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Concise Book of

Medical Laboratory Technology

Methods and Interpretations

Concise Book of

Medical Laboratory Technology

Methods and Interpretations

Ramnik Sood MD (Path, Gold Medalist)

Consultant

Reem Medical and Diagnostic Center

Healthcare Mena Limited

Sharjah

United Arab Emirates

2nd Edition

New Delhi | London | Philadelphia | Panama

The Health Sciences Publisher

Headquarters

Jaypee Brothers Medical Publishers (P) Ltd

4838/24, Ansari Road, Daryaganj

New Delhi 110 002, India

Phone: +91-11-43574357

Fax: +91-11-43574314

Email: jaypee@jaypeebrothers.com

Overseas Offices

J.P. Medical Ltd Jaypee-Highlights Medical Publishers Inc

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Fax: +44 (0)20 3008 6180 Fax: +1 507-301-0499

Email: info@jpmedpub.com Email: cservice@jphmedical.com

Jaypee Medical Inc Jaypee Brothers Medical Publishers (P) Ltd

The Bourse 17/1-B Babar Road, Block-B, Shaymali

111 South Independence Mall East Mohammadpur, Dhaka-1207

Suite 835, Philadelphia, PA 19106, USA Bangladesh

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Phone: +977-9741283608

Email: kathmandu@jaypeebrothers.com

Website: www.jaypeebrothers.com

Website: www.jaypeedigital.com

© 2015, Ramnik Sood

The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent

those of editor(s) of the book.

All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic,

mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers.

All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their

respective owners. The publisher is not associated with any product or vendor mentioned in this book.

Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the

subject matter in question. However, readers are advised to check the most current information available on procedures included and

check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and

duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety

precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property

arising from or relate♥d to use of material in this book.

This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or

services are required, the services of a competent medical professional should be sought.

Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any

have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity.

Inquiries for bulk sales may be solicited at: jaypee@jaypeebrothers.com

Concise Book of Medical Laboratory Technology: Methods and Interpretations

First Edition: 2009

Second Edition: 2015

ISBN 978-93-5152-333-8

Printed at

Jaypee Brothers Medical Publishers (P) Ltd

Dedicated to

the Readers

Preface to the Second Edition

I authored an exhaustive book entitled “Medical Laboratory Technology – Methods and Interpretations” that hit the stands

in mid-eighties in the previous century and is now running in its 6th edition. This was the first such book in the subcontinent and was much appreciated and used by technologists and pathologists alike. The book has seen testimonies in courts

and has been appreciated in the west too. However, in our subcontinent, I was requested by many technologists that they

wanted a little younger sister of the book popularly known as MLT authored by me.

And so was born the Concise Book of Medical Laboratory Technology: Methods and Interpretations. The book essentially

covers everything presented in MLT-6 but in an abridged/shortened and easy-to-digest format. The book is presented in

a flowing noninterrupted format and not in a cumbersome experiment-wise cascading flow. There is no break in the style

that runs smoothly and is easier to absorb and assimilate. As experiments are a part of any course, more stress has been

laid out in the book to understand the intricacies of relevant theories and even troubleshooting all experiments that you

would conduct during the course of your study. As I have written multiple modules for many Universities in India, I did not

have to think for too long to devise a style and format for this book. You will find everything from ESR to PCR and you will

find foam test for bile pigments as also complete automation in urinalysis. You will find basic biochemistry as also detailed

cytogenetics. So whatever be your course or query, you will find it within the covers of this short but sweet book now going

into its second edition.

The book is designed for you not to mug but to understand and elicit the answers from the book of all questions in your

mind. I am aware that this book is used by most of your teachers and tutors too.

Nothing wrong that you are holding now. It will help you all your life!

Ramnik Sood

The first book on Medical Laboratory Technology from the house of Jaypee’s came out in 1985 and has been the best seller

in its class till date. The title “Medical Laboratory Technology – Methods and Interpretations” has seen 6 editions. The latest

one hit the stands in January this year and was released in two volumes. It is a four-color book and has over 1670 pages. The

reader base of all editions of our vastly popular title “MLT” has been upcoming laboratorians, undergraduate and postgraduate

medical students. It was requested by a few institutes to produce a little smaller version of the two-volume set that would

be suitable for the upcoming Laboratory Technology students. So here it is! It is exhaustive yet precise and concise too.

The book will help you to appreciate things as they appear in real life under the microscope and otherwise. All current

technologies find a mention within the covers of this book. Gone are the days when we had to prepare reagents first thing

in the morning (or the days usage); therefore, the current trend of consuming ready-to-use reagents/kits is followed here

to make your job and understanding simpler. So, what is available in the market for all investigations, is what is presented

here. The Tulip Group has very kindly given us the rights to reproduce the text related to all their kits and reagents in this

book. Latest instruments are not forgotten too.

Most important—

Parasitology section is presented in ample detail as it is relevant to all the developing nations.

Quality control/assurance is mentioned in appropriate details. Working is not enough. Working properly and producing

nothing but the most accurate reports are the order of the day. This book will not fail you there. Follow the recommendations to the hilt and you would be running the most accurate laboratory available anywhere.

Should problems arise! The book has “Troubleshooting” section for every possible test mentioned inside. If this happens – then what! If that happens – then what! You will find all answers.

From ESR to PCR – you will find everything.

The book is based on most syllabi as applicable to most institutes in India and elsewhere internationally.

All necessary care has been taken to weed out any discrepancies/typographical errors at the time of going to press.

However, if anything has remained inadvertently, the publishers/author do not take any responsibility for the same in any

manner whatsoever.

Learning can be enjoyable experience, flip a few pages to experience that.

