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Biomedical subjects

P M Ford

Publications and source records attributed to P M Ford.

At least 19 recordsLinked to original sources
PubMed1992

The pathogenesis of nodular regenerative hyperplasia of the liver associated with rheumatoid vasculitis.

Nodular regenerative hyperplasia (NRH) is an uncommon liver disease that typically develops in the setting of a chronic illness such as Felty's syndrome. Although the pathogenesis of NRH has not been defined, vasculitis has been postulated to play an important pathogenetic role in some cases of NRH, even though the association of NRH and vasculitis has been reported rarely. We describe two unusual cases of NRH in patients with Felty's syndrome complicated by rheumatoid vasculitis. Morphometric analysis demonstrated evidence of injury to the hepatic vasculature in the form of loss of small intrahepatic arteries and portal spaces, findings that support the hypothesis that hepatic arteritis plays a role in the development of NRH in cases associated with systemic vasculitis.

Adult↗
PubMed1992

Double-blind randomized controlled trial of flurbiprofen-SR (ANSAID-SR) and diclofenac sodium-SR (Voltaren-SR) in the treatment of osteoarthritis.

A six week, double-blind, randomized, parallel group, multicentre study was conducted in 85 patients with osteoarthritis of the knee and hip to compare the efficacy, tolerability, and safety of Flurbiprofen-SR 200 mg with Diclofenac Sodium-SR 100 mg. Between group comparisons, based on change scores from baseline, we detected no significant differences between the two drugs with respect to efficacy for the majority of outcome measures. There was no significant difference between the groups in the proportion of patients experiencing at least one adverse medical event or in terminations from treatment. We conclude that Flurbiprofen-SR 200 mg is similar in efficacy, tolerability, and safety to Diclofenac Sodium-SR in this trial.

Adolescent↗
PubMed1992

Arthropathies associated with renal disease including dialysis-related amyloid.

In recent years most of the interest in musculoskeletal problems secondary to renal disease has focused on problems occurring in patients with chronic renal failure and specifically in patients on long-term hemodialysis. The musculoskeletal involvement in long-term hemodialysis may involve the joints, soft tissues, or both, and there is presently no good classification to which authors may refer when they report musculoskeletal problems in these patients. There has been intense interest in the past few years in the amyloidosis associated with long-term hemodialysis, and now, apparently, also with peritoneal dialysis. This type of amyloidosis is due to a specific type of amyloid, namely beta 2-microglobulin amyloid. Debate is ongoing about the role of both aluminum toxicity and iron deposition as cofactors affecting the location and extent of amyloid deposits. Debate is also unresolved about the role of specific dialysis membranes in lessening the incidence of dialysis-related amyloid. I review some of these areas as well as interesting new developments in localization of amyloid deposits in patients with chronic renal failure who are on hemodialysis.

Amyloid↗
PubMed1992

Osteoarthritis antirheumatic drug trials. I. Effects of standardization procedures on observer dependent outcome measures.

We designed a study to assess the effects of standardization procedures on reducing interobserver variability for outcome measures given in the current Food and Drug Administration and European League Against Rheumatism guidelines and others selected from the rheumatology literature. Over 2 days, 6 rheumatologists independently examined 6 patients with osteoarthritis (OA) in predetermined order before and after standardizing their examination techniques. An important and beneficial effect of the standardization procedure was observed on the majority of outcome variables. Such reductions in observer variability have the potential to diminish sample size requirements for OA antirheumatic drug studies.

Adult↗
PubMed1992

Osteoarthritis antirheumatic drug trials. II. Tables for calculating sample size for clinical trials.

The calculation of sample size for clinical trials requires knowledge of the standard deviation (SD) of index variables. There are no published lists of SD and it is difficult to locate variance estimates based on relevant populations. In this study we used standardized procedures to determine in 60 patients with osteoarthritis (OA) of the knee the standard deviation of key outcome measures recommended in current Food and Drug Administration and European League Against Rheumatism guidelines for OA clinical trials. These tables will be useful to clinical researchers in selecting outcome measures as well as for calculating sample size requirements for future clinical studies in OA.

Clinical Trials as Topic↗
PubMed1992

Osteoarthritis antirheumatic drug trials. III. Setting the delta for clinical trials--results of a consensus development (Delphi) exercise.

