

Segmental Colitis Associated with Diverticular Disease (SCAD): A Case Report

Segmental colitis associated with diverticular disease (SCAD) is a rare form of diverticular disease due to its autonomy and similarity to inflammatory bowel diseases (IBD). The prevalence of SCAD in patients with diverticulosis ranges from 0.26 to 1.5 %. Here we report the case of a 59 year old female who presented with recurrent and refractory abdominal pain. A 59 year old female presented to the ER with left lower quadrant abdominal pain, loose stools and weight loss for the past 1 year. Stools were watery and mixed with blood. Physical Exam revealed tenderness in the left lower quadrant with no guarding or rebound tenderness. Laboratory examination showed lymphocytosis and CT scan revealed thickened sigmoid colon with few adjacent diverticula. Colonoscopy was performed and it showed few diverticula surrounded by inflammatory changes with erythema, patchy mucosal friability and areas of exudate limited to the sigmoid colon. However, patient reported worsening of abdominal pain and few weeks later a repeat CT scan revealed worsening colonic wall thickening with extensive peri-colonic mesentery stranding/fluid and multiple peri-colonic mesentery lymphadenopathies. She responded to intra venous fluids, ciprofloxacin and flagyl and was discharged on oral antibiotics. She was instructed to follow a high fiber diet, however, her pain and bloody diarrhea recurred within a few weeks of being discharged. She was prescribed 5-ASA 375 mg 4 times a day and a tapering course of prednisone 40mg for one month. On the following visit the patient reported resolution of all her symptoms. The histologically features of SCAD are often indistinguishable from other IBDs on morphologic grounds alone. The correct diagnosis is of great importance, because many patients will respond to therapy aimed at diverticular disease or diverticulitis and do not require immunosuppression. Patient who are refractory to antibiotic therapy should start treatment with immunosuppressive drugs and if symptoms persist they will need a partial surgical colectomy to help relieve the symptoms.

Macrophage Activation Syndrome Associated with Adult-Onset Still's Disease Successfully Treated with Anakinra.

Macrophage activation syndrome (MAS) is a potentially fatal complication of Adult-Onset Still's disease (Still's disease). Whereas an increasing body of evidence supports interleukin-1 (IL-1) blockade as a promising treatment for Still's disease, whether it is therapeutic for MAS associated with Still's disease remains unclear. We report a 34-year-old Caucasian man with one-decade history of TNF-blockade-responsive seronegative arthritis who presented with abrupt onset of fever, serositis, bicytopenia, splenomegaly, hepatitis, and disseminated intravascular coagulation. Striking hyperferritinemia was noted without evidence of infection, malignancy, or hemophagocytosis on bone marrow biopsy. NK cells were undetectable in the peripheral blood, whereas soluble IL-2 receptor was elevated. His multiorgan disease resolved in association with methylprednisolone pulse therapy, Anakinra, and a tapering course of prednisone. This case reinforces the notion that Still's disease is inherently poised to manifest MAS as one of the clinical phenotypes by shedding light on the role of IL-1 underlying both Still's disease and related MAS.

A 36-year-old woman with recurrent high-grade fevers, hypotension, and hypertriglyceridemia

