Background:The lupus anticoagulant (LA) is one of the antiphospholipid antibodies (aPL), which prolong phospholipid- dependent coagulation tests by interfering with coagulation reactions that depend on protein - phospholipid complexes in vitro.
Method:A 25 year old \'healthy\' male Nigerian was screened for the presence of any coagulation abnormality using the KCT, PT and platelet count; after volunteering for his plasma to be used in the preparation of normal pooled plasma in a study.
Results: He was discovered to have a prolonged KCT, PT and normal platelet count. Based on the prolonged KCT his plasma was subjected to mixing studies with various concentration of normal pooled plasma; the KCT index was calculated and a curve was plotted. His KCT index was 1.6 and the curve convex in the left axis suggesting the presence of LA. His past medical history and physical examination were not remarkable.Three months after the initial study, a repeat KCT index was 1.4 and the subject asymptomatic.
Conclusion: From literature review this is the first report of LA in an asymptomatic adult Nigerian; the importance of this finding is discussed.  African Health Sciences  Vol.  7 (3) 2007: pp. 182-18

Bazuaye, Godwin N

Olayemi, Edeghonghon E

PubMed

Olayemi, E E

Bazuaye, G N

AJOL - African Journals Online

African Health Sciences Vol 7 No 3 September 2007 182    Presence of lupus anticoagulant in an asymptomaticNigerian* Edeghonghon E. Olayemi, ** Godwin N. Bazuaye    *Department of Haematology and Blood Transfusion, OACHS, Olabisi Onabanjo, University, P.M.B. 2022, Sagamu, Ogun State.Nigeria, ** Department of Haematology and Blood Transfusion, University of Benin Teaching  Hospital, P.M.B.1111, Benin City, EdoState. NigeriaAbstractBackground: The lupus anticoagulant (LA) is one of the antiphospholipid antibodies (aPL), which prolong phospholipid- dependentcoagulation tests by interfering with coagulation reactions that depend on protein - phospholipid complexes in vitro.Method: A 25 year old ‘healthy’ male Nigerian was screened for the presence of any coagulation abnormality using the KCT, PT andplatelet count; after volunteering for his plasma to be used in the preparation of normal pooled plasma in a study.Results: He was discovered to have a prolonged KCT, PT and normal platelet count. Based on the prolonged KCT his plasma wassubjected to mixing studies with various concentration of normal pooled plasma; the KCT index was calculated and a curve wasplotted. His KCT index was 1.6 and the curve convex in the left axis suggesting the presence of LA. His past medical history andphysical examination were not remarkable. Three months after the initial study, a repeat KCT index was 1.4 and the subject asymptomatic.Conclusion: From literature review this is the first report of LA in an asymptomatic adult Nigerian; the importance of this finding isdiscussed.African Health Sciences 2007; 7(3): 182-184Correspondence author: Olayemi,Department of Haematology and Blood Transfusion, OACHS,Olabisi Onabanjo University, P.M.B. 2022,Sagamu, Ogun State. Nigeria.Email: yemiede@yahoo.comIntroductionThe lupus anticoagulant (LA) is one of theantiphospholipid antibodies (aPL), which prolongphospholipid- dependent coagulation tests by interferingwith  coagulation reactions which depend on protein -phospholipid complexes in vitro1 ; isotypes includeimmunoglobulin G (IgG), immunoglobulin M (IgM),immunoglobulin A (IgA) or combinations of these 2.The presence of the lupus anticoagulant hasbeen associated with certain clinical                             ma-nifestations such as recurrent abortions, arterial andvenous thrombosis, and thrombocytopenia3. Cutaneoussymptoms of this syndrome include leg ulcers and livedoreticularis4. Neurological disorders such as dementia,epilepsy, chorea and migraine5 can also occur. The firstantiphospholipid antibody was detected in patients withsyphilis in 19066 while  the lupus anticoagulant (LA)was first described in 19527.The most commonly detectedantiphospholipid antibodies are lupus anticoagulant,anticardiolipin  and anti-beta 2 glycoprotein 1(â-2GP-1) antibodies1 . LA antibodies are identified by coagula-tion assays, in which they prolong clotting times whileanticardiolipin and anti â-2GP-1 antibodies are detectedby immunoassays that measure immunologic reactivityto a phospholipid or a phospholipid – binding protein.Current criteria for detection of LA antibodies includeprolongation