Ramnik Sood

Preface to the First Edition

Chapter 1. Laboratory 1

Laboratory Set-up 3

Code of Conduct for Medical Laboratory

Personnel 6

Accidents 6

Accidents in the Laboratory 10

Universal Work Precautions (Uwp) for

Laboratory Personnel (Especially in

Relation to Hiv Transmission) 15

Medicolegal Aspects of Clinical Practice 17

Laboratory Instruments 17

Chapter 2. Sterilization 29

Methods Commonly Used for Sterilization 29

Modern Day Disinfection 34

Chapter 3. SI Units 41

Liter 41

Gram 41

Mole (Mol) 41

International Unit (U) 42

Conversion Factors Between Conventional

and System International Units (Siu) 42

Chapter 4. Fundamental Chemistry 52

Indicators 52

Solutes, Solvents and Solutions 52

Periodic Table of Elements 54

Chapter 5. Urine Analysis 56

Composition of Urine 56

Gross Examination of Urine 57

Chemical Examination of Urine 60

Multiple Reagent Strips for Urinalysis 71

Automation in Urinalysis 78

Special Urine Tests 82

Microscopy of the Urinary Sediment 92

Chapter 6. Renal Function and its

Evaluation 104

Renal Physiology in Brief 104

Functions of the Kidney 104

Concentration: Dilution Tests 105

Phenol Red Test 105

Clearance Tests 106

Principles of Precise Tests of Renal

Function 107

Maximal Tubular Capacity (Tm) 108

Contents

Chapter 7. Stool Examination 112

Specimen Collection 112

Inspection of Feces 113

Chapter 8. Medical Parasitology 124

Medical Parasites 124

Intestinal Protozoa of Man 124

Laboratory Examination for

Parasites 201

Chapter 9. Clinical Hematology 205

Ways of Obtaining Blood 205

Anticoagulants 206

Blood Collection System 208

Hemoglobin 210

Anemia 211

Hematocrit/Packed Cell Volume (Pcv) 212

Blood Cell Counts 213

Erythrocyte Indices 216

Complete Blood Count (Cbc) 217

Erythrocyte Sedimentation Rate (Esr) 220

Blood Film Examination 222

Rapid Diagnostics 225

Development of Blood Cells and

Sites of Blood Formation 227

Morphological Types of Red Blood Cells 234

Qualitative Assessment of G6pd

Deficiency 240

Examination of Fetal Hemoglobin 244

Laboratory Diagnosis of Disorders Related to

Rbcs 248

Thalassemias (Reduced Synthesis Rate) 256

Normal White Cell Values and Physiological

Variations 259

White Blood Cells 263

Quality Control in Hematology 270

Chapter 10. Clinical Hematology:

Bleeding Disorders 272

Platelets, Coagulation and Bleeding Disorders:

Laboratory Investigations 272

Laboratory Diagnosis of Platelet Disorders 272

Quality Assurance for Routine Hemostasis

Laboratory 278

Buffered 3.2% Citrate Solution (Profact) 280

Prothrombin Time (Quick One-Stage Method)

Liquiplastin® 283

Sensitive Thromboplastin Reagent for

Prothrombin Time (Pt)

Determination (Isi = 1.0) Uniplastin® 285

xii Concise Book of Medical Laboratory Technology: Methods and Interpretations

Thromboplastin Reagent for

Prothrombin Time (Pt)

Determination, Lyoplastin®

(Lyophilized Reagent, Isi = 1.0) 287

Aptt/Pttk Cephaloplastin Reagent for Partial

Thromboplastin Time (Aptt)

Determination Using Ellagic Acid as

Activator Liquicelin-E® 293

Normal and Abnormal Control Plasmas for

Coagulation Assays Plasmatrol H-I/Ii

® 296

Fibroscreen Thrombin Time Test for Qualitative

Estimation of Fibrinogen Fibroscreen® 297

Fibrinogen Estimation-Quantitative

Fibroquant, Reagent for Quantitative

Estimation of Fibrinogen 299

Fibrinolytic Activity 301

Fdps A Qualitative and Semiquantitative Latex

Slide Test for Detecting Cross

Linked Fibrin Degradation Products in

Human Plasma X-L Fdp 302

Laboratory Diagnosis of Coagulation

Disorders 304

Automation in Coagulation Analysis 305

Troubleshooting 309

Prothrombin Time 310

Dptt/Pttk 312

Fibrinogen Estimation 314

Chapter 11. Blood Banking

(Immunohematology) 317

Blood Group Antibodies 317

Anti-A, Anti-B, Anti-Ab Blood Grouping

Antisera for Slide and Tube Tests 320

Anti-A, Anti-B, Anti-Ab Monoclonal }|Blood

Grouping Antibodies for Slide and Tube

Tests 321

Anti-A1 Lectin Dolichos Biflorus

Lectin for Slide and Tube Tests 322

Anti-H Lectin Ulex Europaeus Lectin

for Slide and Tube Tests 323

Physiological Saline Solution for Serological

Applications (Sodium Chloride 0.9%

W/V) 325

Bovine Serum Albumin 22% Solution

for Serological Applications 325

Concentrated Iso-Osmotic Phosphate Buffered

Saline for Serological Applications 327

Red Cell Preserving Solution for Serological

Applications 328

Abo Grouping 329

Rh Blood Group System 331

Anti-D (Rho) Human (Igg) Polyclonal Blood

Typing Antibodies for Slide

and Modified Tube Tests 333

Anti-D (Rho) (Igm) Monoclonal Blood Typing

Antibodies for Slide and Tube Tests 335

Anti-D (Rho) (Igg) Monoclonal Blood Typing

Antibodies for Slide and Modified Tube

Tests 336

Anti-D (Rho) (Igm + Igg) Monoclonal Blood

Typing Antibodies for Slide and Tube

Tests 338

Anti-human Igg Monospecific Coomb’s

Reagent for Direct and Indirect

Antiglobulin Test 353

Anti-human Globulin Reagent for Direct and

Indirect Antiglobulin Tests 356

Preparing Coomb’s Control Cells Agtrol® 358

Low Ionic Salt Solution for Serological

Applications 359

Stabilized, Activated Papain Enzyme Solution

for Serological Applications 361

Blood Transfusion 363

Trouble Shooting 372

Chapter 12. Cerebrospinal and Other

Body Fluids 382

Cerebrospinal Fluid 382

Synovial Fluid (Sf) 388

Pleural Fluid 389

Pericardial Fluid (Pf) 391

Peritoneal Fluid 392

Amniocentesis and Amniotic Fluid

Analysis, Diagnostic 394

Chapter 13. Semen Analysis 398

Semen Analysis 398

Chapter 14. Sputum Examination 405

Sputum 405

Common Respiratory Disorders 406

Chapter 15. Pregnancy Tests 411

Bioassays 411

Immunologic Methods 412

Slide Test for Pregnancy 412

Slide Test for Pregnancy 414

Elisa Pregnancy Test 416

Dipstick Ict Pregnancy Test 416

Device Ict Pregnancy Test 417

Dipstick Ict, Urine/Serum

Pregnancy Test 418

Device Ict Urine/Serum

Pregnancy Test 419

Troubleshooting 421

Rapid Formats 423

Chapter 16. Examination of

Gastrointestinal Contents 425

Normal Saliva—Constituents 425

Gastric Juice 425

Examination of Duodenal Contents 430

Composition of Bile 430

Pancreatic Function Tests 430

Sweat Electrolytes Pilocarpine

Iontophoresis 432

Contents xiii

Chapter 17. Diabetes Mellitus:

