Platelet Function and Coagulation Profile in Lupus Erythematosus

Regan, Martha G.

doi:10.7326/0003-4819-81-4-462

Cited by 119 publications

(45 citation statements)

References 24 publications

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“…8 - 10 LAs prolong all phospholipid-dependent coagulation tests and appear to act by at least several mechanisms. 8 " 15 LAs have been associated with an increased incidence of systemic arterial and venous thrombotic events 8141617 in patients with and without systemic lupus erythematosus (SLE). 8141618 Ischemic cerebral arterial disease, both transient ischemic attacks (TIAs) and stroke, have been recently documented in association with LAs.…”

Section: Erebral Venous Thrombosis (Cvt) May Resultsmentioning

confidence: 99%

Cerebral venous thrombosis with lupus anticoagulants. Report of two cases.

Levine¹,

Kieran²,

Puzio³

et al. 1987

Stroke

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Section: Erebral Venous Thrombosis (Cvt) May Resultsmentioning

confidence: 99%

Cerebral venous thrombosis with lupus anticoagulants. Report of two cases.

Levine¹,

Kieran²,

Puzio³

et al. 1987

Stroke

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“…Since production of fibrinogen/fibrin degradation products generally depends on clotting followed by fibrinolysis, detection provides only an indirect estimate of clotting. Some investigators have also reported abnormal coagulation studies (23), while others have failed to find consistent changes (26). Since the FPA assay measures the initial alteration of the fibrinogen molecule in the clotting process and does not depend on depletion of clotting factors or the secondary release of fibrin degradation products, its application to studies of patients with SLE may directly define the rate of intravascular coagulation.…”

Section: Discussionmentioning

confidence: 99%

“…A drop of mixed methyl red indicator (15) was added, and the samples were titrated to neutrality by adding 10 N NaOH with a syringe microburet equipped with a finely pulled glass tip. Neutralization of the extract of a 2-ml plasma sample required [25][26][27][28][29][30] /Al of 10 N NaOH, and resulted in dilution of the sample by about 0.01 vol or less. The samples were heated to 500C in a water bath, then removed from the bath and placed under water aspirator vacuum until they began to boil.…”

Section: Methodsmentioning

confidence: 99%

Fibrinopeptide A in plasma of normal subjects and patients with disseminated intravascular coagulation and systemic lupus erythematosus.

Cronlund¹,

Hardin²,

Burton³

et al. 1976

J. Clin. Invest.

108

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A B S T R A C T A radioimmunoassay for fibrinopeptide A (FPA) has been developed. This assay uses rabbit antibodies induced by injection of native FPA-human serum albumin conjugates and 1"I introduced into tyrosine-FPA synthesized in our laboratory. Plasma FPA is separated from fibrinogen by TCA extraction. The assay is capable of detecting as little as 50 pg/ml of FPA.In 20 normal donors this assay revealed a mean concentration of 0.9 ng/ml (0.3 SD). In five patients with disseminated intravascular coagulation, FPA concentrations ranged from 13.0 to 346 ng/ml. Two groups of patients with systemic lupus erythematosus (SLE) whose disease had achieved complete remission were studied; one consisted of four patients with no history of lupus nephritis and another with a history of nephritis. Mean FPA concentrations of 1.5 ng/ml (range, 0.7-1.8 ng/ml) and 2.7 ng/ml (range, 1.1-5.6 ng/ml) were found in these two groups, respectively. Another group of nine patients with active SLE, but without evidence of lupus nephritis, had a mean FPA concentration of 4.5 ng/ml (range, 2.4-7.8 ng/ml). Finally, a group of seven patients with active SLE, including active nephritis, had a mean FPA concentration of 10.2 ng/ml (range, 5.3-17.0 ng/ml).A positive correlation was found between the concentration of plasma FPA and serum DNA-binding activity and an inverse correlation was found between plasma FPA and the concentration of serum C3. No correlation existed between plasma FPA and concentration of serum creatinine. Several possibilities for the origin of plasma FPA in patients with SLE were considered; at present it seems most likely that FPA arises through the action of thrombin on fibrinogen.

