Critical Reviews in Clinical Laboratory Sciences Journal Impact Factor & Information

Publisher: Informa Healthcare

Journal description

Topics: Medical biochemistry; Microbiology and infectious disease; Laboratory hematology; Clinical hematology; Molecular biology; Cellular biology; Toxicology; Advances in pharmacology.

Current impact factor: 3.69

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.692
2013 Impact Factor 7
2012 Impact Factor 3.783
2011 Impact Factor 5.25
2010 Impact Factor 5.741
2009 Impact Factor 4.48
2008 Impact Factor 5.154
2007 Impact Factor 5.037
2006 Impact Factor 6.138
2005 Impact Factor 3.9
2004 Impact Factor 3.444
2003 Impact Factor 3.136
2002 Impact Factor 4.231
2001 Impact Factor 3.931
2000 Impact Factor 3.357
1999 Impact Factor 3.138
1998 Impact Factor 1.96
1997 Impact Factor 3.792
1996 Impact Factor 3.667
1995 Impact Factor 2.625
1994 Impact Factor 2.474
1993 Impact Factor 1
1992 Impact Factor 1.118

Impact factor over time

Impact factor

Additional details

5-year impact 5.55
Cited half-life 9.40
Immediacy index 0.75
Eigenfactor 0.00
Article influence 1.66
Website Critical Reviews in Clinical Laboratory Sciences website
Other titles Critical reviews in clinical laboratory sciences, Chemical Rubber Company critical reviews in clinical laboratory sciences, CRC critical reviews in clinical laboratory sciences
ISSN 1040-8363
OCLC 1151594
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Informa Healthcare

