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The Efficacy of Cefmetazole Against Pyelonephritis Caused by Extended
International Journal of Infectious Diseases 17 (2013) e159–e163 Contents lists available at SciVerse ScienceDirect International Journal of Infectious Diseases jou rnal homepage: www.elsevier.com/locate/ijid The efficacy of cefmetazole against pyelonephritis caused by extended-spectrum beta-lactamase-producing Enterobacteriaceae a, b c d a,e Asako Doi *, Toshihiko Shimada , Sohei Harada , Kentaro Iwata , Toru Kamiya a Department of Infectious Diseases, Rakuwakai Otowa Hospital, Otowachinji-cho 2, Yamashina-ku, Kyoto, Japan b Department of General Internal Medicine, Nara City Hospital, Nara, Japan c Department of Microbiology and Infectious Diseases, Toho University School of Medicine, Ota-ku, Tokyo, Japan d Division of Infectious Diseases, Kobe University Hospital, Chuo-ku, Kobe, Hyogo, Japan e Department of General Internal Medicine, Rakuwakai Otowa Hospital, Otowachinji-cho 2, Yamashina-ku, Kyoto, Japan A R T I C L E I N F O S U M M A R Y Article history: Objectives: Urinary tract infections (UTIs) caused by extended-spectrum beta-lactamase (ESBL)- Received 3 April 2012 producing Enterobacteriaceae are on the increase. Although cefmetazole is stable in vitro against the Accepted 26 September 2012 hydrolyzing activity of ESBLs, no clinical study has ever evaluated its role in infections caused by these Corresponding Editor: William Cameron, organisms. We therefore evaluated the efficacy of cefmetazole compared to carbapenems against Ottawa, Canada pyelonephritis caused by ESBL-producing Enterobacteriaceae. Methods: A retrospective chart review was conducted at a tertiary care hospital from August 2008 to July Keywords: 2010. Chart reviews were done for patients with ESBL-producing organisms in urine identified in the Extended-spectrum beta-lactamase (ESBL) microbiology database. -
Severe Aplastic Anemia
Severe AlAplas tic AiAnemia Monica S. Thakar, MD Pediatric BMT Medical College of Wisconsin Outline of Talk 1. Clinical description of aplastic anemia 2. Data collection forms And a couple of quizzes in between… CLINICAL DESCRIPTIONS What is aplastic anemia? • More than just anemia – Involves low counts in 2 of 3 cell lines: red blood cells (RBC), white blood cells (WBC), pltltlatelets • Should NOT involve dysplasia – EiException: RBC can sometimes be dlidysplastic • Should have NORMAL cytogenetics • If dysplasia (beyond RBCs) or abnormal cytogenetics seen, think myelodysplastic syndrome (MDS) What is “severe” aplastic anemia? • Marrow cellularity ≤25% AND • Two of the following peripheral blood features: – Absolute neutrophil count (ANC) < 0.5 x 109/L – Platelet count <20 x 109/L – Absolute reticulocyte count < 40 x 109/L • “Very” severe aplastic anemia – Same as above except ANC <0.2 x 109/L NORMAL BttBottom Li ne: Severely Reduced HtitiHematopoietic Stem Cell Precursors SEVERE APLASTIC ANEMIA IBIn Bone M arrow Epidemiology • Half of cases seen in first 3 decades of life • Incidence: – 2 cases/m illion in WtWestern countitries – 2‐3 fold higher in Asia • Ethnic predisposition: – Asian • Genetics vs different environmental exposures? • Sex predisposition: M:F is 1:1 Pathoppyhysiology : 3 Main Mechanisms Proposed 1. Immune‐mediated – HthiHypothesis: RdRevved‐up T cells dtdestroy stem cells – Observation: Immunosuppression improves blood counts 2. Stem‐cell “depletion” or “defect” – Hypothesis: Drugs or viruses directly destroy stem cells -
December Is National Aplastic Anemia Awareness Month
