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Stroke
Published in Henry J. Woodford, Essential Geriatrics, 2022
In people aged under 50 with no clear vascular risk factors, especially those with personal or familial histories of thrombosis or rheumatoid arthritis/SLE, a thrombophilia screen (e.g. factor V Leiden, antithrombin III, proteins C and S, and antiphospholipid antibodies) may be considered. It is unclear whether thrombophilias that increase the risk of venous thrombosis also increase the risk of arterial stroke. Even if antiphospholipid syndrome is diagnosed, current guidance suggests a similar management strategy as for other people.6
The Immunobiology of Recurrent Miscarriage
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Marighoula Varla-Leftherioti, Theodora Keramitsoglou, Christina Tsekoura
Approximately 20% of women with recurrent pregnancy loss (RPL) have increased serum levels of autoantibodies, with antiphospholipid antibodies (aPL) predominating [1]. The etiology of the antiphospholipid syndrome is the subject of another chapter and will not be discussed here. Suffice to say, an aPL-related etiology should be suspected in women with ≥3 consecutive pre-embryonic or embryonic pregnancy losses or ≥1 unexplained fetal deaths above 10 weeks of gestation [3]. In women where an aPL-associated etiology is suspected, other autoantibodies may coexist. Such as antithyroid autoantibodies (ATA) (against thyroglobulin [TG] or thyroid peroxidase [TPO]) may be independent markers of “at-risk” pregnancy even with euthyroid status. It is possible that the high rate of miscarriage in the presence of ATA is related to very mild thyroid “underfunction,” with the thyroid gland being less able to adapt to the increased requirements of pregnancy; thus, these women might benefit from thyroid replacement therapy [4]. Furthermore, ATA may represent a generalized activation of the immune system. ATA have been found to coexist with activated T cells in the uterus and with non-organ-specific autoantibodies as well as with increased and hyperactive cytotoxic natural killer (NK) cells in RPL. Hence, treatment with intravenous immune globulin (IVIg), may neutralize the antibodies and also provide the required modulation of immune functioning [5].
Blood and hemostasis
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
A hypercoagulability condition caused by the formation of antibodies against negatively charged phospholipids. The mechanism of the disease process is uncertain, but the abnormal antibodies that are produced appear to activate the coagulation cascades. Symptoms include the recurrence of blood clots (deep vein thrombus, peripheral arterial thrombosis) and a significantly increased risk for stroke and miscarriage. A diagnosis of antiphospholipid syndrome is confirmed by the detection of abnormal antibodies in circulation. Treatment focuses mainly on the use of anticoagulant drugs such as warfarin and heparin.
Evaluation of neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio in pregnant women with systemic lupus erythematosus
Published in Journal of Obstetrics and Gynaecology, 2022
Huseyin Ekici, Metehan Imamoglu, Firat Okmen, Gizem Gencosman, Gunes Ak, Mete Ergenoglu
Foetal growth restriction was defined as birth weight <5th percentile of the normal growth curve. For the diagnosis of preeclampsia, hypertension is defined as a systolic blood pressure of ≥140 mmHg or diastolic blood pressure of ≥90 mmHg on two occasions that are at least four hours apart. The diagnostic criteria for preeclampsia include hypertension with proteinuria occurring at more than 20 weeks of gestation, while preeclampsia in the absence of proteinuria is diagnosed with a new onset of thrombocytopenia (<100,000 mm3), renal insufficiency (creatinine >1.1 mg/dl or more than double the baseline level), elevated liver function tests (ALT/AST >twice the upper limit), pulmonary oedema, cerebral or visual disturbance (ACOG 2020). Foetal loss was defined as foetal death after 22 weeks of gestation and premature birth (preterm) as live birth before 37 weeks of gestation. Diagnosis of antiphospholipid syndrome was established according to the updated Sapporo classification (Miyakis et al. 2006).
Acute portal vein thrombosis in noncirrhotic patients – different prognoses based on presence of inflammatory markers: a long-term multicenter retrospective analysis
Published in Scandinavian Journal of Gastroenterology, 2019
Radan Keil, Jana Koželuhová, Jiří Dolina, Aleš Hep, Radek Kroupa, Vladimír Kojecký, Tomáš Krejčí, Jan Havlín, Ivana Hadačová, Jitka Segethová, Petra Koptová, Zdena Zádorová, Jan Matouš, Barbora Frýbová, Petr Chmátal, Martin Wasserbauer, Jan Šťovíček, Melvin Bae, Tolga Guven, Mahmood Zaeem, Štěpán Hlava
The most commonly detected prothrombotic hematologic factor was a higher level of coagulation factor VIII. Values over 150% were considered pathological [3]. Elevation was found in 49 patients (62.8%). Significantly reduced antithrombin III was found in 27 patients (34.6%), and reduced levels of protein C and S were found in 39 (50.0%) and 36 patients (46.2%), respectively. A significantly elevated blood pellet count was found in 17 (21.8%) patients, four of them had essential thrombocytosis with JAK2 mutation positivity. Positivity for JAK2 was completely present in 10 patients (12.8%). Three patients (3.8%) had diagnosed primary myelofibrosis, 4 (5.1%) patients had essential thrombocytosis, and 3 (3.8%) patients had polycythemia vera. Polycythemia vera was diagnosed 4 years after thrombosis in one patient. Twelve patients (15.4%) had APC resistance or a factor V Leiden mutation. Three (9.4%) females (27, 35, and 54 years old) used hormonal contraception or hormonal substitution therapy. The youngest one was JAK2+ and had elevated factor VIII while the other two had no other risk factors. Antiphospholipid syndrome was excluded in all investigated patients. One patient was positive for anti-beta 2GPI antibodies.
A microvascular myocardial infarction in a 16-year-old girl with antiphospholipid syndrome: a case report
Published in Acta Clinica Belgica, 2019
Jean-Philippe Riga, Attilio Leone, Frédéric Lambot, Olivier Cappeliez, Alain Friart
Myocardial infarction with angiographically non-obstructive coronary disease (MINOCA) is a clinical entity with an average prevalence estimated at 6% of all myocardial infarctions [1]. Compared to infarction with pathological coronary arteries, there are more women [1,2], younger people, and less dyslipidemia among patients with MINOCA [3]. The pathophysiological mechanisms evoked are atherosclerosis, coronary spasm, distal embolization, Tako-Tsubo syndrome, myocarditis, prothrombotic state and hypercoagulability [1,3]. In patients with MINOCA screened for thrombophilia, this condition was found in 14% of patients, including resistance to activated C protein, factor V Leiden deficiency, C protein/S protein deficiency, and factor VII deficiency [1]. The relationship with antiphospholipid syndrome is less documented.