Laboratory Diagnosis 434

Diabetes Mellitus 434

Glycosylated Hemoglobin Kit (Ion Exchange

Resin Method) for the Quantitative

Determination of Glycohemoglobin in

Blood (for in Vitro Diagnostic use Only) 443

Rapid Diagnostics 448

Chapter 18. Liver Function Tests 454

Tests of Excretion by the Liver 454

Evaluation of Synthesis in Liver 457

Evaluation of Enzyme Activity 458

Suggested Liver Function Tests 458

Chapter 19. Clinical Chemistry 461

Colorimetry 461

Photometer 462

Clinical Chemistry 465

Total Proteins 478

Serum Albumin 479

Serum Cholesterol 481

Hdl Cholesterol 484

Blood Glucose 490

Uric Acid 492

Calcium 493

Phosphorus 497

Chloride 500

Serum Iron and Tibc 501

Trace Elements 503

Zinc 503

Zinc (Colorimetric Method) 503

Copper 504

Magnesium 506

Automation in Clinical Chemistry 508

Principles of Quality Assurance and

Standards for Clinical Chemistry 514

Chapter 20. Enzymology 519

Alpha-amylase 519

Lipase 520

Phosphatases 522

Transaminases 530

Gamma-glutamyl Transpeptidase (Ggtp)

Blood 536

Lactic Dehydrogenase 538

Automation in Clinical Chemistry: Random

Access Autoanalyzer 546

Chapter 21. Blood Gases and

Electrolytes 548

Blood Gases 548

Automation in Blood Gas Analysis 556

Avl Compact 2 Blood Gas Analyzer 557

Electrolyte Analysis by Flamephotometer 558

Rapid Diagnostics in Electrolyte Analysis 561

Chapter 22. Serology/Immunology 563

Basic Immunology 563

Technologies 568

Enzyme Immunoassay 572

Chemiluminescence: The Technology 585

Polymerase Chain Reaction 587

Ria 590

Liquid Handling Systems 591

Streptavidin-Biotin Systems 594

Representative Elisa/Clia Techniques 595

Examples of Detailed Elisa

Methods 597

Tests for Syphilis 608

Modified Vdrl Reagent Trepolipin® 610

Toluidine Red Unheated Serum Test for Rapid

Serodiagnosis of Syphilis Redgen® 613

Latex Slide Test for Vdrl Syphfinal 615

Rapid Plasma Reagin (Rpr) Card Test/Carbon

Antigen for Syphilis Testing (Carbogen) 618

One-step Test for Syphilis: Dipstick

Syphicheck® 621

One-step Test for Syphilis (Device)

Syphicheck 622

Third Generation Double Antigen Sandwich

Enzyme-linked Immunosorbent Assay

(Elisa) for the Detection of Antibodies to

Treponema Pallidum in Human

Serum or Plasma Trepolisa 3.0 624

Tests for Typhoid/Enteric Fever Widal

Antigen Set/Antigens for Tube Tests

(Typhochek) 624

Widal Antigen Set/Antigens for Slide

and Tube Tests (Tydal)® 627

Reduced Widal Antigen Set: O and H

for Tube Tests (Vital Widal) 630

Positive Control for Widal Test 631

Rapid Test for Detection Igm Antibodies to

S. typhi in Serum/Plasma/Whole Blood

(Device) Enterocheck – Wb 632

Slide and Tube Test for Detection of Antibodies

to Brucella Abortus/Melitensis Brucel

A/M 635

Slide Screening Test for Brucella Antibodies

(Brucel-Rb)

® 636

Brucellosis Positive Control 638

Rapid Test for Igm and Igg Antibodies

to Dengue Virus: Dengue Fever

(Denguecheck-Wb) (Device) 639

Test for Infectious Mononucleosis

(Immutex) 643

Rapid Test for Igm Antibodies to Leptospira:

Leptospirosis (Leptochek-Wb) (Device) 645

Rapid Test for Malaria Pan/Pv/Pf

(Paramax-3®) (Device) 647

Slide Test for C-reactive Protein (Rhelax

Crp) 650

Slide Test for Antistreptolysin O (Rhelax

Aso®) 653

Slide Test for Rheumatoid Factors

(Rhelax Rf) 656

Slide Test for Anti-deoxyribonucleoprotein

(Rhelax Sle) 659

xiv Concise Book of Medical Laboratory Technology: Methods and Interpretations Australia Antigen Hbsag (Virutex Hbsag) 662

One-Step Test for Hbsag Virucheck Device 664

Hcv Flavicheck Device 665

Toxoplasma Infections 668

Rapid Immunoconcentration

Test for Hiv-1 and Hiv-2

Antibodies Flow through

Method Retroquick-Hiv 669

Rapid Test for Simultaneous/Differential

Detection of total Antibodies to Hiv1 and Hiv-2 in Human Serum/Plasma

Retroscreen 671

Tuberculosis 673

Rapid Test for Detection of Antibodies

to Mycobacterium tuberculosis

(Device) Serocheck-Mtb 676

Tb Igg, Iga, Igm Ab, Mfd Anda 678

Tumor Markers 679

Tumor Markers Standard Methodologies Available on Elisa and Clia, as on Ria too 683

Ca 15-3 (Carcinogenic Antigen 15-3) 683

Ca 19-9 (Carbohydrate Ag 19-9, Gicam

Gastrointestinal Cancer Antigen)

Blood Mfd: Can Ag, 683

Ca 242 Mfd: Can Ag, 684

Ca 125 (Cancer Antigen 125) Mfd:

Monobind 684

Carcinoembryonic Antigen (Cea) Mfd:

Monobind 685

Prostate-specific Antigen (Psa) Total

Prostate Specific Antigen (Tpsa) Elisa,

Mfd: Monobind 685

Prostatic Acid Phosphates (Pap), Blood

Method: Biochemical Analysis 686

Elisa Troubleshooting Aspects 686

Technical Tips 690

Chapter 23. Diagnostic Immunology 693

Qualitative Determination of Plasma Proteins

by Immunoprecipitation 693

Fundamental Quantitative Considerations 698

Turbidimetry 699

An Example of Turbidimetric

Immunoassay 718

C-reactive Protein 720

Turbidimetric Immunoassay for Determination

of C-reactive Protein 722

Turbidimetric Immunoassay for Ultrasensitive

Determination of C-Reactive Protein 723

Turbidimetric Immunoassay for Determination

of Antistreptolysin ‘O’ in Human Serum 724

Turbidimetric Immunoassay for Determination

of Microalbuminuria 724

Immunoglobulins (Ig) 724

Turbidimetric Immunoassay for Estimation of

Immunoglobulin

Iga in Human Serum 725

Turbidimetric Immunoassay for Estimation of

Immunoglobulin Igg in Human Serum 726

Turbidimetric Immunoassay for Estimation of

Immunoglobulin Igm in Human Serum 726

Turbidimetric Immunoassay for Estimation of

Complement C3 in Human Serum 726

Turbidimetric Immunoassay for Estimation of

Complement C4 in Human Serum 727

Turbidimetric Immunoassay for Estimation of

Antithrombin Iii in Human Serum 727

Quantitative Immunoturbidimetric

Assay for Estimation of Fibrinogen 727

Turbidimetric Immunoassay for Estimation of

Lipoprotein (A) in Human Serum 727

Quantitative Turbidimetric

Immunoassay for Estimation of

Apolipoprotein A-I 728

Quantitative Turbidimetric

Immunoassay for Estimation

of Apolipoprotein B 728

Automation in Turbidimetry 729

Chapter 24. The Endocrine System 731

Pituitary Gland 731

Anterior Lobe: Growth Hormone (Gh) 732

Method of Evaluation: StreptavidinBiotin Elisa 733

Corticotropin (Acth) 735

Other Anterior Pituitary Hormones 735

Intermediate Lobe (Pars Intermedia) 736

Posterior Pituitary (Neurohypophysis) 736

Disorders of the Pituitary System 738

Hypothalamus 738

Adrenal (Suprarenal) Gland 738

Mineralocorticoids 738

Glucocorticoids 739

Adrenal Medulla 742

Thyroid 742

Calcitonin 753

Parathyroid 754

Parathyroid Hormone (Intact) Elisa 756

Pancreas 757

Testes 758

Ovary 758

Pineal Gland 759

Hormones and Fertility 759

Male Fertility 760

Female Fertility 763

Algorithm for Evaluating Amenorrhea,

Immunoassays for Lh, Fsh and Prl 768

Adrenal Cortex 775

Adrenal Medulla 777

Testes 779

Steroids 781

17-Β-Estradiol 781

Dheas (Dehydroepiandrosterone Sulfate) 782

∆4-Androstenedione 782

Progesterone 782

17-Alpha-hydroxyprogesterone 783

Total Tri-iodothyronine (T3) 783

Cia™ Insulin (Chemiluminescence

Immunoassay) 788

Contents xv

Chapter 25. Histopathology 791

Preparation of Tissues 791

Routine Staining Procedures 794

Some Staining Techniques in Detail 799

Automation in Histopathology 805

Chapter 26. Cytology 808

Papanicolaou Method of Staining

Smears (Modified) 808

Fnac (Fine-Needle Aspiration Cytology) 809

Smearing Techniques 812

Requirements for Laboratory Set Up 812

Immunoperoxidase Staining for

Cyto and Histopathology 817

Automation in Cytology 818

Chapter 27. Microbiology and

Bacteriology 819

Classification 819

Culture 825

Ready to Pour, Sterilized Pouched Media

for Microbiological Applications

Instaprep 828

Easybact 833

General Instructions for Microbiology 837

Gram-positive Cocci 837

Gram-negative Cocci 839

Anaerobic Spore Bearing Bacilli 840

Aerobic Spore Forming Bacilli 842

Gram-positive Bacilli 842

Mycobacteria 843

Overview of M. tuberculosis: Diagnostic

Approach, Afb Staining, Culture

and Sensitivity 845

Mucolytic, Disinfectant, Specimen

Pretreatment and Buffering System

for Afb Staining and Culture 848

Rapid Two Step Cold Afb Stain 851

Ready to use Lj Solid Medium for

Mycobacterium tuberculosis Isolation 855

Combipack of Solid and Liquid Medium for

Mycobacterium tuberculosis Isolation 857

Primary/Secondary Drug Containing

Lowenstein-Jensen Media Panel Mtb

Sensitivity Tests 861

In Determination of Adenosine Deaminase

Activity in Serum, Plasma and Biological

Fluids 863

Gram-negative Bacilli 865

Spirochetes 871

Gram Stainer 872

Quality Assurance in Bacteriology 872

Color Atlas—Media and Colonies 873

Chapter 28. Mycology 883

Intermediate Superficial Deep Mycoses 884

Deep or Systemic Mycoses 884

Fungi Usually Present as Contaminants but

Which Rarely Cause Disease—Usually in

Patients Chronically Ill from Other

Diseases 885

Mycological Methods 885

Chapter 29. Diagnostic Skin Test 886

Technique of Skin Tests 886

Immunologic Basic for Skin Tests 886

Common Skin Tests 887

Immediate Reaction Type of Skin Tests 887

Delayed Reaction Type of Skin Tests 889

Chapter 30. Cytogenetics 891

Blood Lymphocyte Culture 891

Karyotyping 893

G and Q Bandings 894

Importance of Chromosomal Studies 894

Barr Body Analysis and Buccal Smear for

Staining of Sex Chromatin Mass 895

Chapter 31. World’s Latest and Best

Technologies by Roche 896

Business Areas 896

Revaluating Diagnostics 896

Testing Efficiency and Medical Value 896

Effective Management of Infectious

Diseases 898

Cobas® Modular Platform 900

Your Benefit 900

Cobas® 8000 Modular Analyzer Series 901

Cobas® 8000 Modular Analyzer Series 902

Cobas® 6000 Analyzer Series 903

Cobas® 4000 Analyzer Series 906

Cobas C 311 Analyzer 906

Cobas E 411 Analyzer 906

Cobas C 111 Analyzer 907

Cobas Integra® 400 Plus 908

Cobas P 312 Pre-analytical System 910

Cobas P 512 Pre-analytical System 910

Cobas P 612 Pre-analytical System 911

Cobas P 501 and Cobas P 701

Modular® Pre-analytics Evo 912

Cobas® Connection Modules (Ccm) 913

Cobas® 8100 Automated Workflow Series 914

Cobas® It Solutions 916

Cobas® Middleware Solution 917

Cobas® Laboratory Information System 918

Cobas® Infinity It Solutions 920

Overview of Serum Work Area Tests 921

Ecl—Unique Immunoassay Technology 925

Technology for Homogeneous

Immunoassay Detection 926

Elecsys® Hbsag Ii Quant 926

Elecsys® Hiv Combi Pt 4th Generation (Ag+Ab

Test) 927

The Syphilis Assays 929

Elecsys® Syphilis Immunoassay 929

Elecsys® Torch Panel 930

Elecsys® Troponin T High Sensitive

(Tnt Hs) 931

xvi Concise Book of Medical Laboratory Technology: Methods and Interpretations

Key Benefit: Earlier Diagnosis of Ami 932

Elecsys® Nt-proPnB 932

Elecsys® Tumor Marker Portfolio 933

Elecsys® He4 935

Elecsys® Pro-grp 936

Elecsys® Calcitonin 937

Elecsys® Anti-Tshr 938

Elecsys® Tg Ii 939

Tina-Quant® Lipoprotein (A) Gen 2 Test 940

Tina-Quant® Immunoglobulin A and M

Csf 941

Tina-Quant® Hemoglobin A1c 942

Tina-Quant® Cystatin C Gen 2 942

Elecsys® Preeclampsia 943

