Displaying publications 1 - 20 of 37 in total

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  1. Cheng HM
    Autoimmunity, 1994;19(2):127-33.
    PMID: 7772702 DOI: 10.3109/08916939409009540
    Matched MeSH terms: Antiphospholipid Syndrome/blood; Antiphospholipid Syndrome/immunology
  2. Islam MA, Khandker SS, Alam F, Kamal MA, Gan SH
    Autoimmun Rev, 2018 Mar;17(3):226-243.
    PMID: 29355608 DOI: 10.1016/j.autrev.2017.10.014
    BACKGROUND: Antiphospholipid Syndrome (APS) is an autoimmune multifactorial disorder. Genetics is believed to play a contributory role in the pathogenesis of APS, especially in thrombosis development and pregnancy morbidity. In the last 20 years, extensive research on genetic contribution on APS indicates that APS is a polygenic disorder, where a number of genes are involved in the development of its clinical manifestations.

    AIMS: The aim of this systematic review is to evaluate the genetic risk factors in thrombotic primary APS. Additionally, to assess the common molecular functions, biological processes, pathways, interrelations with the gene encoded proteins and RNA-Seq-derived expression patterns over different organs of the associated genes via bioinformatic analyses.

    METHODS: Without restricting the year, a systematic search of English articles was conducted (up to 4th September 2017) using Web of Science, PubMed, Scopus, ScienceDirect and Google Scholar databases. Eligible studies were selected based on the inclusion criteria. Two researchers independently extracted the data from the included studies. Quality assessment of the included studies was carried out using a modified New-Castle Ottawa scale (NOS).

    RESULTS: From an initial search result of 2673 articles, 22 studies were included (1268 primary APS patients and 1649 healthy controls). Twenty-two genes were identified in which 16 were significantly associated with thrombosis in primary APS whereas six genes showed no significant association with thrombosis. Based on the NOS, 14 studies were of high quality while 6 were low quality studies. From the bioinformatic analyses, thrombin-activated receptor activity (q = 6.77 × 10-7), blood coagulation (q = 2.63 × 10-15), formation of fibrin clot (q = 9.76 × 10-10) were the top hit for molecular function, biological process and pathway categories, respectively. With the highest confidence interaction score of 0.900, all of the thrombosis-associated gene encoded proteins of APS were found to be interconnected except for two. Based on the pathway analysis, cumulatively all the genes affect haemostasis [false discovery rate (FDR) = 1.01 × 10-8] and the immune system [FDR = 9.93 × 10-2]. Gene expression analysis from RNA-Seq data revealed that almost all the genes were expressed in 32 different tissues in the human body.

    CONCLUSION: According to our systematic review, 16 genes contribute significantly in patients with thrombotic primary APS when compared with controls. Bioinformatic analyses of these genes revealed their molecular interconnectivity in protein levels largely by affecting blood coagulation and immune system. These genes are expressed in 32 different organs and may pose higher risk of developing thrombosis anywhere in the body of primary APS patients.
    Matched MeSH terms: Antiphospholipid Syndrome/genetics*; Antiphospholipid Syndrome/immunology
  3. Islam MA, Alam F, Wong KK
    Autoimmun Rev, 2017 May;16(5):512-522.
    PMID: 28279839 DOI: 10.1016/j.autrev.2017.03.005
    BACKGROUND: Antiphospholipid antibodies (aPLs) namely anticardiolipin (aCL) antibody, anti-β2-glycoprotein I (β2GPI) antibody and lupus anticoagulant (LA) are autoantibodies produced against anionic phospholipids and proteins on plasma membranes. Migraine is a primary headache disorder which has growing evidences of autoimmune-mediated pathogenesis and previous studies suggested the presence of aPLs in migraine patients.

    AIMS: The aim of this study was to evaluate the comorbid association between aPLs (aCL, anti-β2GPI and LA) and migraine compared to healthy controls.

    METHODS: Studies were searched through PubMed, ISI Web of Science and Google Scholar databases without restricting the languages and year (up to October 2016) and were selected based on the inclusion criteria. Two authors independently extracted data from the included studies. All analyses were conducted by using random effects model to calculate the odds ratio (OR) and 95% confidence interval (CI). Quality assessment was carried out by using the modified Newcastle-Ottawa Scale (NOS). Publication bias was evaluated via visualization of funnel plots, Begg's and Egger's tests.

