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Biomedical subjects

F P Quismorio

Publications and source records attributed to F P Quismorio.

At least 19 recordsLinked to original sources
PubMed1998

Synergistic effect between IL-10 and bcl-2 genotypes in determining susceptibility to systemic lupus erythematosus.

OBJECTIVE: To determine whether genes participating in programmed cell death, including bcl-2, IL-10, Fas-L, and CTLA-4, may contribute to the genetic predisposition to systemic lupus erythematosus (SLE). METHODS: First, intragenic markers for the bcl-2, IL-10, Fas-L, and CTLA-4 genes were characterized and their extent of polymorphism in normal populations was determined. The allelic distribution of these gene markers in a large Mexican American SLE cohort of 158 patients and 223 ethnically matched controls was determined using fluorescent-labeled primers and semiautomated genotyping. RESULTS: The bcl-2, Fas-L, and IL-10 loci showed significantly different allelic distribution in SLE patients compared with controls, indicating an association between these genes and SLE. No association was found between SLE and the CTLA-4 gene. Further analysis revealed a synergistic effect between susceptibility alleles of the bcl-2 and IL-10 genes in determining disease susceptibility. Alone, the presence of each of these alleles was associated with a moderate increase in SLE risk, while the occurrence of these alleles together increased the odds of developing SLE by more than 40-fold. CONCLUSION: The results suggest that individuals carrying specific genotypes of both bcl-2 and IL-10 are at significant risk of developing SLE.

Abatacept↗
PubMed1996

Pulmonary involvement in primary Sjögren's syndrome.

Interstitial pulmonary fibrosis and tracheobronchial sicca are the most common presentation of pulmonary involvement in primary Sjögren's syndrome. There is wide spectrum of less common manifestations, including pulmonary arterial hypertension, pseudolymphoma, pulmonary lymphoma, lymphocytic interstitial pneumonitis, amyloidosis, and pleurisy. Pulmonary function test abnormalities showing a restrictive pattern and cellular abnormalities in bronchoalveolar lavage fluid for prevalent in patients without respiratory complaints and normal chest radiographs. Long-term prospective controlled studies are needed to determine the clinical course and significance of these findings.

Amyloidosis↗
PubMed1996

Impairments of the protein C system and fibrinolysis in infection-associated stroke.

BACKGROUND AND PURPOSE: Infection/inflammation appears to be an important predisposing risk factor for brain infarction, but little is known regarding underlying molecular mechanisms. We examined the hypothesis that patients with brain infarction preceded by infection/inflammation within 1 week could be identified by a distinctive procoagulant laboratory profile characterized by abnormalities in the protein C system and endogenous fibrinolysis. METHODS: We performed a case-control study examining the relationship between preceding systemic infectious/inflammatory syndromes and selected immunohematologic variables in 36 patients with acute brain infarction and 81 control subjects (community control subjects [n = 47] and hospitalized nonstroke neurological patient controls [n = 34]). RESULTS: The stroke group had a lower mean level of the circulating antithrombotic enzyme activated protein C (APC) (4.33 +/- 0.34% [log-transformed percentage of control value, mean +/- SD]) than community control subjects (4.51 +/- 0.27%, P < .02) or hospitalized neurological patient controls (4.57 +/- 0.31%, P < .005). The lowest circulating APC levels were found in the stroke group with antecedent infection/inflammation within 1 week preceding index brain infarction (4.23 +/- 0.4%, n = 12). Within the stroke group, circulating APC levels were inversely related to IgG isotype anticardiolipin antibody titers (r = -.55, P < .001). Only the stroke group with infection/inflammation within 1 week had elevated plasma C4b binding protein compared with control subjects (141 +/- 61% versus 112 +/- 44%, P < .05). Stroke patients with antecedent infection/inflammation had a distinctively lower ratio of active tissue plasminogen activator to plasminogen activator inhibitor (0.11 +/- 0.04, n = 9) than other stroke patients (0.19 +/- 0.06, n = 9, P < .01) and control subjects (0.22 +/- 0.16, n = 17, P < .02). CONCLUSIONS: Impairments in the protein C pathway and endogenous fibrinolysis may contribute to the increased risk for brain infarction after recent (< or = 1 week) infection/inflammation. A decrease in the circulating anticoagulant APC may be related to elevated antiphospholipid antibody titers.

