Institute of Clinical Pathology and Medical Research ICPMR


Institute of Clinical Pathology and Medical Research ICPMR

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Lippi G.,University of Verona | Sanchis-Gomar F.,Research Institute Of Hospital 12 Of Octubre I12 | Favaloro E.J.,Institute of Clinical Pathology and Medical Research ICPMR
Trends in Pharmacological Sciences | Year: 2016

Despite direct oral anticoagulants becoming a mainstay of anticoagulant therapy, the effective, timely, and safe reversal of their anticoagulant effect remains challenging. Emerging evidence attests that andexanet, a recombinant and inactive variant of native factor X (FXa), competitively inhibits and counteracts the anticoagulant effect of many inhibitors of native activated FXa. © 2016 Elsevier Ltd.

Cai L.,Peking University | Cai L.,Institute of Clinical Pathology and Medical Research ICPMR | Kong F.,Institute of Clinical Pathology and Medical Research ICPMR | Toi C.,Institute of Clinical Pathology and Medical Research ICPMR | And 2 more authors.
International Journal of STD and AIDS | Year: 2010

Lymphogranuloma venereum (LGV) is a sexually transmitted infection caused by Chlamydia trachomatis serovars L1, L2 and L3. Consequently, more specific and sensitive detection methods that are rapid and inexpensive are necessary to differentiate between C. trachomatis serovars. The purpose of this study was to identify and differentiate LGV-related C. trachomatis serovars from rectal swabs using high-resolution melting analysis (HRMA) and multiplex allele-specific polymerase chain reaction (MAS-PCR). Fifteen clinical samples from patients in Sydney were first screened and confirmed as C. trachomatis by using the COBAS®AMPLICOR PCR analyser. The same samples were assayed for C. trachomatis and LGV by HRMA and MAS-PCR of the polymorphic membrane protein H (pmpH) gene. Both methods indicated that two of 15 samples were serovar L2 and the remainder (13/15) other C. trachomatis serovars. Both HRMA and MAS-PCR are inexpensive, rapid, easy methods that are useful tools for the identification of LGV in clinical and research laboratories.

Zhuo F.,Peking University | Zhuo F.,Institute of Clinical Pathology and Medical Research ICPMR | Zhuo F.,Capital Medical University | Xiao M.,Peking University | And 5 more authors.
Clinical Microbiology and Infection | Year: 2011

The prevalence of the newly discovered pneumococcal serotype 6C has increased in some countries since the introduction of seven-valent conjugate pneumococcal vaccine (PCV7). The distribution of invasive serogroup 6 serotypes, in Australia, including 6C and 6D, has not been reported previously. During the period 1999 to 2008, 6097 isolates were referred to the New South Wales Pneumococcal Reference Laboratory for serotyping. Of these, 847 were identified by Quellung reaction as belonging to serogroup 6 and 702 were available for further study. Serotypes were determined by serotype-specific PCR as follows: 6A, 197 (28.1%); 6B, 452 (64.4%); 6C, 52 (7.4%) and one 6D. The average numbers of invasive serogroup 6 isolates, per annum, fell from 62.2 before (2000-2005) to 49.7 after (2006-2008) the introduction of PCV7. The proportions of invasive 6B fell (from 72.4% to 47.3%, p 0.03), those of 6C rose (from 3.3% to 17%, p 0.02) significantly and those of 6A remained fairly constant (24.3% vs 27%, p 0.69) between the two periods. All 6C and 6D and selected 6A and 6B isolates were further characterized by multilocus sequence typing and sequence analysis of cps genes cpsA-cpsB (wzg-wzh) and wchA-wciNbeta-wciO, wciP. Results showed considerable diversity within serotype 6C, apparently as a result of both mutation and recombination. Sequence typing indicates that, in Australia, 6C has been largely derived from 6A. The genetic diversity and rapid increase in incidence of serotype 6C causing invasive pneumococcal disease has potential implications for vaccine efficacy. © 2010 The Authors. Clinical Microbiology and Infection © 2010 European Society of Clinical Microbiology and Infectious Diseases.

Richards R.S.,Charles Sturt University | Nwose E.U.,Charles Sturt University | Nwose E.U.,Institute of Clinical Pathology and Medical Research ICPMR
British Journal of Biomedical Science | Year: 2010