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On author's personal website or institution website
    • Publisher copyright and source must be acknowledged
    • Non-commercial
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • NIH funded authors may post articles to PubMed Central for release 12 months after publication
    • Wellcome Trust authors may deposit in Europe PMC after 6 months
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Cardiac diseases have been extensively studied following diabetes and altered metabolism has been implicated in its initiation. In this context, there is a shift from glucose utilization to predominantly fatty acid metabolism. We have focused on the micro- and macro-environments that the heart uses to provide fatty acids to the cardiomyocyte. Specifically, we will discuss the cross talk between endothelial cells, smooth muscles and cardiomyocytes, and their respective secretory products that allows for this shift in metabolism. These changes will then be linked to alterations in the cardiovascular system and the augmented heart disease observed during diabetes. Traditionally, the heart was only thought of as an organ that supplies oxygen and nutrients to the body through its function as a pump. However, the heart as an endocrine organ has also been suggested. Secreted products from the cardiomyocytes include the natriuretic peptides atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Both have been shown to have vasodilatory, diuretic and antihypertensive effects. These peptides have been extensively studied and their deficiency is considered to be a major cause for the initiation of cardiovascular and cardiometabolic disorders. Another secretory enzyme, lipoprotein lipase (LPL), has been implicated in diabetic heart disease. LPL is a triglyceride-hydrolyzing enzyme that is synthesized within the cardiomyocyte and secreted towards the lumen under various conditions. For example, moderate or short-term hyperglycemia stimulates the release of LPL from the cardiomyocytes towards the endothelial cells. This process allows LPL to contact lipoprotein triglycerides, initiating their break down, with the product of lipolysis (free fatty acids, FA) translocating towards the cardiomyocytes for energy consumption. This mechanism compensates for the lack of glucose availability following diabetes. Under prolonged, chronic conditions of hyperglycemia, there is a need to inhibit this mechanism to avoid the excess delivery of FA to the cardiomyocytes, an effect that is known to induce cardiac cell death. Thus, LPL inhibition is made possible by a FA-induced activation of PPAR β/δ, which augments angiopoietin-like 4 (Angptl4), an inhibitor of LPL activity. In the current review, we will focus on the mediators and conditions that regulate LPL and Angptl4 secretion from the cardiomyocyte, which are critical for maintaining cardiac metabolic homeostasis.
    Critical Reviews in Clinical Laboratory Sciences 01/2015; 52(3):1-12. DOI:10.3109/10408363.2014.997931
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    ABSTRACT: The aim of this review article is to give an update on the state of the art of the immunoassay methods for the measurement of B-type natriuretic peptide (BNP) and its related peptides. Using chromatographic procedures, several studies reported an increasing number of circulating peptides related to BNP in human plasma of patients with heart failure. These peptides may have reduced or even no biological activity. Furthermore, other studies have suggested that, using immunoassays that are considered specific for BNP, the precursor of the peptide hormone, proBNP, constitutes a major portion of the peptide measured in plasma of patients with heart failure. Because BNP immunoassay methods show large (up to 50%) systematic differences in values, the use of identical decision values for all immunoassay methods, as suggested by the most recent international guidelines, seems unreasonable. Since proBNP significantly cross-reacts with all commercial immunoassay methods considered specific for BNP, manufacturers should test and clearly declare the degree of cross-reactivity of glycosylated and non-glycosylated proBNP in their BNP immunoassay methods. Clinicians should take into account that there are large systematic differences between methods when they compare results from different laboratories that use different BNP immunoassays. On the other hand, clinical laboratories should take part in external quality assessment (EQA) programs to evaluate the bias of their method in comparison to other BNP methods. Finally, the authors believe that the development of more specific methods for the active peptide, BNP1–32, should reduce the systematic differences between methods and result in better harmonization of results.
    Critical Reviews in Clinical Laboratory Sciences 12/2014; 52(2). DOI:10.3109/10408363.2014.987720
