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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↗
PubMed1984

Study of HLA antigens in ten multiple-case rheumatoid arthritis families.

We studied the inheritance of HLA haplotypes in 10 families with more than one member affected with adult onset rheumatoid arthritis (RA). The frequency of DR4 was 81% among these patients. Nine families had DR4 bearing haplotypes and homozygosity for DR4 existed in 4 families. In 6 of these families DR4 positive haplotypes were shared among affected members. All but one of the affected sibs shared at least one haplotype with their index case. Ten percent of the unaffected relatives had rheumatoid factor (RF). HLA-DR4 or associated genes appeared to confer susceptibility for RF production and development of RA. However, these haplotypes were inherited also by many sibs who did not develop any manifestations of disease.

Arthritis, Rheumatoid↗
PubMed1982

Increased endothelial cell adherence, aggregation, and superoxide generation by neutrophils incubated in systemic lupus erythematosus and Felty's syndrome sera.

The ability of sera from patients with systemic lupus erythematosus (SLE) and Felty's syndrome to induce increased adhesiveness of normal human neutrophils (PMN) was investigated. PMN from normal healthy donors were incubated in sera from 19 patients with active SLE, 12 with inactive SLE, 20 with Felty's, 24 with rheumatoid arthritis, and 34 normal persons. After incubation, the degree of adherence of the PMN to human endothelial cells in culture, their aggregation, and superoxide (O2-) generation were determined. Sera from patients with both active SLE and Felty's syndrome induced significantly increased PMN adherence to endothelial cells and PMN aggregation in vitro, compared with normal sera. This increased adherence to endothelial cells was maintained after heat treatment (56 degrees C for 30 minutes) of the sera. In O2- generation experiments, sera from patients with active SLE induced significantly increased O2- release from normal PMN using both fresh and heat-treated sera. Sera from Felty's patients demonstrated the same effect with heat-treated sera but not ith fresh sera. When sera from patients with active SLE and Felty's syndrome were used, all three parameters correlated significantly with each other in individual patients. In contrast, sera from the 12 patients with inactive SLE and 24 rheumatoid arthritis patients without Felty's failed to induce significant differences in the three parameters studied when compared with 34 normal controls. Fractionation of 3 SLE sera and 1 Felty's serum on Sephadex G-200 demonstrated that the adherence enhancing factor was present in both IgG and IgG-excluded fractions. The observed increased adhesiveness of PMN induced by SLE and Felty's sera may, at least in part, contribute to the neutropenia which is common in these diseases. Increased O2- release associated with PMN adherence may contribute to endothelial cell damage and vascular injury, which is also a common manifestation of these diseases.

Adult↗
PubMed1982

NAD+-dependent 15-hydroxyprostaglandin dehydrogenase activity in kidney tissue from NZB/NZW F1 hybrid mice.

Prostaglandins, or related compounds, as well as estrogen and androgen are believed to be involved in the processes that lead to the development of murine lupus erythematosus (LE) in NZB/NZW F1 hybrid mice. In this investigation we measured NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) activity in kidney tissue of male and female NZB/NZW F1 hybrid mice and in kidney tissue of male and female mice of other strains. In each case the specific activity of PGDH was significantly greater in kidney tissue of male than in kidney tissue of female mice. However, the specific activities of PGDH in kidney tissues of males of various strains of mice were similar, and the specific activities of PGDH in kidney tissues of females of various strains-including the NZB/NZW F1 hybrid- were similar. Thus, while the lower activity of PGDH in kidney tissues of the female may be important in the pathogenesis of LE, the lower activity of this enzyme is not unique to the kidney of the female NZB/NZW F1 hybrid mouse.

Animals↗
PubMed1981

Human neutrophil swelling induced by immune complexes and aggregated IgG.

Using a Coulter counter method, the effects of various types of IgG-dependent phagocytic stimuli on human neutrophil (PMN) swelling were determined. Human heat aggregated IgG, ovalbumin-antiovalbumin (OV-anti-OV) immune complexes, and opsonized latex particles all induced PMN swelling. The OV-anti-OV immune complexes were effective, whether prepared at antigen-antibody equivalence (insoluble) or at 4 or 9 times antigen excess (soluble). Swelling of PMN occurred at 37 degrees C, but not at 4 degrees C. Complement was not present in any of the experiments. In contrast to the above results, native IgG, OV-anti-OV F(ab')2 immune complexes and unopsonized latex particles did not induce PMN swelling. These results suggest that the PMN swelling observed in this study is due to Fc-dependent, complement-independent membrane stimulation and/or phagocytosis.