Hyperglycaemia-induced oxidative stress is implicated as a cause of increased whole blood viscosity (WBV), which is a clinically modifiable risk factor for cardiovascular disease (CVD). However, whether or not there is variation in WBV at different stages of diabetes mellitus (DM) has yet to be confirmed. The sensitivity of underlying oxidative stress has also yet to be investigated. A total of 154 participants representing different stages of DM pathogenesis were selected for the study. Healthy control, prediabetes, DM and DM+CVD groups were compared for variation in WBV levels. The prevalence of oxidative stress, indicated by abnormal levels of erythrocyte glutathione, malondialdehyde and methaemoglobin, associated with high WBV was evaluated. The results showed a statistically significant difference in WBV between groups (P<0.03). The level of viscosity was significantly lower in the control group relative to the prediabetes group (P<0.01) and DM+CVD group (P<0.04). There was no statistically significant difference between the DM+CVD and prediabetes groups. Greater than 76% prevalence of oxidative stress was shown to be associated with high WBV, reaching 95% prevalence in prediabetes. The study showed that WBV varies between individuals with different stages of diabetic macrovascular pathogenesis, including prediabetes. Redefining the criteria for use of WBV on the basis of sensitivity to underlying oxidative stress, rather than specificity to a disease condition, means that this easily performed test is an option to consider in an all-inclusive laboratory approach to early intervention against future diabetic macrovascular complications. This is particularly important for individuals with subclinical hyperglycaemia.

Favaloro E.J.,Institute of Clinical Pathology and Medical Research ICPMR | Lippi G.,Academic Hospital of Parma
Seminars in Thrombosis and Hemostasis | Year: 2015

A new generation of antithrombotic agents has recently emerged. These provide direct inhibition of either thrombin (factor IIa [FIIa]) or FXa, and are increasingly replacing the classical anticoagulants (heparin and coumarins such as warfarin) in clinical practice for a variety of conditions. These agents have been designated several acronyms, including NOACs, DOACs, and TSOACs, respectively, referring to new (novel; non-vitamin K antagonist) oral anticoagulants, direct oral anticoagulants, and target-specific oral anticoagulants, and currently include dabigatran (FIIa inhibitor), and rivaroxaban, apixaban, edoxaban, and betrixaban (FXa inhibitors). The pervading mantra that NOACs do not require laboratory monitoring is countered by ongoing recognition that laboratory testing for drug effects is needed in many situations. Moreover, since these agents do not require laboratory monitoring, some clinicians inappropriately take this to mean that they do not affect hemostasis tests. This review aims to briefly review the laboratory studies that have evaluated the NOACs against a wide range of laboratory assays to assess utility for qualitative or quantitative measurements of these drugs, as well as interferences that may cause misdiagnosis of hemostatic defects. Point of care testing, including use of alternate samples such as urine and serum, is also under development but is not covered extensively in this review. The main aims of this article are to provide practical guidance to general laboratory testing for NOACs, as well as to help avoid diagnostic errors associated with hemostasis testing performed on samples from treated patients, as these currently comprise major challenges to hemostasis laboratories in the era of the NOACs. © 2015 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York.

Lippi G.,Academic Hospital of Parma | Tripodi A.,University of Milan | Tripodi A.,IRCCS Ca Granda Maggiore Hospital Foundation | Simundic A.-M.,University of Zagreb | Favaloro E.J.,Institute of Clinical Pathology and Medical Research ICPMR
Seminars in Thrombosis and Hemostasis | Year: 2015

D-dimer is the biochemical gold standard for diagnosing a variety of thrombotic disorders, but result reporting is heterogeneous in clinical laboratories. A specific five-item questionnaire was developed to gain a clear picture of the current standardization of D-dimer test results. The questionnaire was opened online (December 24, 2014-February 10, 2015) on the platform Google Drive (Google Inc., Mountain View; CA), and widely disseminated worldwide by newsletters and alerts. A total of 409 responses were obtained during the period of data capture, the largest of which were from Italy (136; 33%), Australia (55; 22%), Croatia (29; 7%), Serbia (26; 6%), and the United States (21; 5%). Most respondents belonged to laboratories in general hospitals (208; 51%), followed by laboratories in university hospitals (104; 26%), and the private sector (94; 23%). The majority of respondents (i.e., 246; 60%) indicated the use of fibrinogen equivalent unit for expressing D-dimer results, with significant heterogeneities across countries and health care settings. The highest prevalence of laboratories indicated they were using ng/mL (139; 34%), followed by mg/L (136; 33%), and μg/L (73; 18%), with significant heterogeneity across countries but not among different health care settings. Expectedly, the vast majority of laboratories (379; 93%) declared to be using a fixed cutoff rather than an age-adjusted threshold, with no significant heterogeneity across countries and health care settings. The results of this survey attest that at least 28 different combinations of measurement units are currently used to report D-dimer results worldwide, and this evidence underscores the urgent need for more effective international joined efforts aimed to promote a worldwide standardization of D-dimer results reporting. © 2015 by Thieme Medical Publishers, Inc.