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    ABSTRACT: Cardiac troponin is the preferred biomarker for defining the acute coronary syndrome and acute myocardial infarction. Currently, the only decision limit formally endorsed with regard to the cardiac troponins is the 99th percentile. This is a “rule-in” criterion, intended to ensure that only persons with the acute coronary syndrome are reviewed. The 99th percentile is an arbitrary cut point and there are many problems associated with its application, including defining a truly healthy population, the difficulty of standardisation of cardiac troponin assays, especially but not only cardiac troponin I, and the effects of age and sex on this parameter. The Emergency Department (ED) screens many more persons for possible acute coronary syndromes than actually have the condition and their needs are best met by a “rule-out” test that enables them to clear their busy departments of the many persons who do not actually have the condition. The needs of the ED are not optimally met using the 99th percentile. The index of individuality for the cardiac troponins is small and significant changes consistent with an acute coronary syndrome can occur without the 99th percentile being exceeded. It appears that the ED may be better served by use of delta troponin changes rather than the 99th percentile, but there are problems with this approach, particularly in persons who present late when troponin release has plateaued. In addition, there are many non-acute coronary syndrome causes for cardiac troponin release. The needs of the cardiologist and the ED physician are so different that it may be inappropriate for both groups to use the same diagnostic criteria for cardiac troponin, and it is of great importance that cardiac troponin measurement be used as only one part of the assessment of the person presenting with possible acute coronary syndrome.
    Critical Reviews in Clinical Laboratory Sciences 11/2014; 52(1). DOI:10.3109/10408363.2014.972497
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    ABSTRACT: Abstract Calcium, the fifth most common element in the body, plays major physiological functions. Measurement of blood calcium is one of the most commonly ordered laboratory tests in assessments of calcium homeostasis and disease diagnosis. Hypercalcemia is an increased level of calcium in the blood. This disorder is most commonly caused by primary hyperparathyroidism and malignancy. However, other less common causes of elevated calcium levels need to be considered when making a differential diagnosis. This review is intended to provide readers with a better understanding of calcium homeostasis and the causes and pathophysiology of hypercalcemia. Most importantly, this review describes useful approaches for laboratory scientists and clinicians to appropriately diagnose and assess hypercalcemia.
    Critical Reviews in Clinical Laboratory Sciences 10/2014; 52(3):1-13. DOI:10.3109/10408363.2014.970266
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    ABSTRACT: Abstract Severe hyperkalemia is a potentially life-threatening condition requiring immediate medical intervention. Pseudohyperkalemia can be misleading and result in incorrect interpretation and inappropriate patient management. Immediate recognition and appropriate interpretation of pseudohyperkalemia, on the other hand, prevents misdiagnosis and unnecessary intervention. Pseudohyperkalemia is induced by hemolysis and excessive leakage of potassium from cells during or after blood collection. It has been increasingly seen in many hematological disorders such as leukocytosis and thrombocytosis. Reverse pseudohyperkalemia has recently been reported in leukemic patients in whom the plasma potassium levels are greater than the serum potassium levels because of heparin-induced cell membrane damage. Although pseudohyperkalemia has long been recognized and understood, it continues to be misinterpreted. To improve patient care, an algorithm for investigation of pseudohyperkalemia and preventive measures should be established and implemented in the clinical laboratory.
    Critical Reviews in Clinical Laboratory Sciences 10/2014; 52(2):1-11. DOI:10.3109/10408363.2014.966898
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    ABSTRACT: Abstract Oxidative stress refers to cellular or molecular damage caused by reactive oxygen species, which especially occurs in age-related conditions as a result of an imbalance between the production of reactive oxygen species and the antioxidant defense response. Dry age-related macular degeneration (AMD) and exfoliation syndrome (XFS) are two common and complex age-related conditions that can cause irreversible vision loss. Two subtypes of AMD, which is the leading cause of blindness in the Western world, exist: the most prevalent dry type and the most severe wet type. Early dry AMD is characterized by formation of drusen, which are sub-retinal deposits, in the macular area and may progress to geographic atrophy with more dramatic manifestation. XFS is a systemic disorder of the extracellular matrix characterized by the accumulation of elastic fibrils that leads, in most cases, to glaucoma development with progressive and irreversible vision loss. Due to the aging population, the prevalence of these already-widespread conditions is increasing and is resulting in significant economic and psychological costs for individuals and for society. The exact composition of the abnormal drusen and XFS material as well as the mechanisms responsible for their production and accumulation still remain elusive, and consequently treatment for both diseases is lacking. However, recent epidemiologic, genetic and molecular studies support a major role for oxidative stress in both dry AMD and XFS development. Understanding the early molecular events in their pathogenesis and the exact role of oxidative stress may provide novel opportunities for therapeutic intervention for the prevention of progression to advanced disease.
    Critical Reviews in Clinical Laboratory Sciences 10/2014; 52(1):1-16. DOI:10.3109/10408363.2014.968703
