G A McCarty

Publications (12)41.28 Total impact

• Article: Antiphospholipid antibody syndromes and the Internet.

  G A McCarty
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  ABSTRACT: Information regarding the antiphospholipid antibody syndrome is accessible on the Internet, and encompasses both physician specific and patient specific files. The quantity and quality of data available at these sites, however, varies greatly and both search-refining and data manipulating protocols and software need improvement.
  Lupus 11/1996; 5(5):418-24. · 2.34 Impact Factor
• Article: Spectrum of vascular pathology affecting patients with the antiphospholipid syndrome.

  M D Hughson, G A McCarty, R A Brumback
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  ABSTRACT: A thrombotic microangiopathy that is identified in patients with the antiphospholipid syndrome (APS) represents only a part of the vascular pathology that can be associated with antiphospholipid antibodies (aPL). Tissues from two autopsies, four renal biopsies, two skin biopsies, and one amputated leg were obtained from six patients who met criteria for the diagnosis of APS. Three patients had systemic lupus erythematosus (SLE), one had lupus-like disease, and two had a primary APS. Five of the patients were hypertensive. Arteries of three patients disclosed fibrin thrombi along with widespread obstruction by recanalized intimal connective tissue. Small renal, leptomeningeal, and pulmonary arteries showed concentric cellular and fibrous intimal hyperplasia indistinguishable from hypertensive vascular disease. Glomerular capillary and afferent arteriolar thrombi were found in renal biopsies from two SLE patients. One of these SLE patients required a leg amputation in which the popliteal artery demonstrated thrombosis, intimal hyperplasia, and acute inflammation. The findings support clinical and experimental data that indicate aPLs cause thrombosis but suggest diversity in the pathogenetic mechanisms aPLs are capable of promoting. Inflammation seems to be rare and to accompany thrombosis. Intimal hyperplasia is particularly common. Its involvement of renal arteries may contribute to hypertension that develops in some APS patients.
  Human Pathlogy 08/1995; 26(7):716-24. · 2.88 Impact Factor
• Article: Thrombotic cerebral arteriopathy in patients with the antiphospholipid syndrome.

  M D Hughson, G A McCarty, C M Sholer, R A Brumback
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  ABSTRACT: A distinctive type of chronic cerebral vasculopathy was identified in the small leptomeningeal arteries of patients with high levels of serum antiphospholipid antibodies. This study characterizes the vascular lesions and investigates their pathogenesis. A comparative study of cerebrovascular disease in patients dying of systemic lupus erythematosus (SLE) and the antiphospholipid syndrome. Cerebrovascular disease observed in autopsies on a patient with primary antiphospholipid syndrome and a patient with SLE and antiphospholipid syndrome was compared with findings on two SLE patients who did not have serum antiphospholipid antibodies and with findings on 15 patients having diseases in which pathological changes of meningeal arteries might be anticipated or are known to occur (six patients with hypertensive cerebrovascular disease, one patient with thrombotic thrombocytopenic purpura, seven patients with marantic or bacterial endocarditis, and one patient with a left ventricular mural thrombus). Multiple blocks of brain tissue were studied by serial histologic sections and histochemical and immunohistochemical methods. Immunofluorescent and electron microscopic (EM) studies were performed on kidneys and EM studies on brain and choroid plexus in each case of antiphospholipid syndrome. Leptomeningeal arteries of antiphospholipid syndrome patients disclosed fibrin thrombi and widespread obstruction by a proliferation of intimal fibrous tissue or myointimal cells. The fibrous and cellular segments of obstructed arteries frequently contained fibrin thrombi and displayed varying stages of recanalization. In late stages of organization, fibrous webs were formed across arterial lumens. Obstructed arteries were traced to small infarcts localized to an underlying column of cortical gray matter. None of the tissues from antiphospholipid syndrome patients showed evidence of an active or healed inflammatory vasculitis or of vascular immune complex deposits. Recanalized thrombi, fibrous and cellular occlusions, and fibrous webs were not found in the leptomeningeal arteries of patients who did not have the antiphospholipid syndrome. The cerebrovascular changes of the antiphospholipid syndrome are derived from a chronic thrombotic microangiopathy. The findings support the hypothesis that antiphospholipid antibodies can cause recurring episodes of intravascular thrombosis.
  Modern Pathology 12/1993; 6(6):644-53. · 4.79 Impact Factor
• Article: A distinctive autoantibody profile in black female patients with lupus nephritis.