December Is National Aplastic Anemia Awareness Month What Is Aplastic Anemia? Aplastic anemia is a non-cancerous disease that occurs when the bone marrow stops making enough blood cells. The body makes three types of blood cells: red blood cells, which contain hemoglobin and deliver oxygen to all parts of the body white blood cells, which help fight infection platelets, which help blood clot when you bleed These blood cells are made in the bone marrow, which is the soft, sponge-like material found inside bones. The bone marrow contains immature cells called stem cells that produce blood cells. Stem cells grow into red cells, white cells, and platelets or they can make more stem cells. In patients who have aplastic anemia, there are not enough stem cells in the bone marrow to make enough blood cells. Picture of blood cells maturing from stem cells. Experts believe that aplastic anemia is an autoimmune disorder. This means that the patient’s immune system (which helps fight infection) reacts against the bone marrow and the bone marrow is not able to make blood cells. Stem cells are no longer being replaced and the left over stem cells are not working well. Therefore, the amount of red cells, white cells, and platelets begin to drop. If blood levels drop too low, a person can feel very tired (from low red cells), have bleeding or bruising (from low platelets), and/or have many or severe infections (from low white cells). What Are the Key Statistics About Aplastic Anemia? Aplastic anemia can occur in anyone of any age, race, or gender. -
Consideration of Antibacterial Medicines As Part Of
Consideration of antibacterial medicines as part of the revisions to 2019 WHO Model List of Essential Medicines for adults (EML) and Model List of Essential Medicines for children (EMLc) Section 6.2 Antibacterials including Access, Watch and Reserve Lists of antibiotics This summary has been prepared by the Health Technologies and Pharmaceuticals (HTP) programme at the WHO Regional Office for Europe. It is intended to communicate changes to the 2019 WHO Model List of Essential Medicines for adults (EML) and Model List of Essential Medicines for children (EMLc) to national counterparts involved in the evidence-based selection of medicines for inclusion in national essential medicines lists (NEMLs), lists of medicines for inclusion in reimbursement programs, and medicine formularies for use in primary, secondary and tertiary care. This document does not replace the full report of the WHO Expert Committee on Selection and Use of Essential Medicines (see The selection and use of essential medicines: report of the WHO Expert Committee on Selection and Use of Essential Medicines, 2019 (including the 21st WHO Model List of Essential Medicines and the 7th WHO Model List of Essential Medicines for Children). Geneva: World Health Organization; 2019 (WHO Technical Report Series, No. 1021). Licence: CC BY-NC-SA 3.0 IGO: https://apps.who.int/iris/bitstream/handle/10665/330668/9789241210300-eng.pdf?ua=1) and Corrigenda (March 2020) – TRS1021 (https://www.who.int/medicines/publications/essentialmedicines/TRS1021_corrigenda_March2020. pdf?ua=1). Executive summary of the report: https://apps.who.int/iris/bitstream/handle/10665/325773/WHO- MVP-EMP-IAU-2019.05-eng.pdf?ua=1. -
WO 2010/025328 Al
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date 4 March 2010 (04.03.2010) WO 2010/025328 Al (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 31/00 (2006.01) kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, (21) International Application Number: CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, PCT/US2009/055306 DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (22) International Filing Date: HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, 28 August 2009 (28.08.2009) KR, KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, (25) Filing Language: English NO, NZ, OM, PE, PG, PH, PL, PT, RO, RS, RU, SC, SD, (26) Publication Language: English SE, SG, SK, SL, SM, ST, SV, SY, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: 61/092,497 28 August 2008 (28.08.2008) US (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (71) Applicant (for all designated States except US): FOR¬ GM, KE, LS, MW, MZ, NA, SD, SL, SZ, TZ, UG, ZM, EST LABORATORIES HOLDINGS LIMITED [IE/ ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, TJ, —]; 18 Parliament Street, Milner House, Hamilton, TM), European (AT, BE, BG, CH, CY, CZ, DE, DK, EE, Bermuda HM12 (BM). -
Aplastic Anemia Pre-HSCT Data (Form 2028)