Defining the minimum clinically important difference or delta to be detected in a clinical trial depends on a number of factors including the research hypothesis, patient characteristics, the nature of the intervention and the trial design. In 2 studies, we have developed standardized procedures for conducting outcome measurement based on current Food and Drug Administration and European League Against Rheumatism guidelines for osteoarthritis clinical trials, and determined the standard deviation for these outcome measures. In the final component of this series of studies, we have used a Delphi technique to establish estimates for delta, and calculated the sample size requirements under 2 different conditions of Type I and Type II error probabilities.

Clinical Trials as Topic↗
PubMed1990

Heterogeneity of laboratory test results for antiphospholipid antibodies in patients treated with chlorpromazine and other phenothiazines.

Ninety-seven psychiatric patients who have been treated with the antipsychotic drug chlorpromazine or another phenothiazine have been investigated for the presence of antiphospholipid antibodies. A variety of coagulation studies and specific antiphospholipid immunoassays were performed to define the spectrum of antigen specificity of these antibodies. Coagulation studies showed an increasing sensitivity for the lupus anticoagulant with reagents of differing phospholipid content. Prolonged activated partial thromboplastin times (APTTs) were found in five patients with the use of an insensitive APTT reagent and in 14 patients with a lower phospholipid content reagent. In every case, attempted correction of the clotting time with normal plasma was unsuccessful. Twenty-one patients had abnormal kaolin clotting time profiles. In seven of these patients, test results with both APTT reagents had been normal. Antibody reactivity was tested against three negatively charged phospholipids, phosphatidyl-serine, cardiolipin, and phosphatidylinositol. Only five patients demonstrated reactivity against phosphatidylinositol, whereas high antibody titers were observed in 28 patients against one or both of phosphatidylserine and cardiolipin. Twenty-three of these patients were found to have elevated anticardiolipin-specific IgM antibodies. Overall, 41 of the patients had at least one laboratory abnormality suggestive of antiphospholipid antibody activity. Seven of the 26 patients, taking phenothiazines other than chlorpromazine, had positive test results for antiphospholipid antibodies. No clinical thromboembolic events were recorded in any patient. These findings demonstrate the heterogeneity of antiphospholipid antibody specificity induced in patients treated with various phenothiazine drugs and indicate that none of these patterns of reactivity marks a predisposition for thromboembolism in this population.

Adult↗
PubMed1990

Premature stroke in a family with lupus anticoagulant and antiphospholipid antibodies.

Lupus anticoagulant and antiphospholipid antibodies are associated with thromboembolic phenomena in individuals both with and without systemic lupus erythematosus. A 32-year-old woman (the index case) with lupus anticoagulant, multiple cerebrovascular events, and a family history of premature stroke raised the possibility of a familial diathesis. Histories or interviews, examinations, and blood tests were obtained for 23 members of four generations of her family. Four individuals had suffered strokes and three more had suffered neurologic symptoms. Two living individuals who had suffered strokes, two individuals with neurologic symptoms, and five asymptomatic individuals had antiphospholipid activity in their blood. In addition, a cousin of the index case was found to have systemic lupus erythematosus and antiphospholipid activity. Elevated concentrations of von Willebrand factor antigen were found associated with some positive lupus anticoagulant assays, the highest concentrations in the two individuals with stroke. The characteristic presentation of the index case and her good response to treatment suggests that further studies of families in whom antiphospholipid antibodies may represent a risk factor for stroke is worthwhile.

Adult↗
PubMed1989

Amyloidosis.

Explore the source record for details and available documents.

Alzheimer Disease↗
PubMed1989

The association of pulmonary hypertension with rheumatoid arthritis.

Pulmonary hypertension due to vasculitis is a rare complication of rheumatoid arthritis (RA). We describe 2 patients with RA and pulmonary hypertension who died with a clinical diagnosis of idiopathic pulmonary hypertension. In each case postmortem examination revealed severe pulmonary vasculitis as the actual cause of the hypertension. Subclinical systemic vasculitis was found in one case and hepatic nodular regenerative hyperplasia in both cases. Pulmonary vasculitis must be included in the differential diagnosis of pulmonary hypertension associated with RA. Open lung biopsy should be considered in this clinical setting in an attempt to identify this potentially treatable cause of pulmonary hypertension.

Adult↗
PubMed1988

Association of lupus anticoagulant with severe valvular heart disease in systemic lupus erythematosus.

Two cases of systemic lupus erythematosus with hemodynamically significant mitral valve dysfunction and associated lupus anticoagulant are reported. Both patients underwent valve replacement and both had thrombus formation on the mitral valve, one pre- and the other postoperatively. Both patients suffered a number of extracardiac thromboses at different times in the course of their illness. The contribution of the lupus anticoagulant to the thrombotic problems, and its possible relationship to the pathogenesis of Libman-Sacks endocarditis are discussed.