Antigen-Antibody Complex↗
PubMed1981

Neurological complications of connective tissue and other "collagen-vascular" diseases.

A variety of neurological complications may occur in the various connective tissue and "collagen-vascular" diseases. Most of these complications are due to vasculitis affecting various sites in the central or peripheral nervous system. While the evidence for definitive vasculitis in SLE is not strong, small vessel damage usually is present in anatomic sites which correlate well with clinical features. Although patients with rheumatoid arthritis also may have vasculitis, neurological complications are usually related to nerve compression by rheumatoid nodules or the arthritic process itself. Considerable controversy exists regarding the accuracy of various diagnostic tests. While corticosteroids are the mainstay of therapy for these conditions, there are no definitive studies proving their efficacy.

Arthritis, Rheumatoid↗
PubMed1981

Beneficial effect of an essential fatty acid deficient diet in NZB/NZW F1 mice.

New Zealand Black by White (B/W) hybrid mice spontaneously develop a disease similar to systemic lupus erythematosus (SLE). Subepidermal immunoglobulin deposits (Se-Ig) and antibodies to double-stranded DNA (anti-dsDNA) develop in aging mice. Death from glomerulonephritis occurs at 8 to 12 mo. Previous findings suggest that epidermal DNA:anti-dsDNA complexes form in situ since Se-Ig correlates with anti-ds DNA and Se-Ig accumulation is augmented by increased epidermal proliferation (presumably due to enhanced epidermal DNA release). Since essential fatty acid (EFA) deficiency is known to increase epidermal proliferation we have studied the effect of an essential fatty acid deficient EFA-d diet on: (1) Se-Ig, anti-dsDNA, and (3) survival. Ten-mo B/W mice on an EFA-d diet were compared with 14 controls on a calorically equivalent standard diet. Both groups were initiated on their diets at 2 mo of age. Only female mice were used. All were weighed weekly; tested for anti-ds DNA (Crithidia luciliae assay) each month; and biopsied for direct immunofluorescence (IF) staining of skin at 6, 7.5, 9, 10.5, and 12 mo. Tissue (skin and kidney) was also obtained for light and IF microscopy. Weights in the 2 study groups were essentially identical. All disease manifestations examined were strikingly altered in the EFA-d animals. Only 2 of 14 (14%) control animals survived to 9 mo and both had anti-dsDNA and Se-Ig. In contrast, 8 of 10 (80%) EFA-d mice were alive at 9 mo and none had anti-dsDNA or Se-Ig. The kidneys from EFA-d mice at 10 mo were normal; however, all kidneys from 7 to 9 mo control mice were abnormal by both light and IF microscopy. Eight of the 10 EFA-d mice were alive at 10 mo. None had Se-Ig but one had anti-dsDNA. At 16 mo (4 mo after controls had died) 7 of 10 EFA-d mice were living and 60% were anti-ds DNA positive. These findings strongly suggest that (1) SE-Ig is present in mice with anti-dsDNA and severe renal disease and (2) EFA-d produces a profoundly beneficial effect in the disease process.

Animals↗
PubMed1981

Increased superoxide generation by normal granulocytes incubated in sera from patients with psoriasis.

Sera from patients with untreated psoriasis were found to induce increased superoxide anion (O-2) generation when incubated with normal granulocytes (PMNs) and zymosan. Sera from patients receiving systemic chemotherapy induced O-2 generation which was similar to that of normal sera and significantly lower than sera from the untreated patients. O-2 production was measured by superoxide dismutase inhibitable ferricytochrome C reduction and was dependent on the presence of both zymosan and a heat labile serum factor. Serum C3c and C5 levels were elevated in both treated and untreated groups of psoriasis patients while C4 was elevated only in untreated patients. serum ceruloplasmin, a O-2 scavenger, was not decreased in patients with psoriasis, and consequently does not account for the increased O-2 generation. These data suggest that sera from patients with psoriasis have an increased capacity to activate PMNs. Activation of PMNs in cutaneous and joint lesions may play a pathogenic role in psoriasis.

