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Biomedical subjects

M D Lockshin

Publications and source records attributed to M D Lockshin.

At least 91 records · Page 5Linked to original sources
PubMed1989

Pregnancy does not cause systemic lupus erythematosus to worsen.

To evaluate risk for exacerbation of systemic lupus erythematosus (SLE) during pregnancy, we prospectively evaluated 80 pregnant women with SLE for manifestations of disease activity. Fifty-three of these women were not taking prednisone at the time of conception. Disease activity was scored in 4 ways: global assessment, prednisone therapy, cumulative number of organ systems with abnormalities, and display of abnormalities of each organ system. No patient received prophylactic therapy to prevent disease exacerbation. Thrombocytopenia, proteinuria, and hypocomplementemia were the most common abnormalities and were usually attributable to the pregnancy complications of preeclampsia and anticardiolipin antibody syndrome rather than to SLE. If all possible abnormalities were attributed to SLE, disease exacerbation occurred in less than 25% of all patients; if only SLE-specific abnormalities were counted, disease exacerbation occurred in less than 13%. Worsening of SLE is uncommon in pregnancy, and prophylactic prednisone therapy is unnecessary.

Female↗
PubMed1989

Aortic insufficiency and mitral regurgitation in patients with systemic lupus erythematosus and the antiphospholipid syndrome.

PURPOSE, PATIENTS, AND METHODS: Heart disease has not been well characterized in patients with systemic lupus erythematosus (SLE) and the antiphospholipid syndrome. During a prospective study of cerebrovascular disease in autoimmune disease and SLE, 11 lupus patients were identified with an antiphospholipid syndrome characterized by significant cardiac valvular disease in addition to cerebral infarction, deep vein thromboses, and thrombocytopenia. Patients were reviewed for criteria for systemic lupus and underwent echocardiographic studies and measurements of anticardiolipin antibodies, VDRL, and the lupus anticoagulant. RESULTS: Eight of the 11 patients had aortic insufficiency, two of whom had associated mitral regurgitation. Three patients had mitral regurgitation alone. Microscopic analysis of a surgically excised aortic valve indicated typical Libman-Sacks verrucous endocarditis. Infective endocarditis was ruled out in all patients. CONCLUSION: This report expands previous descriptions of antiphospholipid syndromes by describing a subset of lupus patients with significant aortic and mitral valvulitis in addition to circulating antiphospholipid antibodies, thrombocytopenia, and recurrent thromboses.

Adult↗
PubMed1989

Prednisone does not prevent recurrent fetal death in women with antiphospholipid antibody.

Effects of therapy, antibody titer, and pregnancy history on pregnancy outcome were evaluated in pregnancies of women with antiphospholipid antibody. Prior fetal death and a high antiphospholipid antibody titer (greater than 40 IgG phospholipid units) contributed independently, in an additive manner, to current fetal loss. Twenty-one pregnancies occurred in asymptomatic women who had both prior fetal death and a high IgG antiphospholipid antibody titer. In this very high-risk group, 9 of 11 (82%) of pregnancies treated with prednisone, 10 to 60 mg/day, ended in fetal death, compared with 5 of 10 (50%) not treated with prednisone (p approximately 0.01, life-table analysis). Of pregnancies treated with aspirin, 80 mg/day, 9 of 14 (64%) treated and 5 of 7 (71%) not treated with prednisone had a fetal death (difference not significant). Prednisone does not improve, and may worsen, current fetal outcome in asymptomatic pregnant women with a high antiphospholipid antibody titer and prior fetal death.

Aspirin↗
PubMed1989

What is SLE?

Explore the source record for details and available documents.

Humans↗
PubMed1988

Neonatal lupus risk to newborns of mothers with systemic lupus erythematosus.