Elecsys® Vitamin D Total 945

Elecsys® Il-6, Pct and Tina-Quant® Crp 945

Elecsys® Tacrolimus and Cyclosporine 947

Hemostasis Testing 949

Multiplate® Analyzer 949

Urinalysis 951

Urinalysis From Roche 951

Combur-Test® Strip 951

Urisys 1100® Analyzer 952

Cobas U 411 Urine Analyzer 953

Cobas® 6500 Urine Analyzer Series* 954

Point-of-Care Testing 956

Cobas Poc it Solution 958

Cobas bge Link Software 960

Cobas B 121 System 961

Cobas B 221 System 962

Cobas B 123 Poc System 963

Accu-Chek® Inform Ii System 964

Accu-Chek® Safe-T-Pro Plus 965

Cobas H 232 Poc System 966

Roche Cardiac® Trop T Sensitive Test 967

Coaguchek® Xs System 968

Coaguchek Xs Plus System 969

Accutrend® Plus System 970

Reflotron® Plus System 971

Cobas B 101 System 972

Molecular Diagnostics 974

Solutions from Roche for Molecular

Diagnostics 974

Cobas P 630 Instrument 977

Cobas® Ampliprep Instrument 978

Cobas® Taqman® Analyzer and Cobas®

Taqman® 48 Analyzer 979

Cobas® Ampliprep/Cobas® Taqman® Hcv

Qualitative and Quantitative Tests, V2.0 980

Cobas® Taqman® Mtb Test 981

Cobas P 480 Instrument 982

Cobas® 4800 System V2.0 983

The Cobas® Hpv Test 985

The Cobas® Oncology Tests 985

Cobas® Mrsa/Sa Test 987

Cobas® Cdiff Test 987

Cobas® Hsv 1 and 2 Test 988

Cobas S 201 System 988

Lightcycler® Systems 990

Lightcycler® 2.0 Instrument 991

Test Kits, Validated for Ivd 992

Lightcycler® Septifast Test 992

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ABSTRACT

Lysophosphatidic acid (LPA) is a bioactive phospholipid mediator that has been found to ameliorate nonsteroidal anti-inflammatory drug (NSAID)-induced gastric injury by acting on lysophosphatidic acid type 2 receptor (LPAR2). In this study, we investigated whether LPAR2 signaling was implicated in the development of NSAID-induced small intestinal injury (enteropathy), another major complication of NSAID use. Wild-type (WT) and Lpar2 deficient (Lpar2-/-) mice were treated with a single, large dose (20 or 30 mg/kg, i.g.) of indomethacin (IND). The mice were euthanized at 6 or 24 h after IND treatment. We showed that IND-induced mucosal enteropathy and neutrophil recruitment occurred much earlier (at 6 h after IND treatment) in Lpar2-/- mice compared to WT mice, but the tissue levels of inflammatory mediators (IL-1β, TNF-α, inducible COX-2, CAMP) remained at much lower levels. Administration of a selective LPAR2 agonist DBIBB (1, 10 mg/kg, i.g., twice at 24 h and 30 min before IND treatment) dose-dependently reduced mucosal injury and neutrophil activation in enteropathy, but it also enhanced IND-induced elevation of several proinflammatory chemokines and cytokines. By assessing caspase-3 activation, we found significantly increased intestinal apoptosis in IND-treated Lpar2-/- mice, but it was attenuated after DBIBB administration, especially in non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mice. Finally, we showed that IND treatment reduced the plasma activity and expression of autotaxin (ATX), the main LPA-producing enzyme, and also reduced the intestinal expression of Lpar2 mRNA, which preceded the development of mucosal damage. We conclude that LPAR2 has a dual role in NSAID enteropathy, as it contributes to the maintenance of mucosal integrity after NSAID exposure, but also orchestrates the inflammatory responses associated with ulceration. Our study suggests that IND-induced inhibition of the ATX-LPAR2 axis is an early event in the pathogenesis of enteropathy.

PMID:37816857 | DOI:10.1038/s41401-023-01175-7

21:49

PubMed articles on: Cardio-Oncology

Allogeneic mitochondrial transplantation ameliorates cardiac dysfunction due to doxorubicin: An in vivo study

Biomed Pharmacother. 2023 Oct 7;168:115651. doi: 10.1016/j.biopha.2023.115651. Online ahead of print.

 

ABSTRACT

Doxorubicin (DOX) is a topoisomerase II inhibitor used in cancer therapy. Despite its efficacy, DOX causes serious adverse effects, such as short- and long-term cardiotoxicity. This work aimed to assess the short- and long-term cardiotoxicity of DOX and the role of inflammation and antioxidant defenses on that cardiotoxicity in a mice model. Adult CD-1 male mice received a cumulative dose of 9.0 mg/kg of DOX (2 biweekly intraperitoneal injections (ip), for 3 weeks). One week (1W) or 5 months (5M) after the last DOX administration, the heart was collected. One week after DOX, a significant increase in p62, tumor necrosis factor receptor (TNFR) 2, glutathione peroxidase 1, catalase, inducible nitric oxide synthase (iNOS) cardiac expression, and a trend towards an increase in interleukin (IL)-6, TNFR1, and B-cell lymphoma 2 associated X (Bax) expression was observed. Moreover, DOX induced a decrease on nuclear factor erythroid-2 related factor 2 (Nrf2) cardiac expression. In both 1W and 5M, DOX led to a high density of infiltrating M1 macrophages, but only the 1W-DOX group had a significantly higher number of nuclear factor κB (NF-κB) p65 immunopositive cells. As late effects (5M), an increase in Nrf2, myeloperoxidase, IL-33, tumor necrosis factor-α (TNF-α), superoxide dismutase 2 (SOD2) expression, and a trend towards increased catalase expression were observed. Moreover, B-cell lymphoma 2 (Bcl-2), cyclooxygenase-2 (COX-2), and carbonylated proteins expression decreased, and a trend towards decreased p38 mitogen-activated protein kinase (MAPK) expression were seen. Our study demonstrated that DOX induces adverse outcome pathways related to inflammation and oxidative stress, although activating different time-dependent response mechanisms.

PMID:37833616 | DOI:10.1007/s10753-023-01908-0

21:49

PubMed articles on: Cardio-Oncology

Right ventricle toxicity in cancer treatment: a focused review on cardiac imaging

Future Cardiol. 2023 Sep;19(11):537-545. doi: 10.2217/fca-2022-0024. Epub 2023 Oct 13.

ABSTRACT

Background: The right ventricle (RV) remains the 'forgotten chamber' in the clinical assessment of cancer therapy-related cardiac dysfunction (CTRCD). Aim: We aimed to review the role that various cardiac imaging modalities play in RV assessment as part of the integrative management of patients undergoing cancer therapy. Discussion: RV assessment remains challenging by traditional 2D echocardiography. In this review we discuss other parameters such as right atrial strain, and other echocardiographic modalities such as 3D and stress echocardiography. We also elaborate on the specific role that cardiac magnetic resonance imaging and equilibrium radionuclide angiocardiography can play in assessing the RV. Conclusion: Biventricular function should be monitored following chemotherapy for early detection of subclinical CTRCD and possible solitary RV changes.