of at least one phospholipid – dependentcoagulation assay1.KCT has been shown to have aspecificity  of up to 93% for LA 8 and it is able to detectLA at a much greater dilution in normal plasma than thetissue thromboplastin inhibition test (TTI) or the diluteRussell’s viper venom time (DRVVT )9. KCT is also moresensitive to the presence of LA than TTI10 .Case ReportO.U. a 25 year old male Nigerian who was a final yearstudent in one of the universities in the south-south geo-political zone of Nigeria; volunteered to have his plasmaused to prepare normal pooled plasma in a studyapproved by the University of Benin Teaching Hospitalethics committee.As a pre-condition to having his plasma pooledalong with those of other volunteers we had to carry outtests to ensure that he did not have any clottingabnormalities, this included  platelet count, prothrombintime (PT) and kaolin clotting time (KCT). It was duringthis that he was detected to have a prolonged KCT andslightly prolonged PT.On further investigation O.U has lived arelatively healthy life, there was neither any past historyof thrombosis nor family history of thrombosis, bothAfrican Health Sciences Vol 7 No 3 September 2007 183parents and all his siblings are alive and well. The patienthad not been previously transfused; he is not a knownepileptic neither has he ever suffered from migraineheadaches. He has never taken any drug such as phenytoinor chlorpromazine which have been associated with LA.On general examination he was a healthy youngman, he was not pale, was  afebrile and anicteric, he hadno lymphadenopathy, did not have any petechiae orechymotic spots. His chest was clinically clear, pulserate was 78/ minute, regular and of  good volume. Onlythe first and second heart sounds were present and hisblood pressure was 110/70 mmHg. No abdominalorgans were palpable. He had no neurological deficits.Method and ReultsKaolin clotting time (KCT) was performed asdescribed previously11,12 .The procedure was carried outin duplicates and the average was taken as the clottingtime.Due to the prolonged KCT, we decided to carryout mixing tests on his plasma using the KCT; in theTable 1: Results of Laboratory InvestigationsInvestigation ResultKCT 188 seconds (163 seconds)KCT Index 1.6 (1.4)PT 17 seconds (16.5 seconds)Packed cell volume 0.41 (0.43)Platelet count 300,000/mm3 ( 273,000/ mm3 )White blood cell count 5,300/mm3 ( 6,200/mm3 )ESR 12 mm/hour (Westergren)Direct antiglobulin test NegativeIndirect antiglobulin test NegativeHIV screen NegativeFigure in brackets is the repeat laboratory investigations after 3 monthsfollowing proportions of normal plasma (NP) andsubject’s plasma (SP). NP/SP: 100/0, 90/10, 80/20,50/50, 20/80, 10/90 and 0/100 as earlier described 12. he KCT index, which is the ratio of KCT at 20% subjectplasma to KCT at 100% normal plasma was thencalculated as shown below.KCT (80% Normal Plasma: 20% Subject’s Plasma)    = />1.2              KCT 100% Normal PlasmaA ratio of greater than or equal to 1.2 was taken to signifythe presence of  LA12. Normal KCT and PT in ourlaboratory is 60-110 seconds and 10 -14 secondsrespectively.  Results of laboratory investigations carriedout are shown in table 1. A graph of KCT of variousmixtures of SP in normal pooled plasma was also plotted,this curve was convex in the left axis, and in keepingwith earlier studies by Exner et al 11, such a shape issuggestive of the presence of LA ( Figure 1).FIGURE 1 KCT OF VARIOUS MIXTURES OF SUBJECT'S PLASMA IN NORMAL POOLED PLASMA0204060801001201401601800 20 40 60 80 100 120% PROLONGED SUBJECT'S PLASMA IN NORMAL POOLED PLASMAKCT (SECONDS)Series1African Health Sciences Vol 7 No 3 September 2007 184DiscussionLA is commonly associated with patients whohave systemic lupus erythematosus (SLE) and otherautoimmune disorders, though recently, it has beenshown that LA may be responsible or at least play asignificant role in recurrent foetal loss.LA and other aPL have been previouslydescribed in asymptomatic subjects from other parts ofthe world. In fact, it has been said that up to 2% of thenormal population may be positive for aPL and it is notknown what percentage of this would go on to developthrombosis or other signs and symptoms ofantiphospholipid syndrome (APS); though only about0.2% have high titres13.  