Antibodies, Anticardiolipin↗
PubMed1995

The elusive search for geographic clusters of systemic lupus erythematosus. Critical review.

OBJECTIVE: To ascertain whether there are any geographic clusters of systemic lupus erythematosus (SLE), and critically review 2 previous reports of these clusters. METHODS: A literature review of all epidemiologic surveys relevant to SLE published since 1966 was undertaken. This included a search of abstracts and reports, in addition to peer-reviewed publications. RESULTS: Two geographic clusters were identified in the literature. A report purporting that contaminated ground water in southwest Tucson, Arizona was associated with significantly increased symptoms of SLE was flawed since no patients were examined, discarded criteria were used, and incorrect definitions were employed by the nonrheumatologist authors. Another study, which identified a cluster in Nogales, Arizona, used generally valid methodology. However, the authors' conclusion that a 94/100,000 prevalence of SLE was evidence of an excessive increase in this 92% Hispanic/Native American community is not consistent with published surveys among Hispanic and Native American populations. CONCLUSION: No valid claims of SLE geographic clusters have been published.

Arizona↗
PubMed1995

Hypergammaglobulinemic purpura of Waldenstrom associated with systemic lupus erythematosus: report of a case and review of the literature.

A patient with hyperglobulinemic purpura of Waldenstrom and systemic lupus erythematosus is reported. The coexistence of these two conditions which share a number of common clinical and laboratory features is rare. Treatment of the patient with prednisone, colchicine and hydroxychloroquine led to the improvement of the cutaneous vasculitis and a drop in ESR, serum gamma globulins and IgM and IgG rheumatoid factors. The features of nine other cases and the immunopathogenesis of the disease are reviewed.

Adult↗
PubMed1995

Polyarteritis nodosa-like vasculitis in human immunodeficiency virus infection.

Human immunodeficiency virus (HIV) infection can present with musculoskeletal syndromes including systemic vasculitis. We describe vasculitis resembling polyarteritis nodosa (PAN) in 2 HIV-infected individuals and review reported cases to emphasize clinical features. Our patients presented with digital gangrene and had vasculitis confirmed by angiography. In reports in the literature, patients have presented with digital ischemia and gangrene, peripheral neuropathy and constitutional symptoms. The diagnosis has been confirmed by angiography and by nerve and muscle biopsy. Treatment with systemic corticosteroids has afforded short term benefits to patients; however the effectiveness of alternative therapy and longterm prognosis remain unclear.

Adrenal Cortex Hormones↗
PubMed1994

Budd-Chiari syndrome associated with antiphospholipid antibodies in a child: report of a case and review of the literature.

Budd-Chiari syndrome, hypertension, and thrombocytopenia developed in a 6-year-old girl as manifestations of primary antiphospholipid antibody syndrome (APS). She improved with systemic corticosteroid and anticoagulation therapy. Anticardiolipin antibodies were found in the patient, her mother and 3 siblings, suggesting the importance of genetic factors. The clinical features of an APS in children is reviewed.

Abdominal Pain↗
PubMed1993

Magnetic resonance imaging of the brain in neuropsychiatric systemic lupus erythematosus.