PMID:37830360 | DOI:10.2217/fca-2022-0024

21:49

PubMed articles on: Cardio-Oncology

A dual role of lysophosphatidic acid type 2 receptor (LPAR2) in nonsteroidal anti-inflammatory drug-induced mouse enteropathy

Acta Pharmacol Sin. 2023 Oct 10. doi: 10.1038/s41401-023-01175-7. Online ahead of print.

 

ABSTRACT

BACKGROUND: Current treatment of acute leukemia is based on anthracycline chemotherapy. Anthracyclines, despite improving patient survival, have serious cardiotoxicity and therefore cardiac monitoring should be a priority. The purpose of this study is to explore the possible early predictors of anthracycline-induced subclinical cardiotoxicity(AISC)in acute leukemia patients.

METHODS: We conducted a prospective observational study involving 51 patients with acute leukemia treated with anthracycline. Demographic data, clinical variables, echocardiography variables and biochemical variables were collected at baseline and after 3 cycles of chemotherapy. Patients were divided into the AISC and No-AISC groups according to changes of global longitudinal peak systolic strain. Regression models and receiver operating characteristic curve analysis were used to explore the relationship between the variables and AISC.

RESULT: 17 of the patients suffered subclinical cardiotoxicity after 3 cycles of anthracycline treatment. Multiple logistic regression analysis showed a significant association of DBil (OR 0.612, 95% CI 0.409-0.916, p = 0.017), TBil (OR 0.841, 95% CI 0.717-0.986, p = 0.033), PLT (OR 1.012, 95% CI 1.002-1.021, p = 0.016) and Glu (OR 1.873, 95% CI 1.009-3.475, p = 0.047) with the development of AISC. After 3 cycles of chemotherapy, there was a significant difference in PLT between the AISC and NO-AISC groups. Moreover, the dynamic changes in PLT from baseline to after 3 cycles of chemotherapy were each statistically significant in the AISC and NO-AISC groups. The combination of PLT and N-terminal pro-B-type natriuretic peptide (NT-proBNP) had the highest area under curves (AUC) for the diagnosis of AISC than PLT and NT-proBNP alone (AUC = 0.713, 95%CI: 0.56-0.87, P = 0.017).

CONCLUSION: Total bilirubin (TBil), direct bilirubin (DBil), platelets (PLT) and blood glucose (Glu) are independent influencing factors for AISC in acute leukemia patients receiving anthracycline therapy. Bilirubin may be a protective factor and PLT may be a contributing factor for AISC. The combination of baseline PLT and baseline NT-proBNP shows satisfactory predictive ability for AISC in acute leukemia cases treated with 3 cycles of chemotherapy.

PMID:37833648 | PMC:PMC10571315 | DOI:10.1186/s12885-023-11060-5

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PubMed articles on: Cardio-Oncology

The Role of Nrf2 and Inflammation on the Dissimilar Cardiotoxicity of Doxorubicin in Two-Time Points: a Cardio-Oncology In Vivo Study Through Time

Inflammation. 2023 Oct 14. doi: 10.1007/s10753-023-01908-0. Online ahead of print.

 

ABSTRACT

BACKGROUND: Aponermin, a circularly permuted tumor necrosis factor-related apoptosis-inducing ligand, is a potential death receptor 4/5-targeted antitumour candidate. Previous phase 1/2 studies have demonstrated the efficacy of aponermin in patients with relapsed or refractory multiple myeloma (RRMM). To confirm the superiority of aponermin plus thalidomide and dexamethasone (aponermin group) over placebo plus thalidomide and dexamethasone (placebo group) in RRMM, a randomized, double-blinded, placebo controlled phase 3 trial was performed.

METHODS: Four hundred seventeen patients with RRMM who had previously received at least two regimens were randomly assigned (2:1) to receive aponermin, thalidomide, and dexamethasone or placebo, thalidomide, and dexamethasone. The primary endpoint was progression-free survival (PFS). Key secondary endpoints included overall survival (OS) and overall response rate (ORR).

RESULTS: A total of 415 patients received at least one dose of trial treatment (276 vs. 139). The median PFS was 5.5 months in the aponermin group and 3.1 months in the placebo group (hazard ratio, 0.62; 95% confidence interval [CI], 0.49-0.78; P < 0.001). The median OS was 22.4 months for the aponermin group and 16.4 months for the placebo group (hazard ratio, 0.70; 95% CI, 0.55-0.89; P = 0.003). Significantly higher rates of ORR (30.4% vs. 13.7%, P < 0.001) and very good partial response or better (14.1% vs. 2.2%, P < 0.0001) were achieved in the aponermin group than in the placebo group. Treatment with aponermin caused hepatotoxicity in some patients, as indicated by the elevated alanine transaminase, aspartate transaminase, or lactate dehydrogenase levels (52.2% vs. 24.5%, 51.1% vs. 19.4% and 44.9% vs. 21.6%, respectively), mostly grade 1/2, transient and reversible. The main grade 3/4 adverse events included neutropenia, pneumonia and hyperglycemia. The incidence of serious adverse events was similar between the two groups (40.6% vs. 37.4%). There was no evidence that aponermin leads to hematological toxicity, nephrotoxicity, cardiotoxicity, or secondary tumors.

CONCLUSIONS: Aponermin plus thalidomide and dexamethasone significantly improved PFS, OS and ORR with manageable side effects in RRMM patients who had received at least two prior therapies. These results support the use of aponermin, thalidomide, and dexamethasone as a treatment option for RRMM patients.

TRIAL REGISTRATION: The trial was registered at http://www.chictr.org.cn as ChiCTR-IPR-15006024, 17/11/2014.

PMID:37838670 | PMC:PMC10576321 | DOI:10.1186/s12885-023-11489-8

21:49

PubMed articles on: Cardio-Oncology

Influencing factors of anthracycline-induced subclinical cardiotoxicity in acute leukemia patients

BMC Cancer. 2023 Oct 13;23(1):976. doi: 10.1186/s12885-023-11060-5.

 

ABSTRACT

BACKGROUND: This review focuses on multimodality imaging of cardiotoxicity in cancer patients, with the aim of evaluating the effectiveness of different techniques in detecting and monitoring cardiac changes associated with cancer therapy.

METHODS: Eight studies were included in the review, covering various imaging modalities such as cardiac magnetic resonance imaging, echocardiography, and multigated acquisition scanning.

RESULTS: Cardiac magnetic resonance imaging emerged as the most definitive modality, offering real-time detection, comprehensive assessment of cardiac function, the ability to detect early myocardial changes, and superior detection of cardiotoxicity when compared to the other imaging modalities. The studies also emphasize the importance of parameters such as left ventricular ejection fraction and global longitudinal strain in assessing cardiac function and predicting cardiotoxicity.