Like other autoantibodies,prevalence increases with age14 .LA has been describedin children15 . In patients with SLE, the prevalence ofaPL is much higher, ranging from 12-30 % foranticardiolipin antibodies16 and 15-34 % for LA 16,17. Inour environment, LA has been described in women withpre-eclampsia 18; multiparous women 19, as well as insickle cell disease patients 20;  we believe that this is thefirst time LA is being reported in an asymptomatic maleNigerian.Patients may have laboratory evidence of aPLwithout clinical consequences 1. The presence of LA in ahealthy subject may lead to confusing results of theclotting profile as the presence of LA is known to becapable of prolonging the PT, APTT, KCT and othermeasures of haemostasis. Also it may lead to endless andoften expensive investigations in an attempt to uncoverthe presence of APS, SLE or other cause.  It is for thesereasons that we are reporting this case  to create awarenessof this possibility in our environment and save otherwisehealthy patients from unnecessary laboratory investiga-tions and anxiety.Three months after the subject was detected ashaving LA, his KCT was still prolonged with an index of1.4 (Table1). However he has remained healthy and hassince completed his tertiary education and is currentlyin paid employment.In conclusion, LA has been described in healthysubjects from other parts of the world we have herereported its presence in a healthy male Nigerian.References1.  Levine JS, Branch W, Rauch J. The antiphospholipid syn-drome. N Engl J Med .2002; 346:752-763.2. Westerman MP, Green D, Gilman-Sachs A. et al.Antiphospholipid antibodies, protein C and S, andcoagulation changes in sickle cell disease. J Lab Clin Med1999; 134: 352-362.3. Cuadrado MJ, Mujic F, Munoz E, Khamastha MA, HughesGR. Thrombocytopaenia in the antiphospholipid antibodysyndrome. Ann Rheum Dis 1997; 56:194-196.4. Miori L, Bellosta M, Miori E, Rabbiosi G. Clinical mani-festations associated with the presence of lupus anticoagu-lant. J Ital Dermatol Venereol. 1989; 124:107-110.5. Chapman J, Shoenfeld Y. Neurological and neuroendocrine-cytokine interrelationship in the antiphospholipid syn-drome. Ann N Y Acad Sci. 2002; 966:415-424.6. Wassermann A, Neisser A, Bruck C. Eine serodiagnosticheReaktion bei Syphilis. Deutsche Med Wochenschr 1906;32:745-746.7. Conley CL, Hartmann RI. A haemorrhagic disorder causedby circulating anticoagulant in patients with disseminatedlupus erythematosus. J Clin Invest. 1952; 31:62-62.8. Ferro D, Saliola M, Quintarelli C. et al. Methods fordetecting lupus anticoagulant and their relation tothrombosis and miscarriage in patients with systemic lu-pus erythematosus. J Clin Pathol. 1992; 45: 332-338.9. Exner T. Comparison of two simple tests for the lupusanticoagulant. Am J Clin Pathol. 1985; 83: 215-218.10. Lesperance B, David M, Rauch J, Infante-Rivard C, RivardGE. Relative sensitivity of different tests in the detectionof low titre lupus anticoagulant. Thromb Haemost. 1988;60: 217-219.11. Exner T, Rickard KA, Kronenberg H. A sensitive testdemonstrating lupus anticoagulant and its behavioural pat-terns. Br J Haematol 1978; 40:143-151.12. Laffan MA, Bradshaw A: Investigation of a thrombotictendency. In: Dacie JV, Lewis SM. Eds. PracticalHaematology, Ed.8: ChurchillLivingstoneEdinburgh1994:P. 351-354.13. Lockshin MD. Answers to the antiphospholipid – antibodysyndrome. N Engl J Med. 1995; 332:1025-1027.14. Petri M. Epidemiology of the antiphospholipid antibodysyndrome. J Autoimmun 2000; 15:145-151.15. Quintero-Del-Rio AL. Antiphospholipid antibodies inpaediatrics. Curr Rheumatol Rep.2002 Oct; 4: 387-91.16. Cervera R, Khamashta MA, Font J et al; Systemic lupuserythematosus: clinical and immunologic patterns of diseaseexpression in a cohort of 1,000 patients. Medicine (Balti-more) 1993; 72:113-124.17. Love PE, Santoro SA. Antiphospholipid antibodies:anticardiolipin and the lupus anticoagulant in systemic lu-pus erythematosus (SLE) and in non- SLE disorders:prevalence and clinical significance. Ann Intern Med 1990;112: 682-698.18. Awodu OA, Shokunbi WA, Ejele OA. Lupus anticoagulantin Nigerian women with preeclampsia. West Afr J Med2003; 22:240-242.19. Awodu OA, Ejele OA, Shokunbi WA, Enosolease ME.Prevalence of lupus anticoagulant in multiparous womenin Benin City. Niger Postgrad Med J 2003; 15: 145-151.20. Olayemi E, Halim NKD, Durosinmi MA, Awodu OA. Lu-pus anticoagulant in Nigerian children with homozygoussickle cell disease. Annals of African Medicine 2005; 3:122-126.

Presence of lupus anticoagulant in an asymptomatic Nigerian

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