    RESULTS: The database searches produced 1995 articles, 13 of which were selected (912 migraineurs and 822 healthy controls). 8.59%, 15.21% and 4.11% of the migraineurs exhibited aCL, anti-β2GPI and LA which was 4.83, 1.63 and 3.03 times higher, respectively, than healthy controls. A significant presence of aCL (OR: 3.55, 95% CI: 1.59-7.95; p=0.002) or anti-β2GPI antibodies (OR: 2.02, 95% CI: 1.20-3.42; p=0.008) was observed in migraine patients, however, LA was not significantly associated (OR: 2.02, 95% CI: 0.50-8.37; p=0.320). Majority of the studies (n=10 of 13) demonstrated NOS score of 7 or above and no significant publication bias was observed.

    CONCLUSION: Migraine might be an autoimmune-associated neurologic disorder. The presence of aCL or anti-β2GPI antibodies was significant in migraine patients compared to healthy controls, suggesting an involvement of these autoantibodies in migraine attack.
    Matched MeSH terms: Antiphospholipid Syndrome/complications*; Antiphospholipid Syndrome/immunology
  4. Islam MA, Alam F, Kamal MA, Wong KK, Sasongko TH, Gan SH
    CNS Neurol Disord Drug Targets, 2016;15(10):1253-1265.
    PMID: 27658514 DOI: 10.2174/1871527315666160920122750
    Neurological manifestations or disorders associated with the central nervous system are among the most common and important clinical characteristics of antiphospholipid syndrome (APS). Although in the most recently updated (2006) APS classification criteria, the neurological manifestations encompass only transient ischemic attack and stroke, diverse 'non-criteria' neurological disorders or manifestations (i.e., headache, migraine, bipolar disorder, transverse myelitis, dementia, chorea, epileptic seizures, multiple sclerosis, psychosis, cognitive impairment, Tourette's syndrome, parkinsonism, dystonia, transient global amnesia, obsessive compulsive disorder and leukoencephalopathy) have been observed in APS patients. To date, the underlying mechanisms responsible for these abnormal neurological manifestations in APS remain unclear. In vivo experiments and human observational studies indicate the involvement of thrombotic events and/or high titers of antiphospholipid antibodies in the neuro-pathogenic cascade of APS. Although different types of neurologic manifestations in APS patients have successfully been treated with therapies involving anti-thrombotic regimens (i.e., anticoagulants and/or platelet antiaggregants), antineuralgic drugs (i.e., antidepressants, antipsychotics and antiepileptics) and immunosuppressive drugs alone or in combination, evidence-based guidelines for the management of the neurologic manifestations of APS remain unavailable. Therefore, further experimental, clinical and retrospective studies with larger patient cohorts are warranted to elucidate the pathogenic linkage between APS and the central nervous system in addition to randomized controlled trials to facilitate the discovery of appropriate medications for the 'non-criteria' neurologic manifestations of APS.
    Matched MeSH terms: Antiphospholipid Syndrome/complications*; Antiphospholipid Syndrome/immunology
  5. Neoh KK, Tang ASN, Looi I, Anita BM
    Case Rep Nephrol, 2020;2020:8828864.
    PMID: 33294240 DOI: 10.1155/2020/8828864
    We report a case of a 21-year-old man with underlying nephrotic syndrome (NS) secondary to minimal change disease, who developed an ischemic stroke with left hemiparesis. He received intravenous thrombolysis followed by a mechanical thrombectomy. After mechanical thrombectomy, he developed acute kidney injury which subsequently required haemodialysis. Further workup revealed that he had concomitant antiphospholipid syndrome (APS) and NS. He was started on vitamin K antagonist anticoagulant. This case report illustrates the importance of workup in identifying causes of ischemic stroke in a young patient.
    Matched MeSH terms: Antiphospholipid Syndrome
  6. Islam MA, Alam F, Gan SH, Cavestro C, Wong KK
    Cephalalgia, 2018 03;38(3):568-580.
