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Biomedical subjects

E R Hurd

Publications and source records attributed to E R Hurd.

At least 19 recordsLinked to original sources
PubMed1987

Kaposi's sarcoma in rheumatoid arthritis.

Cutaneous Kaposi's sarcoma developed eight months after initiation of prednisone treatment in a 58-year-old man with systemic rheumatoid disease (rheumatoid arthritis, Felty's syndrome, rheumatoid vasculitis, and myositis). This patient did not have the acquired immune deficiency syndrome. Review of the literature suggests that the onset of his Kaposi's sarcoma may have been related to immunosuppressive therapy with corticosteroids.

Arthritis, Rheumatoid↗
PubMed1979

Increased C1q binding immune complexes in Felty's syndrome: comparison with uncomplicated rheumatoid arthritis.

Sera from patients with Felty's syndrome (FS) and rheumatoid arthritis (RA) were examined for the presence of circulating immune complexes (IC) by using the 125I-C1q binding and monoclonal rheumatoid factor (mRF) techniques. Of 15 patients with FS, 9 (60%) had high 125I-C1q binding as compared to 3 of 26 RA patients (12%). The average C1q binding was significantly higher in the FS patients than in the RA patients without FS. C1q binding in both FS and RA patients was significantly higher than a group of 90 normal controls. In addition, serum C4 levels were significantly lower in the FS patients than in the RA patients. In contrast to these findings, IC levels in FS and RA patients were very similar when measured by the mRF technique. These studies indicate that FS patients have higher levels of complement-fixing IC in their sera than RA patients without FS. These findings raise the possibility that the complement-fixing IC found in these patients may play a role in the pathogenesis of neutropenia of FS.

Adult↗
PubMed1978

Comparison of the presence of immune complexes in Felty's syndrome and rheumatoid arthritis.

Evidence has been found to document the presence of circulating immune complexes in all patients with Felty's syndrome. The sera of all 12 patients studied showed intermediate complexes by analytical ultracentrifugation. The sera of 9 of 12 patients (75%) showed precipitin lines upon immunodiffusion against IgM rheumatoid factor. Both findings were statistically increased above those in a matched group of patients with classic rheumatoid arthritis. The presence of circulating immune complexes in the sera of the Felty patients was consistent with the observation that large inclusions containing IgG, IgM, and complement were phagocytized by normal polymorphonuclear cells when incubated with sera of Felty patients. Normal polymorphonuclear cells phagocytosed inclusions from 77% of Felty sera, compared with 27% classic rheumatoid arthritis sera. It is suggested that the uptake of immune complexes by polymorphonuclear cells plays a role in the neutropenia of Felty's syndrome.

Antigen-Antibody Complex↗
PubMed1978

Presence of leucocyte inclusions in spleen and bone marrow of patients with Felty's syndrome.

The spleens from two patients with Felty's syndrome and the bone marrow from one patient with Felty's syndrome were examined for the presence of intracytoplasmic inclusions in neutrophils when stained with antibodies to IgG, IgM, IgA, and betalc. Four normal spleens from trauma patients were similarly examined. In both spleens and the bone marrow from the Felty patients, large inclusions were noted. In none of the four normal spleens were large inclusions present. These studies suggest that phagocytosis of immune complexes by neutrophils in Felty patients may induce sequestration of these cells in the spleen and bone marrow.

Bone Marrow↗
PubMed1978

Association of interstitial nephritis with tubule cell injury and proliferation in NZB/NZW mice.

The relationship between renal interstitial mononuclear cell infiltration and renal tubule cell (TC) proliferation has been examined in (NZB X NZW) F1 hybrid (B/W) and control mice. TC proliferation was measured by tritiated thymidine ([3H]TdR) injection, autoradiographic examination of kidney sections and enumeration of labelled tubule cells. In B/W mice interstitial infiltration began at 5 months and reached a peak at 9 months. Proliferation of TC began at 7 months and also reached a peak at 9 months. Control mice consisting of NZB, CBA/J and C57Bl/6J mice showed no increase with age. When the percentages of labelled TC in areas adjacent to interstitial infiltrates and distant from them were compared, the TC adjacent to infiltrates showed an approximately four-fold greater amount of labelling. Ultrathin light and electron microscopic sections demonstrated TC injury in areas in close proximity to infiltrates. These studies suggest that mononuclear cells in the interstitial infiltrate may be injurious to TC, leading to a sequence of injury and subsequent regeneration of these cells. In diseases in which interstitial nephritis is present, such as Sjögren's syndrome, the interstitial infiltrate may contribute to the observed TC dysfunction.