Instructions for Aplastic Anemia Pre-HSCT Data (Form 2028) This section of the CIBMTR Forms Instruction Manual is intended to be a resource for completing the Aplastic Anemia Pre-HSCT Data Form. E-mail comments regarding the content of the CIBMTR Forms Instruction Manual to: [email protected]. Comments will be considered for future manual updates and revisions. For questions that require an immediate response, please contact your transplant center’s CIBMTR liaison. TABLE OF CONTENTS Key Fields ............................................................................................................. 2 Disease Assessment at Diagnosis ........................................................................ 2 Laboratory Studies at Diagnosis ........................................................................... 5 Transfusion Status from Diagnosis to the Start of the Preparative Regimen ........ 7 Laboratory Findings Prior to the Start of the Preparative Regimen ....................... 8 Aplastic Anemia Pre-HSCT Data Aplastic Anemia is a disease in which the bone marrow does not produce enough red blood cells, white blood cells, or platelets for the body. The disease can be idiopathic, or can be caused by environmental exposure, pharmaceutical or drug exposure, or exposure to viral hepatitis. Symptoms of aplastic anemia include, but are not limited to pallor, weakness, frequent infection, and/or easy bruising. The Aplastic Anemia Pre-HSCT Data Form is one of the Comprehensive Report Forms. This form captures aplastic -
Complete Article
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, Apr. 1991, p. 773-775 Vol. 35, No. 4 0066-4804/91/040773-03$02.00/0 Copyright © 1991, American Society for Microbiology Susceptibilities of Mycobacterium fortuitum biovar. fortuitum and the Two Subgroups of Mycobacterium chelonae to Imipenem, Cefmetazole, Cefoxitin, and Amoxicillin-Clavulanic Acid RICHARD J. WALLACE, JR.,* BARBARA A. BROWN, AND GRACE 0. ONYI Department of Microbiology, The University of Texas Health Center, Tyler, Texas 75710 Received 1 October 1990/Accepted 15 January 1991 MICs of imipenem, cefoxitin, cefmetazole, and amoxicillin-clavulanic acid were determined against 100 strains ofMycobacteriumfortuitum and 200 strains ofMycobacterium chelonae. Imipenem and cefmetazole were more active against M. fortuitum than cefoxitin was, and imipenem (which inhibited 39% of strains at 8 ,ug/ml) was the only beta-lactam active against M. chelonae subsp. chelonae. Rapidly growing mycobacteria cause a variety of infec- Laboratory of the University of Texas between 1987 and tions, the majority of which involve skin and soft tissues 1990 were tested. Identification to the species level was (22). Antimicrobial therapy based on in vitro susceptibilities performed by standard methods (14, 21), and identification combined with surgical debridement are the indicated ther- to the subspecies level was by carbohydrate utilization tests apy for patients with serious cutaneous disease (9, 20). and/or drug susceptibility patterns (14, 15). Long-term drug therapy of 3 to 6 months is usually needed One hundred isolates of M. fortuitum biovariant fortui- (20). Amikacin is the most common drug used for serious tum, 141 isolates of M. chelonae subsp. abscessus, and 59 disease, often in combination with cefoxitin (8, 9, 20). -
Cefmetazole Pop Up
Cefmetazole Antibiotic Class: Second-Generation Cephalosporin (2nd generation cephamycin) Antimicrobial Spectrum: Staphylococcus aureus (methicillin susceptible), Coagulase negative Staphylococci, Streptococcus pneumoniae (penicillin susceptible), Streptococcus spp (less activity for Gram positives compared to 1st and 2nd generation cephalosporins), Haemophilus influenzae, Moraxella catarrhalis, Neisseria meningitides, Neisseria gonorrhoeae, Enterobacteriaceae, E. coli Bacteroides spp. Mechanism of Action: Cephalosporins exert bactericidal activity by interfering with bacterial cell wall synthesis and inhibiting cross-linking of the peptidoglycan. The cephalosporins are also thought to play a role in the activation of bacterical