History of the present illness The patient had been admitted 6 months earlier to an outside hospital with a high-grade fever, an erythematous rash on her lower extremities, and pain in her legs. She had a history of bipolar disorder and schizoaffective disorder, and had been treated with the antipsychotic medications ziprasidone and quetiapine fumarate. An initial evaluation for infections was negative, and broadspectrum antibiotics failed to relieve the fever. The patient’s fevers were attributed to the neuroleptic malignant syndrome (Table 1). Her fevers continued unabated to temperatures as high as 103°F, despite discontinuation of her antipsychotic medications and treatment with bromocriptine. She was transferred to another hospital for further evaluation and management. At the transfer hospital, the patient exhibited a transient increase in her creatine kinase level to 1,389 units/liter (normal value 240). Assays for antinuclear antibodies, antibodies to double-stranded DNA, and extractable nuclear antigens (Ro, La, Sm, and RNP) were negative, as were anti–Jo-1 antibodies. A magnetic resonance image of the lower leg showed muscle edema with localized infarction. A muscle biopsy showed perivascular inflammatory infiltrates consistent with an inflammatory myopathy. Prednisone 60 mg/day was started and azathioprine was considered, but the patient’s localized rash and leg pain resolved spontaneously before treatment with azathioprine was started. The patient was prescribed a tapering course of prednisone for presumed dermatomyositis, and did not experience recurrent episodes of fever, rash, or leg pain while receiving glucocorticoids (Table 1). No photographic record of the patient’s original rash exists. Within one week of discharge, the patient developed recurrent fevers and was readmitted to a third hospital. Her dose of prednisone at that time was unknown. She was later found to have a urinary tract infection caused by Escherichia coli and was treated with trimethoprim/sulfamethoxazole. Despite antibiotic treatment, the patient continued to have intermittent high-grade fevers and episodes of hypotension, with blood pressure as low as 70/40 mm Hg (Table 1). She was transferred to a fourth hospital. Upon transfer, the patient had a temperature of 104°F, sinus tachycardia (140–160 beats/minute), hypotension, and a hematocrit of 20%. There was no rash despite the development of intermittent high-grade fever. Multiple cultures were negative for infection. The patient underwent a bone marrow biopsy that showed a hypercellular marrow, and a peripheral smear showed some dysplastic myeloid forms and blasts. These were interpreted as being consistent with reactive changes associated with anemia of chronic disease. A second muscle biopsy finding showed mild perivascular inflammatory infiltrates in the endomysium, consistent with an inflammatory myopathy. However, further analysis by electron microscopy and immunohistochemical staining demonstrated no definitive evidence of such a condition. Antibodies against the membrane attack complex of complement, the major histocompatibility complex, CD20, CD3, laminin , Brown-Brenn stain, and NADH reductase were negative. The final interpretation of the muscle biopsy finding was nonspecific and possibly the result of trauma or ischemia at needle entry sites. The patient continued receiving prednisone without a Richard C. Chou, MD, PhD (current address: DartmouthHitchcock Medical Center, Lebanon, New Hampshire), Judith A. Ferry, MD: Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Charles A. Dinarello, MD: University of Colorado School of Medicine in Denver, Aurora; Paola Dal Cin, PhD: Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts. Address correspondence to Richard C. Chou, MD, PhD, Section of Rheumatology, Department of Medicine, Dartmouth-Hitchcock Medical Center, 1 Medical Center Drive, Lebanon, NH 03756. E-mail: Richard.C.Chou@hitchcock. org. Submitted for publication January 29, 2009; accepted in revised form September 14, 2009. Arthritis Care & Research Vol. 62, No. 1, January 15, 2010, pp 128–136 DOI 10.1002/acr.20024 © 2010, American College of Rheumatology

Lymphoma‐Associated Polymyositis in Dogs

Lymphoma‐Associated Polymyositis in Dogs

Oral Steroids in Initial Treatment of Acute Sciatica

Many physicians use prednisone to treat acute sciatica with the hope of speeding recovery. There is little clinical evidence to support this practice. Our objective was to determine whether early administration of oral prednisone affects parameters related to recovery from acute sciatica. In this double-blind, controlled clinical trial, 27 patients were sequentially assigned to receive either a 9-day tapering course of prednisone (n = 13) or placebo (n = 14) within 1 week of developing sciatic symptoms. Patients and investigators were blinded to the drug administered. Follow-up assessment was done weekly for 1 month and then monthly for 5 months. Prednisone and control groups showed no statistically significant differences in physical findings, use of nonsteroidal anti-inflammatory drugs or narcotic medications, or rates of patients returning to work at any time interval studied. Compared with controls, patients who received prednisone had more rapid rates of improvement from baseline in pain, mental well-being, and disability scores. These changes were subtle but statistically significant. Patients who received prednisone tended to receive fewer epidural injections for pain. Early administration of oral steroid medication in patients with acute sciatica had no significant effect on most parameters studied. It did, however, lead to slightly more rapid rates of improvement in pain, mental well-being, and disability scores. The impact of oral steroids on other outcomes is suggested by this study, but its small sample size limited its statistical power.