  G A McCarty, J B Harley, M Reichlin
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  ABSTRACT: Lupus nephritis has often been associated with anti-DNA, but, based on the findings in eluate studies, it appears that other antigen-antibody reactions, such as those involving anti-Ro/SS-A, anti-nuclear RNP (anti-nRNP), and/or anti-Sm, may also contribute to the pathogenesis of nephritis. In the present investigation, we identified and further studied a distinctive precipitin profile present in black women with nephritis. Longitudinal clinical and serologic studies of a cohort of university-based systemic lupus erythematosus (SLE) patients (n = 120) were carried out over an 8-year period. A subset of 20 black female patients was identified, of whom 8 had lupus nephritis (group I) and 12 did not (group II). Group I was characterized by a distinct precipitin profile consisting of anti-Ro/SS-A, anti-SM, and anti-nRNP, but no anti-La/SS-B. SLE disease duration at presentation was significantly shorter in group I than in group II (mean 1.94 years versus 5.21 years; P = 0.02). The distinctive precipitin profile of anti-Ro/SS-A, anti-Sm, and anti-nRNP occurred exclusively in group I patients (6 of 8, versus 0 of 12 in group II; P < 0.001). In white lupus nephritis patients, this precipitin profile was not seen. While the mechanism responsible for the relationship of this distinctive serologic profile to the development of nephritis in black female lupus patients remains to be determined, its presence may be used as a marker for severe and progressive renal disease.
  Arthritis & Rheumatism 12/1993; 36(11):1560-5. · 7.87 Impact Factor
• Article: Renal thrombotic microangiopathy in patients with systemic lupus erythematosus and the antiphospholipid syndrome.

  M D Hughson, T Nadasdy, G A McCarty, C Sholer, K W Min, F Silva
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  ABSTRACT: Current studies indicate that a thrombotic microangiopathy (TMA) identifies patients with systemic lupus erythematosus (SLE) who are at high risk of progressing to end-stage renal disease. We have observed two patients with SLE and one patient with a primary antiphospholipid syndrome (APS) who developed acute renal insufficiency with thrombocytopenia. Renal biopsies showed a TMA characterized by thrombi or by cellular and mucoid intimal hyperplasia of small arteries and arterioles. No arterial or arteriolar immune-complex deposits were detected by immunofluorescent or electron microscopy. Biopsies from one SLE patient and the APS patient showed no immune-complex glomerular disease. Both had serum antiphospholipid antibodies (aPL). aPL were not detected in the serum of the other SLE patient who had an active lupus nephritis. Acute renal failure and thrombocytopenia resolved in each case following treatment by plasmapheresis or prednisone and heparin. None of the patients were initially treated with cytotoxic drugs. As more knowledge is gained, the accurate identification of renal vascular lesions in SLE or related diseases could influence renal prognosis and choice of therapy. The cases reported here provide further evidence that a TMA can cause acute renal failure independent of lupus nephritis. TMA should be distinguished from other forms of renal vascular disease, particularly a noninflammatory lupus microangiopathy, which is probably mediated by subendothelial immune-complex deposits. The absence of immunoglobulin deposits in vessels involved by a TMA indicates that microvascular thrombosis is promoted by mechanisms other than those usually attributed to immune-complex disease. Phospholipid reactive antibodies may be pathogenetic in some cases.
  American Journal of Kidney Diseases 09/1992; 20(2):150-8. · 5.43 Impact Factor
• Article: Management of antiphospholipid antibody positivity and elective orthopedic procedures.

  W M Schnitz, K A Lister, G A McCarty
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  ABSTRACT: Current management of primary or secondary antiphospholipid antibody (aPL) syndromes with known embolic phenomena requiring anticoagulation is empiric in the setting of elective orthopedic procedures. Short-term withdrawal of warfarin with continuance of aspirin and glucocorticoid therapy was undertaken for sequential bilateral knee replacements in a lupus patient with aPL. Her course was successfully managed without thrombo-embolic complications.
  Lupus 06/1992; 1(3):187-9. · 2.34 Impact Factor
• Article: The antiphospholipid antibody syndrome in the emergency department setting--livedo reticularis and recurrent venous thrombosis.