cell autolysins which may contribute to bacterial cell lysis. Pharmacodynamics: Cephalosporins exhibit time-dependent killing (T > MIC) Pharmacokinetics: Dose of 2g: Cmax: 140 mcg/L; Protein binding: 85%; Half-life: 1-1.5 hours; Table 10 Adverse Effects: Hypersensitivity: Maculopapular rash, Urticaria, Pruritis, Anaphylaxis/angioedema, eosinophilia Hematologic: Hypoprothrombinemia, Neutropenia, Leukopenia, Thrombocytopenia GI: Diarrhea, C. difficile disease Renal: Interstitial nephritis Table 14 Dosage: IV: Powder for reconstitution: 1g, 2g Dosing in adults: 2g IV q 6-12h Dosing in pediatrics: Not Recommended Disease state based dosing: Renal failure: CrCl > 90: Standard dosing CrCl 50-90mL/min: 1-2g q12h CrCl 30-49mL/min: 1-2g q16h CrCl 10-29mL/min: 1-2g q24h CrCl < 10mL/min: 1-2g q48h Hepatic failure: No dosing -
Drug Induced Encephalopathy in Patients with Chronic Kidney Disease: a Case Series Haque WMM*A, Samad T*B, Rahim Mab, Saha Skc, Iqbal Sd
Case Series Drug Induced Encephalopathy in Patients with Chronic Kidney Disease: A Case Series Haque WMM*a, Samad T*b, Rahim MAb, Saha SKc, Iqbal Sd Abstract: Drug induced encephalopathy is an established side effect of many drugs when used in a higher dose. Though we do not encounter this side effect frequently in our day to day practice, yet with renal impairment this is not uncommon. Even with a reduced dose many of these can precipitate encephalopathy in this special group of patients. We are presenting here a series of seven such cases of drug induced encephalopathy in patients with renal impairment. Key words: Chronic kidney disease, Drug induced encephalopahty, encephalopathy. (BIRDEM Med J 2018; 8(2): 172-176 ) Introduction accumulation of the drug due to lower clearance but Altered level of consciousness in a patient of chronic also alteration of blood brain barrier permeability, kidney disease (CKD) is commonly attributed to the alteration of protein binding of drug and several other advanced stage of uremia. However there are several mechanisms can lead to the brain toxicity2. There are other causes which can alter central nervous system different classes of drugs having the potential to (CNS) functions. Electrolytes disturbances, precipitate encephalopathy in higher dose, however hypoglycemia, sepsis, liver dysfunction, thiamin in patient with compromised renal function these deficiency and last but not the least drug toxicity can drugs even in lower dose can lead to profound lead the metabolic encephalopathy in patients with encephalopathy. We had encountered seven such CKD1. In these group of patients not only the cases of drug induced encephalopathy in CKD patient from July 2015 to June 2016 in nephrology Author Information department of BIRDEM General Hospital, Here we a. -
Rituximab: Is It Possible to Link Both Autoimmune Haemolytic Anemia and Aplastic Anemia Regarding the Etiology and Management? Mina T
icine: O ed pe M n l A a r c e c e n s e s G General Medicine: Open Access Kellani MT, Gen Med (Los Angeles) 2016, 4:3 DOI: 10.4172/2327-5146.1000e110 ISSN: 2327-5146 Editorial Open access Rituximab: Is it Possible to Link Both Autoimmune Haemolytic Anemia and Aplastic Anemia Regarding the Etiology and Management? Mina T. Kelleni* Pharmacology Department, Faculty of Medicine, Minia University, Minia, Egypt *Corresponding author: Kelleni MT, Ph, M, Pharmacology department, aculty of Medicine, Minia niversity, Minia, Egypt, Tel: 201200382422; E- mail: [email protected] Rec Date: June 28, 2016; Acc Date: June 29, 2016; Pub Date: June 30, 2016 Copyright: © 2016 Kelleni MT. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Citation: Mina Kellani T (2016) Rituximab: Is it Possible to Link Both Autoimmune Haemolytic Anemia and Aplastic Anemia Regarding the Etiology and Management? Gen Med (Los Angeles) 4: e110. Editorial References In the past few years, rituximab has been recognized as a safe and 1. Abadie K, Hege KM (2014) Severe refractory autoimmune hemolytic effective emerging treatment for autoimmune hemolytic anemia anemia with five-year complete hematologic response to third course of (AIHA) [1,2]. Rituximab was also considered as a preferred second- treatment with rituximab: a case report. Journal of medical case reports 8: line therapy of warm antibody hemolytic anemia in adults in some 175. major European centers and it was shown that second-line treatment 2. -