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    ABSTRACT: Celiac disease is a complex immune-mediated disorder that is triggered by ingestion of gluten and related proteins in genetically susceptible individuals. Under conditions of increased intestinal permeability, gluten-derived peptides can travel across the intestinal epithelium and undergo deamidation catalyzed by the tissue transglutaminase (TTG) enzyme. This renders them immunogenic in individuals expressing specific human leukocyte antigen (HLA) DQ heterodimers. The resulting immune response is characterized by the production of antibodies against both deamidated gliadin peptides (DGP) and TTG, generation of pro-inflammatory cytokines and activation of cytotoxic T cells. This response damages the intestinal epithelium resulting in the wide range of gastrointestinal and systemic symptoms observed in those with celiac disease. Celiac disease diagnosis has traditionally been based on biopsy and histological examination of the small intestine. While this approach is still considered the gold standard, it is invasive and susceptible to both false-positive and false-negative results. Several laboratory tests have become available to aid in the diagnosis and monitoring of celiac disease, and are the focus of this review. These include serological tests for celiac disease-specific antibodies such as anti-endomysial antibodies, anti-TTG antibodies and anti-DGP antibodies of both the immunoglobulin A (IgA) and immunoglobulin G (IgG) class, genetic tests to elucidate HLA DQ status and ancillary tests such as total IgA. While some have suggested that laboratory tests may replace intestinal biopsy in specific circumstances, others maintain that this procedure remains a critical component of celiac disease diagnosis. We review the analytical methodology, strengths, weaknesses, diagnostic performance and clinical utility of the various laboratory tests for celiac disease. Potential future markers and tests that are now considered obsolete are also discussed. Current clinical practice guidelines for the diagnosis and management of celiac disease from the European Society for Pediatric Gastroenterology, Hepatology and Nutrition, the American College of Gastroenterology and the World Gastroenterology Organisation are summarized, and important differences between these guidelines are highlighted.
    Critical Reviews in Clinical Laboratory Sciences 09/2014; 51(6). DOI:10.3109/10408363.2014.958813
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    ABSTRACT: Personalized medicine is an emerging field with a goal of applying genomic information as a predictor of disease risk as well as individualization of drug therapy. For optimization of drug therapy, significant progress has been made in the past decade in linking genetic variation in genes associated with drug disposition to prediction of drug response and adverse reactions. For most drugs in clinical use, the interplay of many factors, including genetics, demographics, drug–drug interactions, disease states and the environment, result in the interindividual variability observed during drug therapy. Broadly speaking, such determinants of drug response are mediated through modulation of drug concentrations reflective of pharmacokinetic factors, as well as drug targets, often referred to as pharmacodynamics. It is clear that for personalized medicine to become clinically meaningful, genomic as well as clinical and environmental influences must be considered together. We show, for a number of drugs in clinical use, that genomics-guided treatment options not only are becoming feasible but are also on the cusp of showing superiority in terms of clinical outcomes as well as cost-benefit. One of the most widely studied drugs with regard to genomics-guided dosing options is the oral anticoagulant, warfarin. Genetic polymorphisms in the gene encoding cytochrome P450 2C9 (CYP2C9) and those in the target gene responsible for the warfarin anticoagulant effect, vitamin K epoxide reductase (VKORC1), account for much of the variability in the warfarin maintenance dose; however, routine genotyping in warfarin therapy remains controversial. We will outline the importance of understanding all of the variables that mediate warfarin response as the prerequisite to successful utilization of genotype-guided warfarin therapy. Similarly, HMG Co-A reductase inhibitors, commonly known as statins, also display wide interindividual variability in plasma concentration, response and toxicity due in part to polymorphisms in transporter genes, including SLCO1B1 and ABCG2. Genetic factors are also important considerations in treatment with other therapeutic agents discussed, including clopidogrel and tamoxifen. Implementation of personalized medicine-based treatment options for these and other drugs, the pharmacokinetics or pharmacodynamics of which are impacted by functional genetic variations, will require overcoming a number of challenges, including cost, turnaround time, and demonstration of clinical benefit, as well as better training of health care professionals about genomics in general, and pharmacogenomics in particular.
    Critical Reviews in Clinical Laboratory Sciences 09/2014; 52(1). DOI:10.3109/10408363.2014.950407