Animals↗
PubMed1977

Macrophage migration inhibitory factor in rheumatoid pericarditis.

The pericardial effusion in a case of rheumatoid pericarditis was studied to determine whether immune complexes and mediators of cellular immunity, represented by migration inhibitory factor (MIF), were present. MIF-like activity was detected in the pericardial fluid, but only traces of immune complexes were revealed by ultracentrifugation. The MIF-like activity was partially characterized by column fractionation and sugar inhibition tests. The role of lymphokines in the pathogenesis of this case of rheumatoid pericarditis is strongly suggested.

Aged↗
PubMed1977

Phagocytosis of immune complexes by polymorphonuclear leucocytes in patients with Felty's syndrome.

The possible role of phagocytosis of circulating immune complexes by neutrophils in the production of the neutropenia of Felty's syndrome has been investigated. Normal neutrophils phagocytosed massive inclusions from the sera from twelve of fifteen patients with Felty's syndrome when incubated with these sera. Such inclusions were phagocytosed from only three of fifteen patients with seropositive RA who did not have Felty's syndrome. Normal neutrophils were more effective than patient neutrophils with regard to phagocytosis of inclusions from the patients' serum suggesting a defect in phagocytic function of Felty's neutrophils. The titre of granulocyte-reactive antinuclear antibodies did not appear to be related to the degree of neutropenia. The data suggest that phagocytosis of circulating immune complexes by neutrophils may interfere with the function of these cells in combating infection and also render them susceptible to removal from the circulation thus leading to the development of neutropenia.

Antibodies, Antinuclear↗
PubMed1977

Quantitative studies of immunoglobulin deposition in the kidney, glomerular cell proliferation and glomerulosclerosis in NZB/NZW F1 hybrid mice.

Using the NZB and NZB/NZW F1 (B/W) hybrid mouse as a model for systemic lupus erythematosus, an effort has been made to quantitate: (1) immune complex deposition in the glomeruli by immunofluorescent staining of immunoglobulin, (2) glomerular cellular proliferation by radioautographic measurement of [3H]Tdr incorporation into the glomerular cells in vivo, and (3) glomerular scarring by PAS staining. The relationship between these changes and increasing age has been examined. By radioautography it was observed that dividing glomerular cells were labelled in vivo after injection of [3H]Tdr. This provided a reproducible measure of the proliferative process in the nephritis of B/W mice. In C57B1/6J and CBA/J mice, which have a low incidence of glomerular disease, little change in the amount of glomerular cell proliferation was observed with increasing age. The NZB strain of animals showed a somewhat increased level of proliferation but this did not increase with age. In striking contrast, glomerular cell proliferation in the B/W mice increased rapidly with age. The earliest change observed in the kidney was the deposition of immunofluorescent material in the mesangium and glomerular capillary basement membrane beginning between 3 and 5 months of age and reaching a peak at 9 months. Increase in glomerular cell proliferation began about 2 months after the onset of immune complex deposition but also reached a maximum at 7 months. Glomerular sclerosis was the last change to appear and continued after the other two parameters measured has begun to decline. These data suggest that the deposition of immune complexes in the glomerulus may be an important triggering mechanism for renal cell proliferation and glomerulosclerosis in the B/W mouse. The techniques described would provide a sensitive and reproducible quantitative method for analysing the differential effects of various types of treatment of immune complex nephritis in animals.

Age Factors↗
PubMed1977

The mechanism of action of cyclophosphamide on the nephritis of (NZB x NZW)F1 hybrid mice.