Cephalosporins Can Be Prescribed Safely for Penicillin-Allergic Patients ▲
JFP_0206_AE_Pichichero.Final 1/23/06 1:26 PM Page 106 APPLIED EVIDENCE New research findings that are changing clinical practice Michael E. Pichichero, MD University of Rochester Cephalosporins can be Medical Center, Rochester, NY prescribed safely for penicillin-allergic patients Practice recommendations an allergic reaction to cephalosporins, ■ The widely quoted cross-allergy risk compared with the incidence of a primary of 10% between penicillin and (and unrelated) cephalosporin allergy. cephalosporins is a myth (A). Most people produce IgG and IgM antibodies in response to exposure to ■ Cephalothin, cephalexin, cefadroxil, penicillin1 that may cross-react with and cefazolin confer an increased risk cephalosporin antigens.2 The presence of of allergic reaction among patients these antibodies does not predict allergic, with penicillin allergy (B). IgE cross-sensitivity to a cephalosporin. ■ Cefprozil, cefuroxime, cefpodoxime, Even penicillin skin testing is generally not ceftazidime, and ceftriaxone do not predictive of cephalosporin allergy.3 increase risk of an allergic reaction (B). Reliably predicting cross-reactivity ndoubtedly you have patients who A comprehensive review of the evidence say they are allergic to penicillin shows that the attributable risk of a cross- U but have difficulty recalling details reactive allergic reaction varies and is of the reactions they experienced. To be strongest when the chemical side chain of safe, we often label these patients as peni- the specific cephalosporin is similar to that cillin-allergic without further questioning of penicillin or amoxicillin. and withhold not only penicillins but Administration of cephalothin, cepha- cephalosporins due to concerns about lexin, cefadroxil, and cefazolin in penicillin- potential cross-reactivity and resultant IgE- allergic patients is associated with a mediated, type I reactions. -
AAMDSIF Aplastic Anemia Presentation
Aplastic Anemia Emma Groarke, MD, FRCPath Staff Clinician, Bone Marrow Failure Service National Heart, Lung, and Blood Institute National Institutes of Health AA MDS 18th May, 2019 Introduction . Aplastic Anemia . Immune mediated . What is it and what causes it? . Diagnosis . Treatment . Immunosuppression . Transplant . Pure Red Cell Aplasia . What is it and what causes it? . Ongoing research 2 A historical disease Aplastic Anemia . Rare blood disorder . 2-3 per million / year . Low blood counts and empty bone marrow . Peak age distributions . 10-25 years old and >60 years old 4 Causes of Aplastic Anemia . Immune system destroying bone marrow cells . “idiopathic” . 70% . Inherited abnormal genes . Telomere diseases . Fanconi anemia . Bone marrow toxins . Rare Young, N. S. (2018). "Aplastic Anemia." N Engl J Med 379(17): 1643-1656. 5 Mechanism of Aplastic Anemia . Immune system attacks the bone marrow . Active lymphocytes (T cells) . Increase in inflammation . Cells die Young, N.S. et al. Blood.2006 6 Aplastic Anemia Young, N. S. (2018). "Aplastic Anemia." N Engl J Med 379(17): 1643-1656. Marrow is “empty” Courtesy of Dr. Stanley Schreier, American Society of Hematology Image Bank 8 How does it affect the patient? . Neutropenia (low white cells) . Risk of infection - If less than 500 – risk of infection - If less than 200 – high risk of infection . Thrombocytopenia (low platelets) . Risk of bleeding - Risk of bleeding with trauma / procedures if <50 - Some risk bleeding <20 - Higher risk bleeding <10 – Platelet transfusion . Anemia (low red cells or hemoglobin) . Red cells carry oxygen in the blood - Symptoms include: - Tiredness - Shortness of breath . If hemoglobin <7 or symptoms - blood transfusion 9 Clonal evolution .