We prospectively studied 91 infants born to women with systemic lupus erythematosus (SLE) or with SLE-like disease. Thirty-eight infants, including 3 sets of twins, were born to women who had anti-Ro, anti-La, or anti-RNP antibodies. Four infants had definite neonatal lupus, and 4 had possible neonatal lupus. No prospectively studied infant had congenital heart block. The presence of neonatal lupus did not correlate with the titer of anti-Ro antibodies. During the same time period, 2 additional babies with neonatal lupus and congenital heart block were born to mothers not previously known to have SLE. Taken together, these findings confirm the association of anti-Ro antibody with neonatal lupus, but indicate that life-threatening neonatal lupus is rare in children born to mothers who are known to have SLE, even when antibodies to Ro, La, or RNP are present. Prophylactic therapy is therefore not indicated for these women. An important proportion of mothers bearing children with neonatal lupus do not have recognized SLE and, currently, cannot be prospectively identified.

Antibodies↗
PubMed1988

IgG but not IgM anti-phospholipid antibody binding is temperature dependent.

We examined the effect of temperature on the measurement of enzyme-linked immunosorbent assay (ELISA)-defined human polyclonal antiphospholipid antibody. Both IgG and IgM antibodies were easily demonstrable when sera were incubated on phospholipid-coated ELISA plates at 4-22 degrees C. When incubations were done at 37-45 degrees C IgG antibody binding markedly decreased but IgM antibody binding did not. Warming the phospholipid-coated ELISA plate alone, the serum alone, the buffer alone, or the blocking reagent alone had no effect. When the antigen content of the wells was increased fourfold the effect of warming still occurred. The effect of warmth was reversible and was seen with affinity-purified antibody as well as with whole serum. Phospholipid vesicles in suspension, however, absorbed antibody in a dose-dependent fashion at 4, 22, and 42 degrees C. These results indicate that antibody binding to phospholipid is temperature dependent when phospholipid is adherent to the solid phase. Whether the change in IgG-phospholipid interaction results from a change in antigen or in antibody remains unknown.

Antigen-Antibody Reactions↗
PubMed1988

IgG subclass and light chain distribution of anticardiolipin and anti-DNA antibodies in systemic lupus erythematosus.

The IgG subclass and light chain distribution of anticardiolipin and anti-DNA antibodies were determined in serum samples from patients with systemic lupus erythematosus. With an enzyme linked immunosorbent assay (ELISA) and mouse monoclonal antibodies to individual subclasses, significant differences in the distributions of IgG2, IgG3, and IgG4 subclasses were observed between anticardiolipin and anti-DNA antibodies. Whereas anti-DNA antibodies were predominantly IgG1 and IgG3, all subclasses of anticardiolipin were detected with a prevalence ranging from 34% (IgG3) to 57% (IgG1). Clinical complications were found slightly more frequently (83%) in patients with sera containing the non or weak complement fixing subclasses (IgG2 and IgG4) than in patients with sera containing complement fixing (IgG1 and IgG3) subclasses (62%). Light chain analysis by ELISA showed a trend towards use of kappa chains for anti-DNA and lambda chains for anticardiolipin antibodies. These findings further emphasise the differences between anti-DNA and anticardiolipin antibodies in terms of their origins and potential mechanisms for producing tissue injury.

Antibodies, Antinuclear↗
PubMed1987

Antibody to cardiolipin, lupus anticoagulant, and fetal death.

We compared the concordance and predictive powers of activated partial thromboplastin time (APTT) and of IgG and IgM antibody to cardiolipin (aCL), for predicting fetal death in 50 pregnant women with systemic lupus erythematosus (SLE) and/or lupus anticoagulant. Overall concordance of any abnormal determination of aCL during pregnancy with any abnormal determination of APTT was 76% (0.05 less than p less than 0.10). Fetal death occurred in 6/12 (50%) of patients with high APTT compared to 5/20 (16%) of patients with low APTT; fetal death occurred in 10/13 (77%) of patients with abnormal aCL and in 2/37 (5%) of patients with normal aCL. Sensitivity for predicting fetal death was .55 for APTT and .85 for aCL; specificity was .81 for APTT and .92 for aCL. Abnormalities of APTT and aCL are sufficiently frequently discordant to prevent equation of the 2 assays. ACL is the better assay for predicting fetal death.

Antibodies↗
PubMed1987

Hazards of lupus pregnancy.

