Search PubMed⌕ Search

Biomedical subjects

E V Potter

Publications and source records attributed to E V Potter.

At least 37 records · Page 2Linked to original sources
PubMed1977

Occult lupus nephropathy: a correlated light, electron and immunofluorescent microscopic study.

Renal biopsies obtained from four adolescent girls who developed symptomatic thrombocytopenia with serologic evidence of systemic lupus erythematosus, without clinical signs of renal involvement, showed glomerular disease by electron and immunofluorescent microscopy with light microscopic changes in two cases. Subsequently, three of the patients developed proteinuria, and repeat biopsies from all four showed appearances ranging from resolution to significant glomerulitis. The findings illustrate the variable patterns of occult glomerulitis in lupus, and highlight the value of correlating light, electron and immunofluorescent studies in renal pathology.

Adolescent↗
PubMed1976

Absence of ristocetin aggregation factor from the skin of a patient with von Willebrand's disease.

Samples of apparently normal skin from one patient with von Willebrand's disease (vWD) and five patients without vWD were examined with fluorescein-tagged antiserum to the component of factor VIII required for aggregation of platelets by ristocetin (VIII-R.A.F.). No evidence of VIII-R.A.F. was found in the vWD skin, while bright granules were seen on and/or in the endothelial cells of dermal capillaries in all patients without vWD. VIII-R.A.F. granules were also found in the interstitial vasculature of all of twelve renal-biopsy specimens from patients without vWD. These observations support the concept that an abnormality of the vascular endothelium is involved in the pathogenesis of vWD.

Blood Platelets↗
PubMed1976

Failure of AHF concentration to control bleeding in von Willebrand's disease.

A newly available dried concentrate of antihemophilic factor (Profilate, Abbott Laboratories) was compared with standard, blood-bank prepared cryoprecipitate in the control of bleeding in a patient with von Willebrand's disease. Profilate effectively raised plasma levels of factor VIII but produced only half the expected increase in plasma ristocetin aggregation factor (RAF), and this RAF did not bind readily to the platelets in the presence of ristocetin. Furthermore, the Profilate had little effect upon the bleeding time or the clinical hemorrhage. In contrast, the cryoprecipitate did increase plasma RAF to the expected level, and this RAF bound readily to the patient's platelets in the presence of ristocetin. Cryoprecipitate promptly controlled bleeding. We conclude that the RAF present in Profilate retains in vitro activity but is incapable of augmenting platelet function in vivo.

Adult↗
PubMed1976

Immunoglobulin E in renal disease.

Samples of renal tissue from 373 patients were examined for the presence of immunoglobulin E (IgE) by immunofluorescent techniques. Only trace to ++ amounts ( on a scale of ++++) were found in 20 patients: 4/9 with post-streptococcal acute glomerulonephritis (GN), 5/30 with GN associated with systemic lupus erythematosus, 3/20 with membranous GN, 1/4 with Goodpasture's syndrome, 2/18 with recurrent microhematuria and focal GN, 1/5 with hemolytic anemia and uremia, 3/73 with renal homografts, and 1/5 with dermatomyositis. No IgE was found in 18 patients with lipoid nephrosis, 8 of whom were being treated with prednisone, nor in 5 patients with focal glomerular sclerosis and the nephrotic syndrome. Serum IgE was measured in 9 of the 20 patients with glomerular deposits of this globulin. With one exception, levels of IgE were within the range generally considered to be normal. However, they were greater than the mean of this range in all but two and near the highest limits of normal in most. Neither the amounts of serum IgE nor the degree of proteinuria could be related to the intensity of stain for IgE in the glomeruli of these patients.

Adolescent↗
PubMed1976

Platelet-bound ristocetin aggregation factor in normal subjects and patients with von Willebrand's disease.

Antiserum specific for that part of the factor VIII complex designated ristocetin aggregation factor (VIIIRAF) was prepared by immunizing rabbits with VIIIRAF derived from the plasma of a hemophilic patient with circulating antibody to factor VIII procoagulant activity (VIIIcoag). The rabbit antiserum prevented ristocetin-induced platelet aggregation and platelet retention by glass-bead columns. Although the antiserum also inactivated VIIIcoag in normal plasma, it did not inactivate VIIIcoag which had been dissociated from VIIIRAF by chromatography in 1 M NaCl, thus establishing the antigenic specificity of these two factors. When the VIIIRAF antibody was conjugated with fluorescein isothiocyanate and used to examine platelets from normal subjects and patients with von Willebrand's disease, the normal platelets showed a granular fluorescence similar to that observed with antifibrinogen serum whole von Willebrand platelets showed no fluorescent staining. The normal platelets retained the VIIIRAF granules during 18 hours incubation and 5 washings in artificial medium while the von Willebrand platelets failed to acquire granules after 18 hours in normal plasma. When the unstained platelets from patients with von Willebrand's disease were suspended in normal plasma and then aggregated by the addition of ristocetin, the aggregates not only stained brightly for VIIRAF, but fluorescent granules could be seen on individual platelets in the aggregates. These observations suggest that ristocetin causes the binding of VIIIRAF to platelets as well as platelet-to-platelet adhesion.

Blood Platelets↗
PubMed1975

Immunoglobulins and complement components in synovial fluid of patients with acute rheumatic fever.

Three components of complement and six other serum proteins were assayed in synovial fluid and serum samples from 25 patients with acute rheumatic fever in Trinidad. The resulting data indicate a relative decrease in both early and late components of complement within the synovial fluids which suggests local activation by immune complexes. Such activation of complement within the joint spaces may play a primary role in development of the inflammatory arthritis of acute rheumatic fever.

Adolescent↗
PubMed1975

Salivary immunoglobulins and streptococcal antibodies in patients with acute rheumatic fever.

Evidence of a local immunologic response to recent pharyngeal infection with group A streptococci was sought in 23 patients with acute rheumatic fever. Salivas from these patients were examined and compared with salivas from control subjects. As assayed, both IgG and IgA values ranged between 8 and 170 mg. per 100 ml. in 10-fold concentrated samples of saliva. When these values were corrected for the concentration of the samples and for the use of serum IgA standards, the following mean values were obtained: for patients with acute rheumatic fever, IgG was 4.5 mg. per 100 ml. and IgA was 8.7 mg. per 100 ml.; for control subjects, IgG was 5.0 mg per 100 ml. and IgA was 9.9 mg. per 100 ml. IgM was present in amounts of 1 to 2 mg. per 100 ml. in 2 patients and 7 control subjects. Antistreptolysin O titers correlated with amounts of IgG in the saliva samples while antihyaluronidase, antigroup A carbohydrate, and antiteichoic acid titers did not. None of the antibody titers correlated with the IgA content of the saliva samples. Furthermore, saliva antibody titers did not differ between patients with acute rheumatic fever and control subjects.

Acute Disease↗