    PMID: 28952322 DOI: 10.1177/0333102417694881
    Background The occurrence of antiphospholipid antibodies (aPLs) and headache comorbidity in the presence or absence of underlying autoimmune diseases remains unclear. Aim The aim of this review was to summarize the relationship between headache and aPLs based on evidences from cohort studies and case reports, in addition to examining the treatment strategies that resolved headache in aPLs-positive individuals.
    Methods A comprehensive literature search was conducted through PubMed, ISI Web of Science and Google Scholar. A total of 559 articles were screened and the appropriate articles were selected based on quality and level of evidence.
    Results Cohort studies (n = 27) from Europe, North America and Asia demonstrated comorbidity of aPLs and headache in antiphospholipid syndrome, systemic lupus erythematosus (SLE) and neuropsychiatric SLE patients. Significantly higher association between migraine and aPLs was observed (n = 170/779; p 
    Matched MeSH terms: Antiphospholipid Syndrome/epidemiology
  7. Ng HK, Chong MF, Azhany Y, Zunaina E
    Clin Ophthalmol, 2014;8:2359-63.
    PMID: 25473262 DOI: 10.2147/OPTH.S71712
    Systemic lupus erythematosus (SLE) is a chronic, multisystem, autoimmune disease that can affect any part of the human body including the eyes. Common blinding ocular manifestations include central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), severe vaso-occlusive retinopathy, and optic nerve involvement. Antiphospholipid syndrome (APS) in lupus is usually associated with large vessel occlusions and needs prompt treatment with anticoagulant. We are reporting two cases of APS in SLE patients that presented with CRVO (case 1) and vaso-occlusive lupus retinopathy (case 2). Both cases were positive for antiphospholipid antibody (APA) and were treated with immunosuppression, anticoagulant, and laser treatment. Thus, screening for APA is vital in SLE patients with lupus retinopathy, as prompt treatment with anticoagulants is important to prevent further vascular thrombosis, which worsens the visual prognosis.
    Study site: Ophthalmology clinic, Hospital Raja Permaisuri Bainun, Ipoh, Perak, Malaysia
    Matched MeSH terms: Antiphospholipid Syndrome
  8. Teh CL, Leong TS
    Clin Rheumatol, 2015 Jan;34(1):175-8.
    PMID: 24831689 DOI: 10.1007/s10067-014-2671-6
    We performed a cross-sectional study of all antiphospholipid syndrome (APS) patients during an 8-year period (2006-2013) to describe the clinical features, serology profiles, treatment regimes, and outcomes in our center. There were a total of 59 patients in our study with the female to male ratio of 9:1. They have a mean age of 41.6 ± 12.1 years and a mean duration of illness of 38.4 ± 68.5 months. The majority of patients presented with vascular thrombosis (69.5 %) with equal arterial and venous involvements. Twenty-six patients (44.1 %) presented with obstetric complications with recurrent abortions (32.2 %) as the main manifestation. Most patients were on daily warfarin doses of 2-6 mg (91.0 %) with target INR of 2-3. There was neither recurrent thrombosis nor bleeding complications documented. There were 80 % live births following treatment in our patients.
    Matched MeSH terms: Antiphospholipid Syndrome*; Antiphospholipid Syndrome/blood; Antiphospholipid Syndrome/complications; Antiphospholipid Syndrome/diagnosis*
  9. Ong SG, Cheng HM, Soon SC, Goh E, Chow SK, Yeap SS
    Clin Rheumatol, 2002 Sep;21(5):382-5.
    PMID: 12223986 DOI: 10.1007/s100670200102
