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Biomedical subjects

M D Lockshin

Publications and source records attributed to M D Lockshin.

At least 37 records · Page 2Linked to original sources
PubMed2000

Ovulation induction and in vitro fertilization in systemic lupus erythematosus and antiphospholipid syndrome.

OBJECTIVE: During ovulation induction (OI), ovarian stimulation is accomplished by hormonal manipulation, which includes administration of gonadotropins, gonadotropin-releasing hormone agonists, follicle-stimulating hormone, and luteinizing hormone. In in vitro fertilization (IVF), progesterone is often added. Because of the possibility of hormone-associated flare or thrombosis, patients with systemic lupus erythematosus (SLE) and primary antiphospholipid syndrome (primary APS) undergoing OI/IVF are potentially at increased risk. The present study was conducted in order to assess this risk. METHODS: Nineteen women who underwent 68 cycles of OI/IVF were studied by interview and retrospective chart review. RESULTS: Four OI/IVF cycles (25%) in SLE patients resulted in increased lupus activity and 2 (13%) in ovarian hyperstimulation syndrome. One patient with primary APS who was given heparin during multiple cycles developed osteopenia. No thrombosis occurred. Pregnancy complications included toxemia, lupus flare, gastrointestinal hemorrhage due to Mallory-Weiss tear, polygestation, and diabetes. Postpartum complications included nephritis flare, costochondritis, and suicidal depression. Lupus flares occurred at expected rates. Five of 16 cycles (31%) in 7 SLE patients, 5 of 48 cycles (10%) in 10 primary APS patients, and 0 of 5 cycles in 2 women with antiphospholipid antibody (without SLE or primary APS) resulted in liveborn children, including multiple gestations (3 twin sets with 4 surviving infants and 2 triplet sets with 3 surviving infants). Seven of 14 living children (50%) were premature, 3 had neonatal lupus, and 1 had pulmonic stenosis. Five surviving infants (38%) had complications unrelated to prematurity. CONCLUSION: Although OI/IVF can be successful in SLE and primary APS patients, rates of fetal and maternal complications are high.

Adult↗
PubMed2000

Future trends for treatment of APS.

Since the Sapporo Anti-phospholipid Antibody Conference we have learned much about the molecular and genetic biology of antiphospholipid antibody, its mechanisms of pathogenesis, detailed clinical descriptions of illness, including tests of criteria, definitions of subsets of disease, and early intimations about long-term prognosis. There has been wide application of known treatments but little testing of new ones. Rapid advances in the basic science of this illness gives us an opportunity to devise, test, and generally apply targeted biologic agents in order to prevent the short-term and long-term complications of this disease.

Antiphospholipid Syndrome↗
PubMed2000

Primary antiphospholipid syndrome: functional outcome after 10 years.

OBJECTIVE: To analyze the 10 year functional outcome of primary antiphospholipid syndrome (APS). METHODS: We identified 39 patients with primary APS (35 female, 4 male) who developed a first thrombotic or pregnancy event before 1990. Patients meeting American College of Rheumatology criteria for systemic lupus erythematosus or other connective tissue disorders (secondary APS) were excluded. Medical records were reviewed for detailed histories and functional outcomes. RESULTS: At 10 years' followup, 15 patients (38.4%) had organ damage in the form of hemiparesis (n = 8), dementia (n = 3), quadriplegia (n = 1), dilated cardiomyopathy-myocardial infarction (n = 1), vascular insufficiency-massive pulmonary infarction (n = 1), and endstage renal disease (n = 1). Eight patients (20.5%) with organ damage were unable to perform everyday activities important to their quality of life (functionally impaired). Causes of functional impairment were cognitive dysfunction (n = 3), cardiovascular disease (New York Heart Association Functional Classification Class IV) (n = 2), aphasia (n = 1), expressive aphasia (n = 1), and locked-in syndrome (n = 1). CONCLUSION: Functional prognosis is poor in an important minority of primary APS patients with > 10 years of disease. One-third of primary APS patients had organ damage and one-fifth were functionally impaired.

Antiphospholipid Syndrome↗
PubMed1999

Lupus anticoagulant-hypoprothrombinemia syndrome associated with systemic lupus erythematosus: report of 2 cases and review of literature.

We describe two patients whose initial presentation of systemic lupus erythematosus (SLE) was accompanied by haemorrhagic episodes and significant coagulopathy. Further investigation demonstrated positive lupus anticoagulant and decreased Factor II (prothrombin) activity. Both patients were diagnosed with lupus anticoagulant-hypoprothrombinemia syndrome (LAC-HPS) as a result of non-neutralizing antibodies directed against Factor II. LAC-HPS is a rare clinical entity that can occur in association with SLE, transient viral infections, drug reactions or even in healthy individuals. Mixing studies, which can be affected by other coagulation factor inhibitors, play an important role in the diagnosis of LAC-HPS. Factor VII level was decreased in the second patient, a finding that has not previously been reported in association with SLE. In both patients, bleeding stopped promptly and coagulation studies improved significantly with high dose corticosteroids. We discuss the pathogenesis, diagnosis and management of LAC-HPS in patients with SLE.