To determine the utility of magnetic resonance imaging (MRI) of the brain in diagnosing active neuropsychiatric disease in systemic lupus erythematosus (NP-SLE), a prospective study of 51 hospitalized systemic lupus erythematosus (SLE) patients during 64 separate episodes of suspected NP-SLE was initiated. In addition to standard hematology, chemistry, and serological tests, the workup included MRI in all patients. A computed tomographic scan of the brain was obtained in patients enrolled in the first year of the study. Of the 64 neuropsychiatric episodes, 42 were attributable to NP-SLE and 22 were attributed to causes other than SLE. Neuropsychiatric complaints unrelated to lupus included depression (n = 6), seizures (n = 5), headache (n = 3), altered mental status (n = 2), aseptic meningitis (n = 2), cardiovascular accident (n = 2), transient ischemic attack (n = 1), and vertigo (n = 1). The MRI was abnormal in 34 of 64 (53%) episodes. MRI abnormalities were more common in patients with focal neurological deficits (19/26) than in those without focal findings (15/38; P = .008) and in patients with nephritis (19/24) than in those without renal disease (15/40; P = .002). MRI abnormalities were as frequent in NP-SLE (25/42) as in cases with non-NP-SLE-related causes (9/22). Periventricular increased signal (PIS) was a frequent MRI finding (10/64). Enlargement of the prepontine cistern, an MRI finding not previously described in NP-SLE, was seen (14/64). Both findings were associated with the presence of hypertension and lupus nephritis. PIS similar to that seen in our patients has been described in otherwise healthy elderly individuals with risk factors for stroke, suggesting that vascular abnormalities may be important in the etiology of these lesions. In conclusion, abnormalities in brain MRI occur frequently in NP-SLE, especially in patients with focal neurological deficits. However, the presence of similar MRI abnormalities in SLE patients with neuropsychiatric symptoms and findings with non-SLE-related causes limits the specificity of the MRI for diagnosing NP-SLE.

Adolescent↗
PubMed1993

The lipid, lipoprotein, and apolipoprotein effects of hydroxychloroquine in patients with systemic lupus erythematosus.

Lipid, lipoprotein, and apolipoprotein effects of hydroxychloroquine were studied in 18 female patients with systemic lupus erythematosus (SLE) with mild or inactive disease. Patients were case matched (200-400 mg hydroxychloroquine daily vs no hydroxychloroquine) on several factors including daily corticosteroid dose in this cross sectional study. All had normal menstrual cycles; none smoked, used alcohol, were taking lipid altering medications or had other concurrent diseases. Patients taking hydroxychloroquine had 35-54% lower total triglyceride, VLDL-triglyceride, LDL-triglyceride, HDL-triglyceride, VLDL-cholesterol, and apolipoprotein CIII levels (p < 0.03). These results are encouraging in that hydroxychloroquine, in addition to being useful for alleviating the primary symptoms of SLE, may also be useful for ameliorating the adverse effects of corticosteroid therapy on triglyceride-rich lipoprotein metabolism.

Adult↗
PubMed1992

Hematogenous factors and prediction of delayed ischemic deficit after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Delayed ischemic deficits contribute to the high morbidity and mortality rates associated with subarachnoid hemorrhage. We evaluated the potential usefulness of measuring coagulation and hemorheological variables and cardiolipin antibodies for prediction of delayed ischemic deficit after subarachnoid hemorrhage. METHODS: Consecutive patients with subarachnoid hemorrhage were studied. Coagulation and hemorheological variables and cardiolipin antibodies were measured on admission, within 7 days of subarachnoid hemorrhage. A subset of patients was studied on admission and at two subsequent occasions. RESULTS: Sixty-nine patients were studied. Sixty-one of these were without clinical manifestations of vasospasm at admission, and 16 developed delayed ischemic deficit during their hospitalization. None of the laboratory variables measured were significantly different between patients with or without later development of delayed ischemic deficit. Elevation of the fibrin fragment D-dimer was found in the group of eight patients admitted with ischemic symptoms and in 49% (34 of 69) of all patients, but this was not associated with delayed ischemic deficit. Sixteen patients were studied on three occasions; this group showed a significant decrease in hematocrit, an increased white blood cell count, and no change in fibrinogen concentration. Fibrin D-dimer levels rose significantly after surgery (from 5.01 +/- 0.69 to 5.53 +/- 0.58 ln-ng/ml, p less than 0.025) and after onset of delayed ischemic deficit (from 4.71 +/- 0.64 to 5.84 +/- 0.34 ln-ng/ml, p less than 0.01). CONCLUSIONS: Hemostatic measurements, hemorheological variables, and cardiolipin immunoreactivity did not predict delayed ischemic deficit in this population.