    The aim of this study was to investigate the incidence of IgG anticardiolipin antibody (ACL) and IgG anti-beta(2) glycoprotein I antibody (anti-beta2GPI) positivity in patients with primary or secondary antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE), to assess the association between IgG ACL and anti-beta2GPI, and the relationship between the presence of ACL and anti-beta2GPI with the clinical manifestations of APS. IgG ACL and IgG anti-beta2GPI levels were measured in 51 SLE patients, 20 patients with SLE and APS (secondary APS) and 11 primary APS patients using commercially available ELISA kits. Relationships between laboratory data and clinical manifestations of the patients were examined. The incidence of IgG ACL positivity was significantly higher in primary (36.4%) and secondary (40%) APS than in SLE (13.7%) patients (P = 0.02). The incidence of IgG anti-beta2GPI positivity was significantly higher in primary (54.5%) and secondary (35%) APS than in SLE (7.8%) patients (P = 0.0006). Mean levels of IgG ACL and anti-beta2GPI were significantly higher in the primary and secondary APS than in the SLE patients (P = 0.002 for both). A significant relationship was found between IgG ACL and IgG anti-beta2GPI (P = 0.01, R(2) = 0.56). There was a significant correlation between the presence of IgG ACL and a history of thrombosis in the combined primary and secondary APS group, but not in SLE patients. In conclusion, in this study IgG ACL and IgG anti-beta2GPI are closely related and mean levels of IgG ACL and IgG anti-beta2GPI are higher in patients with either primary or secondary APS than in SLE patients.
    Study site: Rheumatology Clinic, University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Antiphospholipid Syndrome/diagnosis; Antiphospholipid Syndrome/immunology*; Antiphospholipid Syndrome/epidemiology
  10. Sugai S
    Curr Opin Rheumatol, 1992 Oct;4(5):666-71.
    PMID: 1419500
    Over the past year, many reports have been published on a variety of clinical manifestations related to antiphospholipid antibodies. The low prevalence of anticardiolipin antibodies with the rare occurrence of thrombosis and a low rate of fetal loss in studies in Malaysia and China showed a potential role for local factors. A study of cross-reactive idiotype of the anticardiolipin antibody suggested that anticardiolipin antibodies are derived from a set of natural autoreactive clones. Regarding the pathogenic role of the antiphospholipid antibody, evidence has been presented that the epitopes formed between cardiolipin and beta 2 glycoprotein I are the targets of the antiphospholipid antibody. Complement activation, abnormalities of natural anticoagulants such as protein S deficiency, and genetic association with DR4, DR7, and DRw53 have also been studied.
    Matched MeSH terms: Antiphospholipid Syndrome/etiology; Antiphospholipid Syndrome/immunology*
  11. Islam MA, Alam F, Sasongko TH, Gan SH
    Curr Pharm Des, 2016;22(28):4451-69.
    PMID: 27229722
    Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by a persistently high titer of antiphospholipid antibodies (aPLs). In addition to pregnancy morbidity, arterial and/or venous thrombosis is another clinical feature of APS. Regardless of the type of APS, the thrombi formed by the induction of aPLs can lead to deep vein thrombosis, pulmonary embolism, myocardial infarction, stroke and gangrene. Although the concept of APS was introduced approximately 32 years ago, its thrombogenic pathophysiology is still unclear. Therefore, patients are treated with anticoagulant and/or antiplatelet regimens just as in other thrombotic disorders even though the thrombotic pathophysiology is mainly aPLs-mediated. In this review, we provided an update of the cellular, auto-immune and genetic factors known to play important roles in the generation of thrombi. Current successful regimens are also outlined along with potential emerging treatment strategies that may lead to the optimum management of thrombotic APS patients.
    Matched MeSH terms: Antiphospholipid Syndrome/drug therapy*; Antiphospholipid Syndrome/physiopathology
  12. Giemza-Stokłosa J, Islam MA, Kotyla PJ
    Curr Pharm Des, 2019;25(27):2909-2918.
    PMID: 31686632 DOI: 10.2174/1381612825666190709202804
    BACKGROUND: Ferritin is a molecule that plays many roles being the storage for iron, signalling molecule, and modulator of the immune response.