CONCLUSION: Due to the common use of HER2 agents and anthracyclines within the breast cancer population, the LVEF as a critical prognostic measurement for assessing heart health and estimating the severity of left-sided cardiac malfunction is a commonly used endpoint. CTRCD rates differed between imaging modalities, with cardiac MRI the most sensitive. The use of multimodal cardiac imaging remains a nuanced area, influenced by local availability, the clinical question at hand, body habits, and medical comorbidities. All of the imaging modalities listed have a role to play in current care; however, focus should be given to increasing the provision of cardiac MRI for breast cancer patients in the future to optimize the detection of CTRCD and patient outcomes thereafter.

PMID:37834939 | PMC:PMC10573256 | DOI:10.3390/jcm12196295

21:49

PubMed articles on: Cardio-Oncology

Aponermin or placebo in combination with thalidomide and dexamethasone in the treatment of relapsed or refractory multiple myeloma (CPT-MM301): a randomised, double-blinded, placebo-controlled, phase 3 trial

BMC Cancer. 2023 Oct 14;23(1):980. doi: 10.1186/s12885-023-11489-8.

 

ABSTRACT

The present review summarizes the beneficial and detrimental roles of reactive oxygen species in myocardial ischemia/reperfusion injury and cardioprotection. In the first part, the continued need for cardioprotection beyond that by rapid reperfusion of acute myocardial infarction is emphasized. Then, pathomechanisms of myocardial ischemia/reperfusion to the myocardium and the coronary circulation and the different modes of cell death in myocardial infarction are characterized. Different mechanical and pharmacological interventions to protect the ischemic/reperfused myocardium in elective percutaneous coronary interventions and coronary artery bypass grafting, in acute myocardial infarction and in cardiotoxicity from cancer therapy are detailed. The second part keeps the focus on ROS providing a comprehensive overview of molecular and cellular mechanisms involved in ischemia/reperfusion injury. Starting from mitochondria as the main sources and targets of ROS in ischemic/reperfused myocardium, a complex network of cellular and extracellular processes is discussed, including relationships with Ca2+ homeostasis, thiol group redox balance, hydrogen sulfide modulation, cross-talk with NAPDH oxidases, exosomes, cytokines and growth factors. While mechanistic insights are needed to improve our current therapeutic approaches, advancements in knowledge of ROS-mediated processes indicate that detrimental facets of oxidative stress are opposed by ROS requirement for physiological and protective reactions. This inevitable contrast is likely to underlie unsuccessful clinical trials and limits the development of novel cardioprotective interventions simply based upon ROS removal.

PMID:37839355 | PMC:PMC10590874 | DOI:10.1016/j.redox.2023.102894

21:49

PubMed articles on: Cardio-Oncology

Multimodal Imaging of Cancer Therapy-Related Cardiac Dysfunction in Breast Cancer-A State-of-the-Art Review

J Clin Med. 2023 Sep 29;12(19):6295. doi: 10.3390/jcm12196295.

 

ABSTRACT

BACKGROUND: Doxorubicin (DOX)-induced cardiotoxicity is an important cause of poor prognosis in cancer patients treated with DOX. Angiotensin IV (Ang IV) has multiple protective effects against cardiovascular diseases, including diabetic cardiomyopathy and myocardial infarction, but its role in DOX-induced cardiotoxicity is currently unclear. In this study, we investigated the effects of Ang IV on DOX-induced cardiotoxicity.

METHODS: The viability of primary cardiomyocytes was measured by Cell Counting Kit-8 assays and Hoechst 33342/propidium iodide staining in vitro. ELISAs (serum cTnT and CK-MB) and echocardiography were performed to assess myocardial injury and cardiac function in vivo. Phalloidin staining, haematoxylin and eosin staining and wheat germ agglutinin staining were conducted to detect cardiomyocyte atrophy. We also performed C11 BODIPY staining, measured the levels of Ptgs2 and malondialdehyde and detected the concentrations of ferrous ions, glutathione and oxidized glutathione to indicate ferroptosis.

RESULTS: Ang IV not only attenuated DOX-induced atrophy and cardiomyocyte injury in vitro but also alleviated myocardial injury and improved cardiac function in DOX-treated mice in vivo. Moreover, Ang IV reversed DOX-induced downregulation of glutathione peroxidase 4 (GPX4) and inhibited ferroptosis both in vitro and in vivo. Knockdown of GPX4 by siRNA abolished the cardioprotective effects of Ang IV. Furthermore, Ang IV increased GPX4 levels and ameliorated ferroptosis in RAS-selective lethal 3-treated primary cardiomyocytes.

CONCLUSIONS: Ang IV ameliorates DOX-induced cardiotoxicity by upregulating GPX4 and inhibiting ferroptosis. Ang IV may be a promising candidate to protect against DOX-induced cardiotoxicity in the future.

PMID:37838222 | DOI:10.1016/j.taap.2023.116713

21:49

PubMed articles on: Cardio-Oncology

Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection

Redox Biol. 2023 Oct 6;67:102894. doi: 10.1016/j.redox.2023.102894. Online ahead of print.

 

ABSTRACT

Cancer and cardiovascular disorders are known as the two main leading causes of mortality worldwide. Cardiotoxicity is a critical and common adverse effect of cancer-related chemotherapy. Chemotherapy-induced cardiotoxicity has been associated with various cancer treatments, such as anthracyclines, immune checkpoint inhibitors, and kinase inhibitors. Different methods have been reported for the management of chemotherapy-induced cardiotoxicity. In this regard, sodium-glucose cotransporter-2 inhibitors (SGLT2i), a class of antidiabetic agents, have recently been applied to manage heart failure patients. Further, SGLT2i drugs such as EMPA exert protective cardiac and systemic effects. Moreover, it can reduce inflammation through the mediation of major inflammatory components, such as Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasomes, Adenosine 5'-monophosphate-activated protein kinase (AMPK), and c-Jun N-terminal kinase (JNK) pathways, Signal transducer and activator of transcription (STAT), and overall decreasing transcription of proinflammatory cytokines. The clinical outcome of EMPA administration is related to improving cardiovascular risk factors, including body weight, lipid profile, blood pressure, and arterial stiffness. Intriguingly, SGLT2 suppressors can regulate microglia-driven hyperinflammation affecting neurological and cardiovascular disorders. In this review, we discuss the protective effects of EMPA in chemotherapy-induced cardiotoxicity from molecular, immunological, and neuroimmunological aspects to preclinical and clinical outcomes.

PMID:37839109 | DOI:10.1016/j.biopha.2023.115686

21:49

PubMed articles on: Cardio-Oncology

Angiotensin IV ameliorates doxorubicin-induced cardiotoxicity by increasing glutathione peroxidase 4 and alleviating ferroptosis

Toxicol Appl Pharmacol. 2023 Oct 12;479:116713. doi: 10.1016/j.taap.2023.116713. Online ahead of print.