Favaloro E.J.,Institute of Clinical Pathology and Medical Research ICPMR | Plebani M.,University of Padua | Lippi G.,Academic Hospital of Parma
Clinical Chemistry and Laboratory Medicine | Year: 2011

A revised framework for the regulation of in vitro diagnostic devices (IVDs) came into force in Australia on July 1, 2010 that aims to 'ensure that public and personal health are adequately protected', but which instead may lead to adverse outcomes in clinical diagnosis and management. The regulatory process aims to regulate all IVDs, including those used by clinical diagnostic laboratories, which are already subject to scrutiny as part of the current laboratory accreditation process. The IVD regulatory process initiated in Australia is similar to that used in Canada, but different to that currently operating in the USA and Europe. However, it is feasible that other countries will in time adopt a similar regulatory framework, given that many countries are involved in the development process. In this opinion paper, the regulatory process for IVDs across several geographies are outlined, as are some benefits and weaknesses of the new regulatory process now applied to Australia, as potentially planned for other regions of the world. © 2011 by Walter de Gruyter.

Wang B.,University of Sydney | Steain M.C.,University of Sydney | Dwyer D.E.,University of Sydney | Dwyer D.E.,Institute of Clinical Pathology and Medical Research ICPMR | And 2 more authors.
Virology Journal | Year: 2011

Background: Positive controls are an integral component of any sensitive molecular diagnostic tool, but this can be affected, if several mutations are being screened in a scenario of a pandemic or newly emerging disease where it can be difficult to acquire all the necessary positive controls from the host. This work describes the development of a synthetic oligo-cassette for positive controls for accurate and highly sensitive diagnosis of several mutations relevant to influenza virus drug resistance. Results: Using influenza antiviral drug resistance mutations as an example by employing the utility of synthetic paired long oligonucleotides containing complementary sequences at their 3' ends and utilizing the formation of oligonucleotide dimers and DNA polymerization, we generated ∼170bp dsDNA containing several known specific neuraminidase inhibitor (NAI) resistance mutations. These templates were further cloned and successfully applied as positive controls in downstream assays. Conclusion: This approach significantly improved the development of diagnosis of resistance mutations in terms of time, accuracy, efficiency and sensitivity, which are paramount to monitoring the emergence and spread of antiviral drug resistant influenza strains. Thus, this may have a significantly broader application in molecular diagnostics along with its application in rapid molecular testing of all relevant mutations in an event of pandemic. © 2011 Wang et al; licensee BioMed Central Ltd.

Chen X.,Capital Medical University | Kong F.,Institute of Clinical Pathology and Medical Research ICPMR | Wang Q.,Institute of Clinical Pathology and Medical Research ICPMR | Li C.,Capital Medical University | And 3 more authors.
Journal of Clinical Microbiology | Year: 2011

A high-resolution melting analysis (HRMA) assay was developed to detect isoniazid, rifampin, and ofloxacin resistance in Mycobacterium tuberculosis by targeting resistance-associated mutations in the katG, mabA-inhA promoter, rpoB, and gyrA genes. A set of 28 (17 drug-resistant and 11 fully susceptible) clinical M. tuberculosis isolates was selected for development and evaluation of HRMA. PCR amplicons from the katG, mabA-inhA promoter, rpoB, and gyrA genes of all 28 isolates were sequenced. HRMA results matched well with 18 mutations, identified by sequencing, in 17 drug-resistant isolates and the absence of mutations in 11 susceptible isolates. Among 87 additional isolates with known resistance phenotypes, HRMA identified katG and/or mabA-inhA promoter mutations in 66 of 69 (95.7%) isoniazid-resistant isolates, rpoB mutations in 51 of 54 (94.4%) rifampin-resistant isolates, and gyrA mutations in all of 41 (100%) ofloxacin-resistant isolates. All mutations within the HRMA primer target regions were detected as variant HRMA profiles. The corresponding specificities were 97.8%, 100%, and 98.6%, respectively. Most false-positive results were due to synonymous mutations, which did not affect susceptibility. HRMA is a rapid, sensitive method for detection of drug resistance in M. tuberculosis which could be used routinely for screening isolates in countries with a high prevalence of tuberculosis and drug resistance or in individual isolates when drug resistance is suspected. Copyright © 2011, American Society for Microbiology. All Rights Reserved.

PubMed | Institute of Clinical Pathology and Medical Research ICPMR
Type: Journal Article | Journal: North American journal of medical sciences | Year: 2012

Medical nutrition therapy (MNT) guidelines acknowledge the need to identify deficiencies of antioxidant vitamins. However, the guidelines contain that such identification is difficult. Thus, there is evidence that available clinical laboratory tests for antioxidant vitamins C and E are not in perspective in clinical practice. Coenzyme-Q(10) and glutathione tests are also available in research laboratories. These indices are invaluable tools for discrete recommendation and monitoring of antioxidant nutrition therapies. This commentary addresses biomarker insight to what the MNT guidelines consider difficult. The importance and limits of the various dietary antioxidants is overviewed. It puts in perspective how clinical laboratory monitoring of vitamins C and E levels can be used to optimize the outcomes of dietary evaluations for diabetes management. Insight to how to interpret the laboratory results is presented. The importance of this commentary is hinged on the premise that the outcome of dietary therapy can be counter-productive when laboratory evaluation or limitations of the antioxidant nutrients are undermined.

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