    METHODS: Different electronic databases were searched in a non-systematic way to find out the literature of interest.

    RESULTS: The level of ferritin rises in many inflammatory conditions including autoimmune disorders. However, in four inflammatory diseases (i.e., adult-onset Still's diseases, macrophage activation syndrome, catastrophic antiphospholipid syndrome, and sepsis), high levels of ferritin are observed suggesting it as a remarkable biomarker and pathological involvement in these diseases. Acting as an acute phase reactant, ferritin is also involved in the cytokine-associated modulator of the immune response as well as a regulator of cytokine synthesis and release which are responsible for the inflammatory storm.

    CONCLUSION: This review article presents updated information on the role of ferritin in inflammatory and autoimmune diseases with an emphasis on hyperferritinaemic syndrome.

    Matched MeSH terms: Antiphospholipid Syndrome/blood
  13. Islam MA, Alam F, Wong KK, Kamal MA, Gan SH
    Curr Vasc Pharmacol, 2017;15(4):313-326.
    PMID: 28056758 DOI: 10.2174/1570161115666170105120931
    Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombosis and/or pregnancy morbidity with persistent levels of antiphospholipid antibodies (aPLs). The development of thrombosis in APS is mediated by aPLs and contributes to the high mortality rate in APS patients. However, although APS has been reported for more than 30 years, there has been no optimal regimen for its prevention or for the management of thrombosis, mainly because the mainstay treatment strategies for managing APS are not targeted towards aPL-mediated thrombotic pathophysiology. Instead, the treatments commonly used are aimed at general thrombotic disorders. Warfarin is the most commonly used vitamin K antagonist (VKA), in addition to anti-platelet medications, such as aspirin and clopidogrel. Over the last decade, novel non-VKA oral anticoagulants, including rivaroxaban, apixaban and dabigatran, as well as immunomodulatory agents, such as rituximab, eculizumab, hydroxychloroquine, statins and sirolimus, have also been used. In this review, we discuss the current treatment strategies and future treatment outlook for thrombotic APS.
    Matched MeSH terms: Antiphospholipid Syndrome/blood*; Antiphospholipid Syndrome/complications; Antiphospholipid Syndrome/drug therapy*
  14. Islam MA, Wong KK, Sasongko TH, Gan SH, Wong JS
    Eur J Rheumatol, 2016 Sep;3(3):139-141.
    PMID: 27733946 DOI: 10.5152/eurjrheum.2015.0068
    Here we present a case report of three familial primary antiphospholipid syndrome (PAPS) patients from Malaysia. The three familial patients comprised two females and one male with a mean age of 26.3 years. The first diagnosis was made between 2005 and 2009, and all patients demonstrated deep vein thrombosis, high levels of IgM and IgG anticardiolipin antibodies, and received warfarin treatment international normalized ratio (INR) 2.0-3.0. The patients ceased to show clinical symptoms after treatment. Recently (August 2014), we investigated whether the levels of antiphospholipid antibodies remained elevated, and we found that seronegativity occurred in the patients. We suspect that prolonged anticoagulant treatment might be one of the causes of reduced levels of antiphospholipid antibodies in these familial PAPS patients.
    Matched MeSH terms: Antiphospholipid Syndrome*
  15. Islam MA, Alam F, Kamal MA, Gan SH, Sasongko TH, Wong KK
    PMID: 28824414 DOI: 10.3389/fnagi.2017.00250
    Growing evidences are supporting towards the involvement of antiphospholipid antibodies [aPLs e.g., lupus anticoagulant (LA), anticardiolipin (aCL) and anti-β2-glycoprotein I (anti-β2-GPI) antibodies] in various neurological manifestations including migraine, epilepsy and dementia in the presence or absence of autoimmune diseases such as antiphospholipid syndrome or systemic lupus erythematosus. The aim of this systematic review and meta-analysis was to assess the presence of aPLs in dementia patients without a diagnosis of any autoimmune disease. Electronic databases (e.g., PubMed, Web of Science, Scopus, ScienceDirect and Google Scholar) were searched without any year or language restrictions and based on the inclusion criteria, nine prospective case-control studies assessing only aCL were included involving 372 dementia patients and 337 healthy controls. No studies were found to assess the presence of both LA or anti-β2-GPI. The study-specific odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using random-effects model. We observed the prevalence of aCL in dementia was higher (32.80%) than that of controls (9.50%) e.g., 3.45 times higher risk of presenting with dementia than the controls, and significant presence of aCL antibodies was detected in dementia patients compared to controls (OR: 4.94, 95% CI: 2.66 - 9.16, p < 0.00001; I2 = 32%, p = 0.16). Publication bias was not observed from Egger's (p = 0.081) and Begg's tests (p = 0.180). Based on the study quality assessment using modified Newcastle-Ottawa Scale for case-control studies, seven of nine studies were of high methodological quality scoring ≥ 7 (median value). In summary, aCL antibodies were significantly present in dementia patients suggesting that aCL antibodies are generated due to the autoimmune-derived effects of dementia or there might be a potential causative role of this autoantibody in dementia pathogenesis.
    Matched MeSH terms: Antiphospholipid Syndrome*
  16. Baig MA, Swamy KB
    Indian J Pathol Microbiol, 2021 1 13;64(1):123-127.
    PMID: 33433421 DOI: 10.4103/IJPM.IJPM_900_19
    Background: In the laboratory, factor VIII can be measured by three different methodologies, such as one-stage clotting assay, two-stage clotting assay, and chromogenic assay. These assays differ in ease of use, variety of reagents available, sensitivity to mild hemophilia A, and interference from lupus anticoagulants (LACs). Certain factor VIII gene mutations can cause discrepancy in results between one-stage activated partial thromboplastin time (APTT) and chromogenic assays.