Fetal death occurs in about 1/3 of pregnancies in patients with systemic lupus erythematosus (SLE). It is largely predicted by lupus anticoagulant (estimated by activated partial thromboplastin time) and/or antibody to cardiolipin. These antibodies are not synonymous. Neonatal lupus appears in a minority of infants born to women with antibody to the Ro/La antigens. Hypocomplementemia is common in SLE pregnancies, as in pregnancy induced hypertension. Lupus exacerbation is uncommon either during or after pregnancy. Prematurity and fetal death are the greatest hazards.

Autoantibodies↗
PubMed1986

The diversity of neurologic events in systemic lupus erythematosus. Prospective clinical and computed tomographic classification of 82 events in 71 patients.

To investigate outcome and pathophysiology of central nervous system (CNS) systemic lupus erythematosus (SLE), we prospectively codified all cases of CNS SLE. Eighty-two events occurred in 71 patients. Four events in four patients were due to infection and were excluded. Twelve events occurred in 11 women with positive antinuclear antibody but negative anti-DNA antibody test reactions and no other manifestation of SLE. Of the remaining 66 events (56 patients), 26 events were "isolated" and 40 "complex." Non-CNS SLE was "active" during 47 events and "inactive" during 19 events. "Isolated" CNS events were equally likely in clinically "active" and "inactive" SLE. Patients with active SLE were as likely to have an episodic or remittent course as were patients with inactive SLE. "Complex" events, however, were more likely to have favorable outcome than were "isolated" events. "Isolated" events without focal CT abnormalities, the only component of CNS SLE that can be called diffuse lupus encephalitis, accounted for only 20% of all neurologic events.

Adolescent↗
PubMed1986

Hypocomplementemia with low C1s-C1 inhibitor complex in systemic lupus erythematosus.

Ninety-three serum and plasma samples from 45 patients with systemic lupus erythematosus were analyzed for the complex formed by C1s and its inhibitor, as well as for C3, C4, C4a desarginine, and staphylococcal protein A-bound immune complexes. There were statistically significant correlations between C1s-C1 inhibitor complex and CH50, between C1s-C1 inhibitor complex and C4, and between C1s-C1 inhibitor complex and C4a desarginine. Serial studies were performed on 24 patients over a period of 6 months. Seven of 21 patients with hypocomplementemia had persistently normal levels of C1s-C1 inhibitor complex, 7 had transiently abnormal levels of C1s-C1 inhibitor complex, and 7 had sustained abnormal levels of C1s-C1 inhibitor complex. Two of 3 pregnant patients with normal levels of complement had abnormal levels of C1s-C1 inhibitor complex. Staphylococcal protein A-bound immune complexes demonstrated no correlation with any of the complement assays. Complement activation, as measured by C1s-C1 inhibitor complex, is often a transient phenomenon in systemic lupus erythematosus patients with persistent hypocomplementemia.

Antigen-Antibody Complex↗
PubMed1986

Changes in anti-lymphocyte and anti-Ia antibodies during pregnancy in systemic lupus erythematosus.

Anti-lymphocyte antibodies reactive with monocyte-depleted lymphocytes, T cells, or B cells were studied in 43 nonpregnant and 23 pregnant systemic lupus erythematosus (SLE) patients. Anti-Ia specificity was assayed in an enzyme-linked immunosorbent assay system. No difference in mean lymphocytotoxicity was noted between pregnant and nonpregnant SLE patients; however, anti-Ia lymphocyte antibody associated with disease activity was lower (P less than 0.01) in pregnant than in nonpregnant SLE patients. Lymphocytotoxic or anti-Ia antibody activity did not reliably predict the outcome of individual pregnancies.

Antilymphocyte Serum↗
PubMed1986

Connective tissue diseases. Goals and strategies of management.

Connective tissue diseases are a source of frustration for both patients and their families. Short-term treatment is aimed at the presenting syndrome, and a specific diagnosis is not needed. Long-term treatment attempts to provide an acceptable quality of life while avoiding complications and disability. Drug therapy includes nonsteroidal antiinflammatory drugs, antimalarial drugs, corticosteroids, and immunosuppressive agents. Joint-protection measures and physical therapy help prevent specific complications. Exacerbations of disease can be traced to several common aggravating factors. Because of the nature of connective tissue diseases, psychosocial problems among patients and their families are common. Physicians who anticipate these problems can help patients learn to cope with a chronic, painful condition.

Adrenal Cortex Hormones↗