Dicloxacillin-Induced Mixed Cholestatic Liver Injury

Purpose: Background: Dicloxacillin (Diclox) is semi-synthetic penicillin (PCN) used for treatment of a variety staphylococcal infections. It is the predominant beta-lactam PCN prescribed in the U.S. Severe liver reactions associated with its use are very rare. Case: A previously healthy 74 year-old white male presented with a 2 week history of jaundice, severe pruritus, dark urine, nausea and anorexia. He received a 10 day course of diclox 250 mg po qid for cellulitis of his right arm one month prior to this presentation. Pretreatment LFT's had been normal. Atorvastatin, which he had taken for three years was discontinued at the onset of his jaundice. He was non-smoker and drank alcohol rarely. His physical exam was remarkable only for scleral icterus and jaundice. An ultrasound of the abdomen was normal. Serological evaluation was negative for viral, autoimmune, chronic cholestatic, and hereditary liver diseases. He was started on ursodiol 300 mg po tid and also received a short tapering course of prednisone. A marked clinical improvement paralleled a decrease in liver enzymes over the course of next several weeks. Discussion: The clinical picture of a mixed cholestatic-hepatocellular injury pattern, significant eosinophilia, and a negative evaluation for other potential causes of liver injury was felt to be most consistent with a diclox-induced drug reaction, likely due to hypersensitivity. The long prior use of atorvastatin with normal LFTs just prior to diclox excluded statin induced hepatopathy. Given the improvement in LFTs and clinical improvement on ursodiol therapy, no liver biopsy was performed. Diclox induced liver injury is rare with an estimated frequency of adverse hepatic events of 1.8 reactions per million daily doses. An immunoallergic reaction mediated through formation of drug modified hepatic protein adducts is the likely mechanism. Older age and a prolonged course of therapy are important risk factors. Mixed cholestatic injury can occur up to several weeks after taking diclox, similar to that seen with amoxicillin-clavulante. Jaundice and pruritus typically are severe and protracted. Conclusion: Bile duct loss has been reported and liver tests may remain abnormal for months after resolution of clinical symptoms, although ursodiol therapy may shorten the course.Table

A Prospective, Controlled Longitudinal Study of the Effects of Oral Corticosteroid Therapy on Bone Mineral Density in Patients with IBD

Purpose: There is very limited data regarding the duration and dose of steroids required to produce bone loss in IBD. The objective of this study is to prospectively determine the rate and degree of bone loss in IBD patients treated with prednisone (pred), compared to a group of IBD patients matched for disease activity not treated with prednisone (non-P). Methods: Pred patients (n = 17) underwent baseline DEXA to determine baseline bone mineral density (BMD) at the lumbar spine (LS), and bilateral hips, and were compared to non-P patients (n = 15) with active disease. DEXA scans were repeated at 3 months after initiating prednisone, or alternate therapy, for non-P patients. Prednisone was started at 40–60 mg/d and tapered according to a fixed schedule based upon clinical response. All patients were treated empirically with oral calcium 1500 mg/d and vitamin D 600 u/d. Results: For pred patients compared with non-P patients, there were no differences in the gender (M:F = 11:6 vs 11:4), age (36 vs. 44), There was a lower proportion of CD patients in the pred group (3/17) than in the non-P group (12/15, p=.001). All women were premenopausal. Patients in both groups had similar baseline disease activity. Pred patients had higher t scores for both LS and hips at baseline. Values for baseline t scores, and 3 month changes in t score and% BMD are shown in the Table below. p values are for differences between the pred and non-P groups.TableThere was also a higher proportion of pred patients with a clinically significant, i.e >5%, decline in BMD at the hips, than in the non-P group (5/17 vs. 0/14, p=.04). Conclusions: In this prospective, controlled study, a < 3 month course of prednisone, led to a significantly greater decline in BMD at the hips (but not at the spine) compared to control patients at 3 months. Significant bone loss at the hips, as defined by a greater than 5% decline in BMD, can be seen as early as 3 months in these patients with active IBD being treated with a tapering course of prednisone, despite concurrent supplemental calcium and vitamin D.

The utility of positron emission tomography in the evaluation of autoimmune hearing loss.