The effects of cyclophosphamide an antinuclear antibody levels, immune complex deposition in renal glomeruli, glomerular cell proliferation and glomerulosclerosis in the (NZB x NZW)F1 hybrid mouse have been investigated in order to better understand the mechanism of action of this drug on nephritis. Five groups of mice were injected daily with this agent (15 mg/kg) by the i.p. route over a 2-month period. Treatment periods began at 1, 3, 5, 7 and 9 months. Each group was killed at the end of the treatment period. During the last week [3H]Tdr(1 mu Ci/g) was injected daily i.p. Immune complex deposition was measured by quantification of glomerular immunofluorescent staining in both capillary loops and mesangium. Glomerular cell proliferation was quantified by measurement of the number of glomerular cells which incorporated [3H]Tdr during in vivo labelling. The number of [3H]Tdr-labelled cells in each of 100 glomeruli was counted using kidney autoradiographs of whole kidney slices. This technique provided a very reproducible and quantitative index of glomerular cell proliferation. Glomerulosclerosis was measured by determining percentage of PAS-positive material in each of 100 counted glomeruli. Immune complex deposition in the kidney preceded the glomerular cell proliferation. The proliferation reached a peak at 9 months of age. Glomerulosclerosis gradually increased with age until the animal's death. Cyclophosphamide significantly decreased antinuclear antibody levels, glomerular cell proliferation, and immunoglobulin staining in the glomeruli. Progression of glomerulosclerosis was significantly arrested. The present findings demonstrate a very significant effect of cyclophosphamide on three important pathological changes which occur in the nephritis of the (NZB x NZW)F1 hybrid mouse and provide information about possible mechanisms underlying these changes.

Animals↗
PubMed1977

Effect of cyclophosphamide on interstitial nephritis and tubule cell proliferation in NZB/NZE mice.

The effect of cyclophosphamide on renal interstitial mononuclear cell infiltration and renal tubule cell (TC) proliferation has been examined in (NZB x NZW)F1 hybrid (B/W) and control mice. TC proliferation was measured by tritiated thymidine (3/Tdr) injection, autoradiographic examination of kidney sections, and enumeration of labeled tubular cells. Cyclophosphamide administered 2 months before sacrifice virtually obliterated interstitial infiltration and significantly decreased tubule cell proliferation at 3, 5, 7, 9, and 12 months of age.

Aging↗
PubMed1976

The differential effects of cyclophosphamide and 6-mercaptopurine on the renal disease and skin immunoglobulin deposits of the NZB-NZW F1 hybrid mice.

The following differential effects of immunosuppressive therapy with Cyclophosphamide (CYCLOPH) and 6-mercaptopurine (6-MP) in the female NZB-NZW F1 hybrid strain have been observed: (1) CYCLOPH but not 6-MP significantly decreased antinuclear antibody level. (2) Both CYCLOPH and 6-MP significantly decreased glomerular cell proliferation. (3) Both CYCLOPH and 6-MP significantly arrested progression of glomerulosclerosis. (4) While CYCLOPH significantly diminished Ig deposition in the glomeruli, 6-MP had no effect on this phenomenon. (5) While CYCLOPH decreased subepidermal globulin deposition in the skin, 6-MP appeared actually to enhance subepidermal staining. Thus, the present studies demonstrated that CYCLOPH was superior to 6-MP in four of the five parameters studied. In the case of one parameter, Ig staining of the skin, 6-MP actually produced enhancement of the staining. Both CYCLOPH and azathioprine which is a derivative of 6-MP, are currently being used for the treatment of human SLE. The present findings suggest that of the two, CYCLOPH may be the drug of choice.

Animals↗
PubMed1975

Subepidermal deposition of immunoglobulin in NZB/NZW F hybrid mice.

The dermal-epidermal junction of NZB/NZW F1 hybrid mice is a site of immunoglobulin (Ig) deposition. This produces a fluorescent band which is very similar to that seen in the skin of patients with systemic lupus erythematosus. The deposition of Ig in the mouse skin is first observed at six months of age and increases in frequency thereafter. After an initial lag of 1 to 2 months, it parallels the age-related deposition of Ig in the kidney. The observed temporal relationship between glomerular and cutaneous Ig deposition supports the concept that the presence of immunoglobulin in the skin is highly indicative of the presence of immune complexes in the kidney.

Animals↗