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“…and is usually due to an acquired platelet dysfunction. 11,12 Sometimes, it heralds a more serious complication, such as immune thrombocytopenia, or as in our patient, the presence of an acquired inhibitor to coagulation factors, commonly to factor VIII. Efforts to suppress such acquired inhibitors with immunosuppressive agents are often successful.…”

Section: Discussionmentioning

confidence: 99%

“…Platelet aggregation study showed slightly reduced aggregation response to all agonists, except ristocetin, which was almost normal, suggesting a mild acquired platelet dysfunction which is not uncommon in SLE. 11,12 Screening for von Willebrand disease was negative, the ristocetin co-factor (RiCoF) assay was 108% (normal 50-200) and platelet aggregation response to ristocetin was almost normal.…”

Section: Case Reportmentioning

confidence: 99%

Treatment of Acquired Factor VIII Inhibitor Associated with Childhood-Onset Systemic Lupus Erythematosus

Islam

Abdullah

1999

Ann Saudi Med

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Acquired inhibitors to factor VIII in non-hemophiliacs are rare, occurring in one of every five million individuals, and can lead to spontaneous hemorrhages.1 They may develop in association with collagen vascular diseases such as systemic lupus erythematosus (SLE), which accounts for only 6% of cases, in malignancy, with certain drugs, and during pregnancy.2 In nearly half of the patients, no underlying cause is apparent. 2 Significant bleeding, soft tissue hematoma and hemarthrosis are common complications, especially with strong inhibitors of more than 10 Bethesda units (BU)/mL.2,3 Treatment consists of active control of bleeding, using high-dose human factor VIII, activated prothrombin complex or porcine factor VIII concentrates, together with aggressive immunosuppression to eliminate the inhibitor. 3More recently, recombinant activated factor VII (rF-VIIa) has been used for the control of bleeding due to inhibitors in hemophiliacs, and was shown to be equally effective in bypassing the inhibitory action in the management of non-hemophiliacs. 4 Immunosuppression using cyclophosphamide (CYC) with or without corticosteroids is a well-established mode of treatment in the management of factor VIII inhibitors with severe bleeding complications. 5,6 Intravenous immunoglobulins (IVIG) were also reported to be successful in the management of acquired factor VIII inhibitor in SLE refractory to other modes of treatment. [7][8][9] We report the successful use of a combination of high-dose human factor VIII, CYC and prednisolone to eliminate factor VIII inhibitor in a patient suffering from documented childhood-onset SLE. Case ReportOur patient was a 16-year-old girl suffering from childhood-onset SLE. Her symptoms started at the age of eight years, and she fulfilled the revised criteria of the American College of Rheumatology for the classification of SLE.10 She had a long history of non-erosive polyarthritis, pleuritis, mouth ulcers and positive antinuclear antibodies (ANA). Titer at diagnosis was 1:1280 coarse speckled pattern. Our patient was initially treated with oral prednisolone. During a follow-up visit nearly eight years after the onset of symptoms, she reported easy bruising. Her only medication at the time was maintenance prednisolone 10 mg daily.Physical examination revealed multiple ecchymoses on the arms, legs and trunk, and slight gum bleeding. Her father had died many years previously from undetermined causes, but her mother, brothers and sisters were all well. The presence of SLE familial element was suspected because two other members of her family, her first-degree maternal cousins, were also suffering from childhood-onset SLE. Unfortunately, HLA phenotyping studies were not done. Her family reported that her two cousins who received follow-up in another hospital, also suffered from easy bruising. One of the cousins was an 11-year-old boy with cutaneous lupus (on topical Synalar 0.025% cream and Coppertone 15 sunscreen, and later, prednisolone 10 mg/day), and the other was his five-year-old sister, w...

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Platelet Function and Coagulation Profile in Lupus Erythematosus

Cited by 119 publications

References 24 publications

Cerebral venous thrombosis with lupus anticoagulants. Report of two cases.

Cerebral venous thrombosis with lupus anticoagulants. Report of two cases.

Fibrinopeptide A in plasma of normal subjects and patients with disseminated intravascular coagulation and systemic lupus erythematosus.

Treatment of Acquired Factor VIII Inhibitor Associated with Childhood-Onset Systemic Lupus Erythematosus

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