To evaluate positron emission tomography as an imaging tool in the diagnosis, evaluation, and management of autoimmune inner ear disease. Autoimmune inner ear disease is a form of cochleovestibular disease associated with variable hearing loss and vertigo for which no reliable diagnostic tests are available. Pilot study of 10 patients with autoimmune inner ear disease and 5 sex-matched and age-matched control subjects without any history of autoimmune inner ear disease, who underwent limited positron emission tomography of the inner ear. Five patients with new or active autoimmune inner ear disease underwent serial positron emission tomography before and after 4 to 6 weeks of a high-dose tapering course of prednisone. The subjects had cranial magnetic resonance imagining, audiometric and vestibular studies, and heat-shock protein (HSP-70) measurements. Reading of the positron emission tomography scans was blinded. Positron emission tomography was normal in 4 of 5 normal control subjects and abnormal in 1 with normal audiometric and vestibular studies and positive HSP-70. Of patients with established and stable autoimmune inner ear disease, 4 of 5 had no positron emission tomography abnormalities and negative HSP-70, and the one with abnormal positron emission tomography shortly thereafter manifested clinically active disease. Of the 5 patients with active autoimmune inner ear disease monitored serially, 4 had an initial abnormal positron emission tomography in at least one ear, which became normal in all but 1 patient after therapy. HSP-70 correlated with disease activity. Only 1 patient with clinically active autoimmune inner ear disease had a normal positron emission tomography before and after therapy (the HSP-70 was positive before therapy and negative after the therapy). Positron emission tomography, especially when combined with HSP-70 determination, may be a useful technique for assessing disease in patients with autoimmune inner ear disease.

A Pilot Study of Steroid Therapy After Emergency Department Treatment of Acute Asthma: Is a Taper Needed?

The purpose of this study was to determine if there is a difference in early relapse rates between patients receiving an 8-day course of 40 mg/day prednisone and those receiving an 8-day tapering course of prednisone. Furthermore, we wished to determine if one regimen is superior to the other for minimizing adrenal suppression. This was a prospective, randomized, double blind clinical trial conducted in an urban, university-affiliated Level 1 trauma center. All asthmatic patients with exacerbation who were judged well enough for discharge home from the emergency department (ED) were eligible for participation. Patients with a history of chronic obstructive pulmonary disease, congestive heart failure, pneumonia, pneumothorax, or other pulmonary process, and asthmatics already using inhaled or oral steroids within 2 weeks of admission to the ED were excluded. Before treatment, a cosyntropin stimulation test was administered to all asthmatics admitted to the ED. All patients treated in the ED then received three doses of aerosolized albuterol, 60 mg of i.v. methylprednisolone, and oxygen. FEV1 was measured before treatment, after each treatment, and 1 h after the third aerosol administration. Patients were then sent home with either an 8-day course of 40 mg/day prednisone or an 8-day tapering course of prednisone (tapering from 40 mg to 0 mg). Patients were asked to return on day 12 for another cosyntropin stimulation test and pulmonary function testing and on day 21 for pulmonary function testing only. Fifteen patients participated: seven received a nontapering dose of prednisone and eight received a tapering dose of prednisone. There were no differences in the FEV1 percent predicted, the incidence of relapse, or the incidence of adrenal suppression between the two groups. In our small study, we found no difference in relapse rate between asthmatics receiving an 8-day tapering dose of prednisone and those receiving 40 mg/day prednisone upon discharge from the ED. Furthermore, no patients had evidence of adrenal suppression from either dosing regimen.

Prednisone Improves Renal Function and Proteinuria in Human Immunodeficiency Virus-associated Nephropathy

To determine if prednisone ameliorates the course of human immunodeficiency virus-associated nephropathy (HIV-AN). Twenty consecutive HIV-infected adults with biopsy-proven HIV-AN (n = 17) or clinical characteristics of HIV-AN (n = 3) with serum creatinine concentrations > 177 mumol/L (2 mg/dL) or proteinuria > 2.0 g/d or both were prospectively evaluated and treated with prednisone at a dose of 60 mg/d for 2 to 11 weeks, followed by a tapering course of prednisone over a 2- to 26-week period. Serum creatinine concentration, 24-hour protein excretion, serum albumin, and steroid-related adverse effects were assessed before and after treatment. Nineteen patients had serum creatinine concentrations > 117 mumol/L (2 mg/dL). Two of them progressed to end stage renal disease (ESRD) in 4 to 5 weeks. In 17 patients serum creatinine levels decreased from 717 +/- 103 mumol/L (8.1 +/- mg/dL) (mean +/- SE) to 262 +/- 31 mumol/L (3.0 +/- 0.4 mg/dL) (P < 0.001). Five patients relapsed after prednisone was discontinued and were retreated. In these 5 the serum creatinine declined from 728 +/- 107 mumol/L (8.2 +/- 1.2 mg/dL) to 344 +/- 47 mumol/L (3.9 +/- 0.5 mg/dL) (P < 0.01) in response to the second course of prednisone. Twelve of 13 tested patients showed a reduction in 24-hour urinary protein excretion with an average decrement from 9.1 +/- 1.8 g/d to 3.2 +/- 0.6 g/d (P < 0.005). Serum albumin increased from 24.4 +/- 3.6 g/L to 29.3 +/- 2.6 g/L (P = NS) in the 11 patients with paired 24-hour urine collections for whom pre- and post-treatment determinations were available. In one non-azotemic patient with nephrotic syndrome, protein excretion declined from 15.2 to 2.2 g/day and the serum albumin increased from 4.0 g/L to 31.0 g/L. The 20 patients have been followed for a median of 44 weeks (range 8 to 107). Eight ultimately required maintenance dialysis. Eleven died from complications of HIV disease 14 to 107 weeks after institution of prednisone; none was receiving prednisone at the time of death. Seven are alive and free from ESRD a median of 25 weeks (range 8 to 81) from the initiation of prednisone therapy. Six patients developed a total of seven serious infections while receiving prednisone, including Mycobacterium avium-complex infection in 2 and CMV retinitis in 3. Prednisone improves serum creatinine and proteinuria in a substantial proportion of adults with HIV-AN. Corticosteroid-related side effects are not prohibitive. A prospective, randomized controlled trial is required to confirm these preliminary results.