  S Kester, D L McCarty, G A McCarty
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  ABSTRACT: We present the case of a 26-year-old man with an exacerbation of apparent chronic asthma with chronic peripheral vascular disease due to recurrent venous thrombosis. Localized livedo reticularis, new cutaneous infarctions, severe venous insufficiency, thrombocytopenia, renal failure, and cerebral supratentorial dysfunction were noted. During hospital admission, antibodies to phospholipids in high titer were present by three different testing methods. Renal biopsy demonstrated significant renal vasculature abnormalities characteristic of hemolytic endovasculopathy, and magnetic resonance imaging showed multiple cerebral infarctions. This case exemplifies the spectrum of presentations and management of the primary antiphospholipid antibody syndrome. The clue to its presence in this patient was the livedo reticularis rash, a cutaneous marker for this syndrome that was evident in the emergency department.
  Annals of Emergency Medicine 03/1992; 21(2):207-11. · 4.13 Impact Factor
• Article: Autoantibodies to phospholipids--new looks at old diseases--a primer for physicians.

  G A McCarty
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  ABSTRACT: Antibodies to negatively charged phospholipids (aPL) are associated with a wide clinical spectrum. Primarily the clinical problems present as localized and/or generalized thromboses, recurrent fetal loss, strokes, and various cytopenias. The clinical settings which would prompt the physician to consider aPL as causal or contributory to pathology in many organ systems are reviewed, and guidelines for screening and confirmatory testing are defined. Since effective treatments do exist to decrease or prevent morbidity, and in some cases, mortality, the generalist as well as the specialist should be aware of the many faces these primary and secondary syndromes present to them in daily practice.
  The Journal of the Oklahoma State Medical Association 03/1992; 85(2):61-8.
• Article: Endothelium as a target for the immune injury in systemic vasculitis.

  P L Meroni, N Del Papa, D Gambini, W Barcellini, G A McCarty, K A Lister
  Contributions to nephrology 02/1992; 99:1-6. · 1.49 Impact Factor
• Article: Aseptic meningitis in association with diclofenac treatment in a patient with systemic lupus erythematosus.

  C Codding, I N Targoff, G A McCarty
  Arthritis & Rheumatism 11/1991; 34(10):1340-1. · 7.87 Impact Factor
• Article: Autoantibodies in scleroderma and polymyositis: an update.

  G A McCarty
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  ABSTRACT: Cutaneous manifestations of systemic connective tissue diseases, such as scleroderma and its variants, polymyositis, and dermatomyositis, often prompt early dermatologic consultation. Indirect immunofluorescent autoantibody determinations using tissue culture substrates are initial screening tests that are highly positive in the majority of patients with scleroderma and its variants, but are less frequently positive in patients with polymyositis and dermatomyositis. When combined with second-level analyses for the multiplicity of precipitin autoantibodies that have been defined in both these major classes of rheumatic diseases, most autoantibodies of both diagnostic and prognostic significance can be defined efficiently and cost-effectively. The major autoantibody specificities characteristic of these connective tissue diseases are summarized in this article, with emphasis on current concepts of their clinical molecular, and possible pathogenetic significance.
  Seminars in dermatology 10/1991; 10(3):206-16.
• Article: Scleroderma: DR antigens, autoantibodies and clinical manifestations.

  G S Alarcón, G A McCarty, P Lanyon, R M Phillips, R T Acton, B O Barger
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  ABSTRACT: The relationship between anticentromere antibodies (ACA), antitopoisomerase I or Scleroderma 70 (Scl-70) antibodies, HLA-DR antigens, and clinical manifestations of scleroderma were examined in 51 patients defined by ARA criteria. No association between a given HLA-DR antigen and either ACA or anti-Scl-70 was found. Statistically significant associations were noted for patients with ACA who had a lower frequency of arthritis and longer disease duration; anti-Scl-70 patients were more likely to be males with a higher frequency of pulmonary, cardiac and sicca symptoms.
  Clinical and experimental rheumatology 5(4):317-21. · 2.15 Impact Factor