Adult↗
PubMed1998

Placental pathology in systemic lupus erythematosus: a prospective study.

OBJECTIVES: Systemic lupus erythematosus and antiphospholipid antibody, often identified in patients with systemic lupus erythematosus, are associated with poor pregnancy outcome. This study distinguishes between the effect of each of these factors on gestational outcome and placental pathologic conditions in pregnant patients with systemic lupus erythematosus. STUDY DESIGN: Thirty-seven pregnancies and 40 placentas from 33 women with systemic lupus erythematosus were studied prospectively. RESULTS: Systemic lupus erythematosus alone, but not systemic lupus erythematosus activity, was associated with increased spontaneous abortions, preterm gestations, and fetal growth restriction. Placental correlates were ischemic-hypoxic change, decidual vasculopathy, decidual and fetal thrombi, chronic villitis, and decreased placental weight. Extensive infarction and fetal death were important antiphospholipid antibody-related findings. CONCLUSIONS: Decidual vasculopathy/coagulopathy appears to mediate the antiphospholipid antibody-related and much of the systemic lupus erythematosus-related deleterious effect on the placenta and gestational outcome. The presence of antiphospholipid antibody largely, but not invariably, predicts fetal death. Antiphospholipid antibody-independent chronic villitis may represent a second mechanism of systemic lupus erythematosus-related change.

Adult↗
PubMed1998

Why do women have rheumatic disease?

If gonadal hormones are responsible for the female predominance (gender discrepancy, sexual dimorphism) that characterizes most autoimmune rheumatic diseases, pregnancy should be a particularly vulnerable period for onset of new disease as well as for exacerbation of established disease. Currently available data support neither the contention: that pregnancy increases incidence nor that it worsens severity of the common illnesses. Moreover, many illnesses pathogenetically similar to rheumatic diseases have the same hormonal background but are not characterized by sexual dimorphism. In nonrheumatic sexually dimorphic illnesses an environmental, behavioral, or genetic reason for gender discrepancy is usually present. To explain sexual dimorphism in the autoimmune rheumatic diseases, the fields of environmental, genetic, chromosomal, and in utero sex differentiation need further exploration.

Female↗
PubMed1998

Corticosteroids during pregnancy.

In pregnancy, pharmacokinetics of corticosteroids changes. Systemic corticosteroids are not teratogenic. Pregnant women receiving corticosteroid therapy suffer the same side effects and benefits as do treated women who are not pregnant. Clinical experience suggests no abnormalities of children of mothers treated with usual doses of prednisone and methylprednisolone throughout pregnancy, but premature rupture of amniotic membranes and low birthweight babies may occur. Betamethasone and dexamethasone are used to treat the fetus. The effect on the fetus of bolus doses of methylprednisolone is unknown. Very little corticosteroid ingested by the mother enters her breast milk. Corticosteroid therapy in pregnancy is appropriate to control clinically active maternal illness; to treat an in utero infant suffering from neonatal lupus-associated carditis; in stress doses (in corticosteroid-treated patients) for labor and delivery: and, pre-delivery, to induce fetal lung maturation.

Adrenal Cortex Hormones↗
PubMed1998

Pregnancy loss and antiphospholipid antibodies.

With the use of low-dose heparin, fetal survival of aPL pregnancies is 70-80%, but prematurity and intrauterine growth restriction are common. It is likely, but not proven, that dysregulated placental coagulation and resultant vasculopathy are the cause of fetal loss. Details of dysregulated coagulation remain to be described. Opportunities remain to determine the role of coagulopathy in repeated pregnancy loss, identify a critical event or window to which intervention might be directed, identify maternal (and fetal) characteristics other than aPL that determine fetal loss, describe toxicity profiles of current treatments, develop more specific, less toxic therapies, and describe long-term fetal and maternal outcomes.

Abortion, Habitual↗
PubMed1998

Why women?

This article examines common suppositions about the reasons for female predominance (gender discrepancy, sexual dimorphism) in the autoimmune rheumatic diseases. It suggests that estrogenic hormones are an insufficient explanation. Many illnesses similar to rheumatic diseases are not characterized by sexual dimorphism, nor by evident autoimmunity, yet the populations affected have the same hormonal background. In most other illnesses that are sexually dimorphic, an environmental, behavioral, or genetic reason is present. It is likely that rheumatic illnesses will have similar explanations. For the autoimmune rheumatic diseases, further work in the fields of environmental, genetic, chromosomal, and in utero sex differentiation is indicated.

Autoimmune Diseases↗
PubMed1997

Why women?

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Autoimmune Diseases↗