Nontapering versus tapering prednisone in acute exacerbations of asthma: A pilot trial

Controversy exists as to whether or not the dose of prednisone should be tapered in patients discharged from the emergency department after initial treatment for an acute exacerbation of asthma. We assessed the rates of relapse and rebound in a group of 28 patients treated with a nontapering course of prednisone and compared their outcomes to an historical control group of 48 patients treated with a typical tapering course of prednisone. We found no significant difference in the rates of relapse or rebound between the nontapering dose patients and the tapering dose patients within either 21 days of discharge or within 10 days after stopping prednisone. Fifty-four percent of study patients reported adverse effects that could be attributed to prednisone. Our preliminary findings suggest that tapering of prednisone may not be needed in these patients.

Ventilatory Management of Respiratory Failure in Asthma

CASE PRESENTATION The patient whom I wish to discuss this morning is unable to be present because she is dead. What I want to talk about is why that happened, and how it could possibly have been prevented. She was a 60-year-old nonsmoking woman who had asthma since the age of 16 years. She had been hospitalized seven times for asthma since 1980, but had never been intubated. She had been given prednisone intermittently, but never for more than 3 months at a time. There was no history of cardiac disease. Fourteen days prior to admission, she complained of dyspnea, went to the emergency department (ED), and was given nebulized albuterol, a theophylline drip, and a bolus of methylprednisolone. She was discharged on a 10-day tapering course of prednisone. She came back to the ED 2 days before admission because the dyspnea had recurred. She was given the same medications,

GRANULOMA ANNULARE AND DISSEMINATED HERPES ZOSTER

A 71-year-old man was admitted to the Wake Forest University/Baptist Hospital Medical Center on February 1, 1989, with pharyngitis and a cutaneous eruption that began that day. The past history was significant for a diagnosis of chronic lymphocytic leukemia (CLL) made in 1984, and for longstanding hypertension, severe coronary artery disease, and prostatic hypertrophy. The patient had required no therapy for his CLL until August, 1988, when he developed hemolytic anemia and was treated with oral chlorambucil, 4 mg/day, and a tapering course of prednisone. By December, 1988, the prednisone therapy had been discontinued, but the patient required hospital admission for pneumococcal pneumonia, which responded well to intravenous antibiotic therapy. One day prior to the current admission the patient complained of persistent fevers, sore throat, productive cough, and headache. He noted a new cutaneous eruption on the day of admission in February, 1989. The past history was positive for occasional herpes stomatitis. The patient did not know if he had previously been infected with varicella. Skin examination revealed multiple (greater than 20), single, and grouped vesicles in a generalized distribution involving the bilateral trunk, head, neck, arms, and legs. The heaviest involvement was on the right posterior auricular area and on the neck. A Tzanck preparation obtained from an early lesion was positive for multinucleated giant cells. Viral culture was negative at 24 hours and at 1 week. A skin biopsy of an early vesicular lesion was performed and revealed intraepidermal vesicles with acantholysis and giant cells.(ABSTRACT TRUNCATED AT 250 WORDS)