    Materials and Methods: The coagulometer for factor VIII assay is Sysmex CS-5100. All data were expressed as mean ± standard deviation (SD).

    Results: A total of 135 cases were studied. Of these, 100 cases were of mild hemophilia A diagnosed by molecular genetics and, 15 cases were positive for LAC, which were confirmed by dilute Russell Viper venom test. Clot-based one-stage APTT assay showed 65% sensitivity and 80% specificity in diagnosing mild hemophilia A cases and out of 15 LAC cases, it showed false positivity in five cases. Chromogenic assay showed 85% sensitivity and 90% specificity in diagnosing mild hemophilia cases and was 100% specific in excluding LAC cases.

    Conclusions: One-stage APTT assay is the most commonly used test for determining factor VIII levels but chromogenic assay are considered as the gold standard and recommended as the reference method by European Pharmacopoeia and ISTH subcommittee. Mild hemophilia A patients with missense mutations show discrepancy between the one-stage clot-based APTT assay and chromogenic assays for determination of factor VIII level and this can lead to misdiagnosis or misclassification of mild hemophilia A. Therefore, it is recommended that both the assays should be used in the evaluation of mild hemophilia cases.

    Matched MeSH terms: Antiphospholipid Syndrome
  17. Wan Ali WASR, Mohd Shahrir MS, Hussein H
    MyJurnal
    A 35-year-old Jordanian gentleman presented with worsening right iliac fossa pain of three-day durations with vomiting, loose stool and intermittent fever. He later underwent laparoscopic surgery, which was subsequently converted to open laparotomy. Intraoperatively, there was thickened bowel with multiple mesenteric lymph nodes, and also thrombosis of the small bowel vein supplying the affected bowel lesion, the diagnosis which was later confi rmed with the histopathological report. Resection with end-to-end anastomosis was done during the surgery. Within one-week post laparotomy, he developed another progressive abdominal pain and distension, vomiting and no bowel opening. He was sent for another exploratory laparotomy. Intraoperatively, there was a gangrenous small bowel segment measuring 130 cm, with an intact large bowel and previous anastomotic site. Resection of 150 cm of the small bowel was subsequently done.
    Matched MeSH terms: Antiphospholipid Syndrome*
  18. Kotyla PJ, Islam MA
    Int J Mol Sci, 2020 Mar 18;21(6).
    PMID: 32197340 DOI: 10.3390/ijms21062076
    MicroRNAs (miRNAs) are single-stranded, endogenous RNA molecules that play a significant role in the regulation of gene expression as well as cell development, differentiation, and function. Recent data suggest that these small molecules are responsible for the regulation of immune responses. Therefore, they may act as potent modulators of the immune system and play an important role in the development of several autoimmune diseases. Antiphospholipid syndrome (APS) is an autoimmune systemic disease characterized by venous and/or arterial thromboses and/or recurrent fetal losses in the presence of antiphospholipid antibodies (aPLs). Several lines of evidence suggest that like other autoimmune disorders, miRNAs are deeply involved in the pathogenesis of APS, interacting with the function of innate and adaptive immune responses. In this review, we characterize miRNAs in the light of having a functional role in the immune system and autoimmune responses focusing on APS. In addition, we also discuss miRNAs as potential biomarkers and target molecules in treating APS.
    Matched MeSH terms: Antiphospholipid Syndrome/immunology*; Antiphospholipid Syndrome/pathology
  19. Le Ho Y, Ahmad Zaidi NA, Salleh A, Abdul Kareem BA
    J Cardiothorac Surg, 2021 Apr 17;16(1):92.
    PMID: 33865405 DOI: 10.1186/s13019-021-01458-2
    BACKGROUND: Antiphospholipid syndrome is an antibody mediated pro-thrombotic state leading to various arterial and venous thromboses. The syndrome can be either primary or secondary to other autoimmune diseases, commonly systemic lupus erythematosus. Cardiac involvement, in particular valvular disease is common in patients with antiphospholipid syndrome, occurring in about a third of these patients. Valvular diseases associated with antiphospholipid syndrome often occur as valve thickening and non-bacterial vegetation or Libman-Sacks endocarditis. Deposits of antiphospholipid immunoglobulin and complement components are commonly observed in the affected valves, suggesting an inflammatory process resulting in valvular vegetation and thickening. Libman-Sacks endocarditis has a high propensity towards mitral valve, although haemodynamically significant valvular dysfunction is rare.