 

ABSTRACT

INTRODUCTION: Patients with myeloproliferative neoplasms (MPNs) and atrial fibrillation (AF) are at increased risk of thrombosis and bleeding. However, the risk of thrombosis and bleeding in patients with AF and MPN compared with the general population with AF is unclear. Additionally, traditional risk scores (CHA2DS2-VASC and HAS-BLED) for risk/benefit estimation of thromboprophylaxis in AF do not account for MPN status. Therefore, we aimed to investigate bleeding and thrombosis risk in patients with MPN hospitalized for AF.

METHODS: We utilized the National Readmission Database (NRD) to identify patients with AF with and without MPN. Primary bleeding and thrombosis outcomes were in-hospital or 30-day readmission for bleeding or thrombosis, respectively. We propensity score (PS) matched patients with and without MPN. Risk of primary outcomes in MPN was assessed in PS matched cohort using logistic regression. Receiver operating characteristic (ROC) curve used to evaluate predictive ability of CHA2DS2-VASC and HAS-BLED of primary thrombosis and bleeding outcomes, respectively.

RESULTS: 24,185 patients without MPN were matched with 1,617 patients with MPN and variables were balanced between groups. Patients with MPN were at increased risk of meeting the thrombosis (OR 1.98, 95% CI 1.23-3.21) but not bleeding (OR 0.87, 95% CI 0.63-1.19) primary outcomes. In MPN, CHA2DS2-VASC predicted thrombosis (C-statistic 0.66, 95% CI 0.54-0.78) but HAS-BLED was a poor predictor of bleeding (C-statistic 0.55, 95% CI 0.46-0.64).

CONCLUSION: In patients with AF, MPN was associated with increased risk of bleeding and thrombosis. HAS-BLED scores did not accurately predict bleeding in MPN. Further investigation is needed to refine risk scores in MPN.

PMID:37839025 | DOI:10.1007/s11239-023-02900-z

21:49

PubMed articles on: Cardio-Oncology

Empagliflozin treatment of cardiotoxicity: A comprehensive review of clinical, immunobiological, neuroimmune, and therapeutic implications

Biomed Pharmacother. 2023 Oct 13;168:115686. doi: 10.1016/j.biopha.2023.115686. Online ahead of print.

 

ABSTRACT

BACKGROUND: Recent studies suggested a relationship between Takotsubo syndrome (TTS) and malignancy. However, clinical outcomes of TTS associated with cancer have not been assessed completely. This study was aimed to investigate the outcomes of patients with TTS and cancer.

METHODS: We performed a systematic review and meta-analysis to evaluate the clinical outcomes of TTS in patients with and without malignancy. We systematically reviewed and analyzed 14 studies (189,210 patients) published in PubMed and Cochrane Library databases until December 2022. The primary outcome was all-cause mortality at the longest follow-up.

RESULTS: The prevalence of current or previous malignancy in patients with TTS was 8.7% (16,461 patients). Patients with TTS and malignancy demonstrated a higher risk of mortality at the longest follow-up than those with TTS alone (odds ratio [OR], 2.41; 95% confidence interval [CI]; 1.95-2.98; P < 0.001). Moreover, cancer was significantly associated with an increased risk of in-hospital or 30-day mortality (OR 2.36; 95% CI, 1.67-3.33; P < 0.001), shock (OR 1.42; 95% CI, 1.30-1.55; P < 0.001), mechanical respiratory support (OR 1.68; 95% CI, 1.59-1.77; P < 0.001), arrhythmia (OR 1.27; 95% CI, 1.21-1.34; P < 0.001), and major adverse cardiac events (OR 1.69; 95% CI, 1.18-2.442; P < 0.001).

CONCLUSIONS: This study revealed significant associations between previous or active cancer and an increased risk of all-cause mortality and in-hospital adverse events in patients with TTS.

PMID:37840966 | PMC:PMC10570743 | DOI:10.3389/fcvm.2023.1244808

21:49

PubMed articles on: Cardio-Oncology

In-Hospital and readmission outcomes of patients with myeloproliferative neoplasms and atrial fibrillation: insights from the National Readmissions Database

J Thromb Thrombolysis. 2023 Oct 15. doi: 10.1007/s11239-023-02900-z. Online ahead of print.

 

ABSTRACT

INTRODUCTION: Due to the cardiotoxicity of cancer treatment and traditional risk factors for cardiovascular disease (CVD) such as obesity, diabetes, dyslipidemia, and hypertension, cancer patients are at higher risk of developing CVD. However, limited research exists on the correlation between chronic kidney disease (CKD) and CVD risk in cancer patients.

METHODS: This cross-sectional study selected cancer patients aged ≥20 years from the National Health and Nutrition Examination Survey (NHANES) conducted from 2015 to 2020. Multivariable logistic regression was used to assess the association between CKD and CVD in cancer patients. Additionally, subgroup analyses were conducted to investigate the association among different groups of cancer patients.

RESULTS: We included 1700 adult cancer patients (52.53% were female). After multivariable adjustment for covariates including traditional CVD factors, CKD was significantly associated with CVD, with an odds ratio (95% confidence interval) and P-value of 1.61(1.18,2.19) and 0.004. Subgroup analyses after multivariable adjustment showed a significant correlation between CKD and increased CVD risk in the following populations: age ≥60 years, males, White ethnicity, and individuals with or without traditional CVD factors (obesity, diabetes, dyslipidemia, and hypertension).

CONCLUSIONS: CKD remains a significant factor in the higher risk of CVD among adult cancer patients in the United States, even after adjustment for traditional CVD risk factors. Therefore, to reduce the risk of CVD in cancer patients, it is important to treat CKD as a non-traditional risk factor for CVD and actively manage it.

PMID:37839394 | DOI:10.1159/000534182

21:49

PubMed articles on: Cardio-Oncology

Clinical outcomes of takotsubo syndrome in patients with cancer: a systematic review and meta-analysis

Front Cardiovasc Med. 2023 Sep 29;10:1244808. doi: 10.3389/fcvm.2023.1244808. eCollection 2023.

 

ABSTRACT

A 75-year-old man underwent chemoradiotherapy for advanced esophageal cancer. After nine years, he was hospitalized for left pyothorax. Consequently, the patient underwent drainage and window opening surgery. He experienced cardiopulmonary arrest but was resuscitated. Based on cardiac catheterization data, the patient was diagnosed with constrictive pericarditis. Unfortunately, extracorporeal circulation did not improve his condition, and he ultimately died. An autopsy revealed adhesion between the pericardium and pleura, especially the pericardium in contact with the left thoracic cavity, which was markedly thickened. This suggests that constrictive pericarditis, a latent complication of chemoradiotherapy, is aggravated by pyothorax.

PMID:37839880 | DOI:10.2169/internalmedicine.2502-23

21:49

PubMed articles on: Cardio-Oncology

Association of chronic kidney disease with cardiovascular disease in cancer patients: a cross-sectional study

Cardiorenal Med. 2023 Oct 14. doi: 10.1159/000534182. Online ahead of print.