Adult↗
PubMed1991

Regression of reactive systemic amyloidosis due to ankylosing spondylitis following the administration of colchicine.

We describe a patient in whom nephrotic syndrome due to renal amyloidosis occurred 4 years into the course of severe ankylosing spondylitis with peripheral joint and extraarticular involvement. Treatment with colchicine was accompanied by reversal of proteinuria, and histologic regression of amyloid deposits was documented from bone marrow obtained from the femoral heads during total hip arthroplasties staged 1 year apart.

Adult↗
PubMed1991

Immunohematologic characteristics of infection-associated cerebral infarction.

We evaluated 50 consecutive patients with acute ischemic stroke to assess the prevalence of systemic infection preceding the neurological event. We analyzed the immunohematologic characteristics of patients with and without signs and/or symptoms of a preceding infectious process. Patients were examined less than or equal to 7 days after cerebral infarction and evaluated for fibrinogen, anticardiolipin antibodies, fibrin D-dimer (a fragment of cross-linked fibrin), plasminogen activator inhibitor-1, and protein S. Of the 50 patients, 17 had symptoms of infection beginning less than or equal to 1 month before the stroke (11 had upper respiratory tract infections, three urinary tract infections, two subacute bacterial endocarditis, and one pneumonia). Compared with patients without infection, patients with infection had significant increases in fibrin D-dimer concentration (5.3 +/- 1.1 versus 4.7 +/- 0.9 log-transformed ng/ml, p less than 0.05) and cardiolipin immunoreactivity, IgG isotype (1.8 +/- 1.3 versus 1.1 +/- 0.9 log-transformed phospholipid units, p less than 0.04), and, when studied less than or equal to 2 days after the stroke, increased fibrinogen levels (459 +/- 126 versus 360 +/- 94 mg/dl, p less than 0.05). In conclusion, infection-associated cerebral infarction is common and is associated with substantial immunohematologic abnormalities.

Adult↗
PubMed1991

Interstitial lung disease and cryoglobulinemia in polymyositis.

Alveolar septal deposits of immunoglobulins and complement were found in the lung biopsy of a patient with polymyositis and interstitial lung disease. Anti-Jo 1 antibody was present in the serum and in isolated mixed cryoglobulins of the patient, suggesting the role of immune complex deposition in the pathogenesis of lung disease. Significant amounts of cryoglobulins were found in 10 of 16 (62.5%) patients with polymyositis/dermatomyositis tested.

Adult↗
PubMed1990

CD8+ lymphocytes from patients with systemic lupus erythematosus sustain, rather than suppress, spontaneous polyclonal IgG production and synergize with CD4+ cells to support autoantibody synthesis.

The cellular requirements for B cell hyperactivity in systemic lupus erythematosus (SLE) were studied. Removal of either CD8+ or CD4+ lymphocyte markedly decreased the spontaneous in vitro production of polyclonal IgG and of antigen-specific (anti-double-stranded DNA and antinucleoprotein) antibodies by SLE peripheral blood mononuclear cells (PBMC). The CD8+ lymphocytes that sustained IgG production were CD3+, HLA-DR+, and their activity was abrogated by preincubation with anti-HLA-DR monoclonal antibody. When both CD4+ and CD8+ cells were removed, the readdition of either subset partially restored polyclonal IgG production, but both cell subsets were required to reconstitute autoantibody production. Purified SLE B cell cultures, which generated only 15% of the IgG produced by unseparated PBMC, were fully reconstituted only by mixtures of CD4+ with CD8+ cells, and with CD8-, CD4-, CD16+ cells. At least part of the support for spontaneous IgG production can be attributed to endogenous interleukin-2 and interleukin-6.