    CASE PRESENTATION: We present a successful aortic valve replacement with cardiopulmonary bypass in a 48 years old lady with antiphospholipid syndrome, who has severe aortic regurgitation as a result of Libman-sacks endocarditis. Antiphospholipid antibodies were positive and the clinical data showed both negative cultures and infective parameters. Surgically resected vegetations revealed sterile fibrinous and verrucous vegetations on aortic valve. Valve replacement and the course of cardiopulmonary bypass was uneventful, and the patient was discharged well.

    CONCLUSIONS: Classically Libman-Sacks endocarditis is often and more commonly associated with autoimmune diseases such as systemic lupus erythematosus, although it can occur in both primary and secondary antiphospholipid syndrome. It is not a common entity, and it is a frequent underestimated disease as most clinicians do not routinely screen for valvular lesion in patients with antiphospholipid syndrome unless they are symptomatic. However, due to its high prevalence of cardiac involvement, clinicians should have a high index of suspicion in the attempt to minimize cardiovascular and haemodynamic complications. Valve surgery in patients with antiphospholipid syndrome carries considerable early and late morbidity and mortality, usually caused by thromboembolic and bleeding events. The perioperative anticoagulation management and haemostatic aspect of antiphospholipid syndrome present an exceptional challenges to clinicians, surgeons, anaesthetists and laboratory personnel.

    Matched MeSH terms: Antiphospholipid Syndrome/complications*
  20. Shaharir SS, Ghafor AH, Said MS, Kong NC
    Lupus, 2014 Apr;23(4):436-42.
    PMID: 24399814 DOI: 10.1177/0961203313518624
    INTRODUCTION: Renal involvement is the most common serious complication in patients with systemic lupus erythematosus (SLE).
    OBJECTIVE: The objective of this article is to investigate and determine the associated factors of disease damage among lupus nephritis (LN) patients.
    METHODS: Medical records of LN patients who attended regular follow-up for at least one year in the Nephrology/SLE Clinic, Universiti Kebangsaan Malaysia Medical Centre (UKMMC), were reviewed. Their Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index scores were noted. Univariate analysis and multivariable regression analysis were performed to determine the independent factors of disease damage in LN.
    RESULTS: A total of 150 patients were included and their follow-up duration ranged from one to 20 years. Sixty (40%) LN patients had disease damage (SDI ≥1). In the univariate analysis, it was associated with age, longer disease duration, antiphospholipid syndrome (APS), higher maximum daily oral prednisolone dose (mg/day), lower mean C3 and C4, higher chronicity index and global sclerosis on renal biopsies (p < 0.05). Patients who received early (≤3 months after the SLE diagnosis) hydroxychloroquine (HCQ), optimum HCQ dose at 6.5 mg/kg/day and achieved early complete remission (CR) were less likely to have disease damage (p < 0.05). After adjustment for age, gender, disease duration and severity, multivariable regression analysis revealed that a higher maximum daily dose of oral prednisolone was independently associated with disease damage while early HCQ and CR were associated with lower disease damage.
    CONCLUSION: Higher maximum daily prednisolone dose predicted disease damage whereas treatment with early HCQ and early CR had a protective role against disease damage.
    KEYWORDS: Antiphospholipid syndrome; lupus nephritis; systemic lupus erythematosus

    Study site: Nephrology/SLE Clinic, Pusat Perubatan Universiti Kebangsaan Malaysia (PPUKM)
    Matched MeSH terms: Antiphospholipid Syndrome/epidemiology*
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