Adolescent↗
PubMed1988

Lupus anticoagulant, antiphospholipid antibodies and migraine.

The records of fifteen patients referred for neurological assessment and found to have lupus anticoagulant or elevated anticardiolipin antibodies were reviewed. The mean age for females in the group was 29.4 years and for males was 35. A diagnosis of migraine, either as an acute or chronic problem, was made in 10 (66%) of these patients. Seven of the 15 patients had ischemic stroke and two patients had other thrombotic complications associated with lupus anticoagulant. Three of the nine female patients with migraine had histories of spontaneous abortions. All migraine patients experienced transient or more prolonged neurological deficits with their headaches. An association between lupus anticoagulant and migraine can only be suggested. Data on the incidence of migraine in patients with lupus anticoagulant in the general medical population does not exist. Furthermore the prevalence of lupus anticoagulant in migraine sufferers is unknown. Therefore further studies are required to investigate this possible association.

Adult↗
PubMed1988

Seasonality comparisons among groups using incidence data.

A new test using incidence data is developed for testing whether two or more groups have the same seasonal pattern. The method fits sine waves to the data with a fundamental period of one cycle per year, and has the possibility of using higher harmonics, when necessary, to adequately model the data. The seasonal pattern can, therefore, have an arbitrary shape. The method allows for different length time intervals and different size populations at risk in the time intervals. Maximum likelihood estimation, based on the Poisson distribution, is used to determine the parameters of the model. Likelihood ratio tests and Akaike's information criterion (AIC) are used to determine the number of harmonics, and to test hypotheses. This method has been used to test for seasonal patterns in the incidence of insulin-dependent diabetes mellitus (IDDM) in Colorado among persons aged 0-17 years. Comparisons of seasonal patterns are made between males and females, and three age groups, each controlling for the other effect as in analysis of variance. Other potential applications of this approach are also discussed. A basic program is available for an IBM-PC to carry out these analyses.

Adolescent↗
PubMed1987

Brain-reactive autoantibody levels in the sera of ageing autoimmune mice.

Brain-reactive autoantibodies are thought to play an important role in mediating central nervous system (CNS) disorders in systemic lupus erythematosus (SLE). In this paper the developmental occurrence of these antibodies in the sera of autoimmune mice, i.e. NZB, NZB/W, MRL/l and BXSB mice were examined. All murine strains tested, whether autoimmune or not, showed some degree of serum reactivity toward brain antigens. Autoimmune mice, however, displayed higher levels of serum brain-reactive antibodies, and at earlier ages, than non-autoimmune mice. Immunofluorescence assays against brain sections and adsorption assays, with both neural and non-neural tissue, indicated a heterogeneity in the specificity of the populations of brain-reactive antibodies present. These studies provide an important step in characterizing the appearance and diversity of brain-reactive autoantibodies, with the goal of better understanding their significance and potential role in mediating CNS dysfunction in SLE.

Aging↗
PubMed1986

Prolonged thrombocytopenia in post-transfusion purpura (PTP) associated with changes in the crossed immunoelectrophoretic pattern of von Willebrand factor (vWF), circulating immune complexes and endothelial cell cytotoxicity.

A 39-year-old multigravida presented with a platelet count of 2 X 10(9)/112 d after a blood transfusion. The clinical presentation was typical of post-transfusional purpura (PTP). She was successfully managed with intensive plasma exchange with plasma replacement. Replacement with albumin saline was unsuccessful. Elevated levels of immune complexes were detected on presentation but were reduced to normal levels by plasma exchange but were elevated again during relapse. Raised levels of circulating platelet aggregates and platelet-aggregating activity were found during relapse but were absent during remission. Crossed immunoelectrophoresis of vWF showed a left shift suggesting the presence of abnormally high molecular weight multimeric forms. In contrast, multimeric assay of the same samples were within normal limits suggesting that the shift noted on crossed immunoelectrophoresis may have resulted from complexing of vWF with some other components. Immunological studies demonstrated the presence of endothelial cell cytotoxicity and lymphocytotoxicity in the patient's serum. It is concluded that the thrombocytopenia observed in PTP may not occur as a direct result of the immunological event initiating the disorder but rather indirectly via the release of vWF consequent upon endothelial cell damage which, either alone or in combination with another factor, possible immune complexes, induces intravascular platelet aggregation and sequestration. There were significant similarities between the case reported and recent observations in thrombotic thrombocytopenic purpura suggesting that these syndromes may have aetiological factors in common.

Adult↗