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    ABSTRACT: Long non-coding RNAs (lncRNAs) are transcripts without protein-coding capacity; initially regarded as “transcriptional noise”, lately they have emerged as essential factors in both cell biology and mechanisms of disease. In this article, we present basic knowledge of lncRNA molecular mechanisms, associated physiological processes and cancer association, as well as their diagnostic and therapeutic value in the form of a decalog: (1) Non-coding RNAs (ncRNAs) are transcripts without protein-coding capacity divided by size (short and long ncRNAs), function (housekeeping RNA and regulatory RNA) and direction of transcription (sense/antisense, bidirectional, intronic and intergenic), containing a broad range of molecules with diverse properties and functions, such as messenger RNA, transfer RNA, microRNA and long non-coding RNAs. (2) Long non-coding RNAs are implicated in many molecular mechanisms, such as transcriptional regulation, post-transcriptional regulation and processing of other short ncRNAs. (3) Long non-coding RNAs play an important role in many physiological processes such as X-chromosome inactivation, cell differentiation, immune response and apoptosis. (4) Long non-coding RNAs have been linked to hallmarks of cancer: (a) sustaining proliferative signaling; (b) evading growth suppressors; (c) enabling replicative immortality; (d) activating invasion and metastasis; (e) inducing angiogenesis; (f) resisting cell death; and (g) reprogramming energy metabolism. (5) Regarding their impact on cancer cells, lncRNAs are divided into two groups: oncogenic and tumor-suppressor lncRNAs. (6) Studies of lncRNA involvement in cancer usually analyze deregulated expression patterns at the RNA level as well as the effects of single nucleotide polymorphisms and copy number variations at the DNA level. (7) Long non-coding RNAs have potential as novel biomarkers due to tissue-specific expression patterns, efficient detection in body fluids and high stability. (8) LncRNAs serve as novel biomarkers for diagnostic, prognostic and monitoring purposes. (9) Tissue specificity of lncRNAs enables the development of selective therapeutic options. (10) Long non-coding RNAs are emerging as commercial biomarkers and therapeutic agents.
    Critical Reviews in Clinical Laboratory Sciences 08/2014; 51(6). DOI:10.3109/10408363.2014.944299
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    ABSTRACT: Contrast-induced nephropathy (CIN) is a common event in hospitals, with reported incidences ranging from 1 to 30%. Patients with underlying kidney disease have an increased risk of developing CIN. Point-of-care (POC) creatinine devices are handheld devices capable of providing quantitative data on a patient’s kidney function that could be useful in stratifying preventive measures. This overview aims to synthesize the current evidence on diagnostic accuracy and clinical utility of POC creatinine devices in detecting patients at risk of CIN. Five databases were searched for diagnostic accuracy studies or clinical trials that evaluated the usefulness of POC devices in detecting patients at risk of CIN. Selected articles were critically appraised to assess their individual risk of bias by the use of standard criteria; 13 studies were found that addressed the diagnostic accuracy or clinical utility of POC creatinine devices. Most studies incurred a moderate to high risk of bias. Overall concordance between POC devices and reference standards (clinical laboratory procedures) was found to be moderate, with 95% limits of agreement often lying between −35.4 and +35.4 µmol/L (−0.4 and +0.4 mg/dL). Concordance was shown to decrease with worsening kidney function. Data on the clinical utility of these devices were limited, but a significant reduction in time to diagnosis was reported in two studies. Overall, POC creatinine devices showed a moderate concordance with standard clinical laboratory creatinine measurements. Several biases could have induced optimism in these estimations. Results obtained from these devices may be unreliable in cases of severe kidney failure. Randomized trials are needed to address the clinical utility of these devices.
    Critical Reviews in Clinical Laboratory Sciences 07/2014; 51(6). DOI:10.3109/10408363.2014.937794
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    ABSTRACT: Abstract This review focuses on the promising potential of nucleic acids in body fluids such as blood and urine as diagnostic, prognostic, predictive and monitoring biomarkers in urologic malignancies. The tremendous progress in the basic knowledge of molecular processes in cancer, as shown in the companion review on nucleic acid-based biomarkers in tissue of urologic tumors, provides a strong rationale for using these molecular changes as non-invasive markers in body fluids. The changes observed in body fluids are an integrative result, reflecting both tissue changes and processes occurring in the body fluids. The availability of sensitive methods has only recently made possible detailed studies of DNA- and RNA-based markers in body fluids. In addition to these biological aspects, methodological aspects of the determination of nucleic acids in body fluids, i.e. pre-analytical, analytical and post-analytical issues, are particularly emphasized. The characteristic changes of RNA (differential mRNA and miRNA expression) and DNA (concentrations, integrity index, mutations, microsatellite and methylation alterations) in serum/plasma and urine samples of patients suffering from the essential urologic cancers of the prostate, bladder, kidney and testis are summarized and critically discussed below. To translate the promising results into clinical practice, laboratory scientists and clinicians have to collaborate to resolve the challenges of harmonized and feasible pre-analytical and analytical conditions for the selected markers and to validate these markers in well-designed and sufficiently powered multi-center studies.
    Critical Reviews in Clinical Laboratory Sciences 05/2014; 51(4):1-32. DOI:10.3109/10408363.2014.914888