Antibody Formation↗
PubMed1990

Cardiac compression in rheumatoid pericarditis.

Rheumatoid pericarditis occurs in approximately one third of rheumatoid arthritis (RA) patients. However, clinically apparent rheumatoid pericarditis is infrequent. The authors found clinical pericarditis in 12 of 960 patients admitted for RA, 5 of whom had manifestations of cardiac compression. These 5 had longer duration of RA, worse functional class, and more extraarticular features than the patients without cardiac compression. Presenting features of cardiac compression included dyspnea, edema, chest pain, and pulsus paradoxus. Treatment of patients with cardiac compression due to rheumatoid pericarditis may include a trial of systemically administered corticosteroids, but this should not delay surgical intervention for impending tamponade. Pericardiocentesis should only be performed as an emergency, life-saving procedure. It may be followed by intrapericardiac injection of corticosteroids, but this does not prevent recurrence. Longer-lasting benefit is obtained by surgical decompression. Two-year mortality in patients with cardiac compression was 100%. The literature on the subject is reviewed.

Adrenal Cortex Hormones↗
PubMed1990

A long-term study of interstitial lung disease in systemic lupus erythematosus.

The clinical course of chronic diffuse interstitial lung disease (ILD) was studied in 14 patients with SLE. The mean duration of follow-up was 7.3 years. All patients had dyspnea on exertion, pleuritic chest pain, chronic cough, and basilar rales. Chest roentgenogram showed diffuse or basilar infiltrates, pleural disease, and elevation of both diaphragms. Systemic corticosteroids were given early in the course of the illness for lung involvement and multisystem disease. Diffusing capacity for carbon monoxide (DLCO) and inspiratory vital capacity (IVC) improved or remained unchanged in the majority of patients. Respiratory complaints improved in all patients; however, two patients died of pulmonary fibrosis and another died of bacterial pneumonia. Alveolar septal deposits of immunoglobulins and complement were found. This study showed that while variability existed among individual subjects, the clinical progression of ILD was slow and tended to improve or stabilize with time.

Adrenal Cortex Hormones↗
PubMed1989

Anticardiolipin antibodies in acquired immunodeficiency syndrome.

We undertook a prospective study of IgG and IgM anticardiolipin antibodies (ACAs) to determine their clinical significance in patients with acquired immunodeficiency syndrome (AIDS). IgG ACAs were found in 24 (92.3%) of 26 patients with AIDS who were hospitalized for pulmonary complaints (group 1) and in 13 (93%) of 14 patients with AIDS-related complex (group 2). In addition, 17 (94%) of 18 patients with AIDS (group 3) who had coagulation tests and were studied retrospectively had IgG ACAs. The prevalence of IgG ACAs in these three groups was significantly higher than in healthy controls, but was comparable to that in 31 consecutive patients with systemic lupus erythematosus (67.7%). The mean titer of IgG ACAs in group 1 was higher than in groups 2 and 3 but was not different from that in the patients with systemic lupus erythematosus. The frequency and titer of IgM ACAs in group 1 (7.6%) or group 2 (14.3%) were not significantly different from those in normal controls (4.7%). In contrast, half of the patients in group 3 had low-titer IgM ACAs. The serum titer of IgG ACAs in patients with AIDS with thrombocytopenia was significantly higher than it was in those with normal platelet counts. There was no association between ACAs and Pneumocystis carinii pneumonia or other infections, cancer, thrombosis, positive VDRL test, or presence of the lupus anticoagulant. The prevalence and titer of IgG or IgM ACAs were not associated with abnormal results of any coagulation test. Although we found IgG ACAs to be associated with thrombocytopenia in AIDS, their presence does not carry exactly the same clinical significance as it does in systemic lupus erythematosus. The high prevalence of ACAs in AIDS, in AIDS-related complex, and in otherwise healthy contacts with antibodies to human immunodeficiency virus suggests that their occurrence may be related to the underlying human immunodeficiency virus infection.

AIDS-Related Complex↗