Ceruloplasmin↗
PubMed1981

Prevention of glomerulonephritis and prolonged survival in New Zealand Black/New Zealand White F1 hybrid mice fed an essential fatty acid-deficient diet.

Female B/W mice spontaneously develop an autoimmune disease that is similar to systemic lupus erythematosus. Antibodies to doublestranded DNA (dsDNA) and antinuclear antibodies develop in aging animals; death from immune complex-mediated glomerulonephritis occurs from 8 to 12 mo of age. It has been reported that prostaglandin (PG)E(1) treatment of such mice prolongs survival. In the present study, four groups of female B/W mice were studied beginning at 6-11 wk of age on the following regimens: (a) a synthetic diet that contained 20% safflower oil, (b) a standard laboratory chow diet, (c) a standard diet together with injections of PGE(1), and (d) an essential fatty acid-deficient synthetic diet that contained 20% coconut oil. All animals were tested monthly for antinuclear antibodies and anti-dsDNA. Kidney tissue was obtained for light and immunofluorescence microscopy when animals were dying. All disease manifestations were altered strikingly in the essential fatty acid (EFA)-deficient animals. Intermediate benefit was seen in PGE(1)-treated animals. 7% of the control animals and 18% of safflower oil-fed animals survived to 10 mo. In contrast, the PGE(1)-treated and EFA-deficient mice had a similar survival rate (78-88%). At age 16 mo, 78% of EFA-deficient mice and 45% of PGE(1)-treated mice were alive. 25% of the PGE(1)-treated and 55% of the EFA-deficient animals survived to 20 mo. Serum anti-dsDNA appeared at age 5 mo in safflower oil-fed and control animals, but not until 9 and 12 mo for PGE(1)-treated and EFA-deficient animals, respectively. All kidneys from 7- to 9-mo-old safflower oil-fed and control animals and the majority of kidneys from PGE(1)-treated animals were abnormal by light and immunofluorescence microscopy. Kidneys from EFA-deficient animals were essentially normal at 10 mo. At 13 mo, all PGE(1)-treated animals examined had significant kidney involvement, whereas none of the EFA-deficient animals had glomerulonephritis. These findings demonstrate that an EFA-deficient diet has a beneficial effect on murine lupus erythematosus.

Age Factors↗
PubMed1981

Human neutrophil aggregation and increased adherence to human endothelial cells induced by heat-aggregated IgG and immune complexes.

Several types of IgG-dependent phagocytic stimuli independent of complement were investigated for their property to induce human polymorphonuclear neutrophil leucocyte (PMN) aggregation and adherence to human endothelial cells (EC) in culture. A Coulter counter method was employed for the detection of cell aggregation. Aggregated IgG, ovalbumin-anti-ovalbumin (OV anti-OV) immune complexes (both insoluble and soluble) and opsonized latex particles induced a significant degree of PMN aggregation which was detectable as early as 2 min after exposure of PMN to these stimuli. This aggregation was dependent on divalent cations (Ca++, Mg++). The same phagocytic stimuli furthermore significantly increased adherence of PMN to cultured human EC and serum-coated plastic. Controls consisting of native IgG, and OV anti-OV complexes prepared from Fab')2 antibody failed to induce either aggregation or increased adherence of PMN. These data suggest that exposure of PMN to IgG-dependent phagocytic stimuli induces increased adhesiveness of PMN and that interaction between the Fc-receptor of PMN and the Fc-portion of phagocytic stimuli is essential for this effect.

Antigen-Antibody Complex↗
PubMed1980

Increased granulocyte adherence in psoriasis and psoriatic arthritis.

Circulating polymorphonuclear leukocytes (PMN) from patients with psoriasis and psoriatic arthritis were found to be significantly more adherent to nylon fiber columns when compared with both normal and nonpsoriatic patient control groups. The increased adherence correlated positively with the extent of disease and was highest in those patients with psoriatic arthritis. Total leukocyte and PMN counts were increased in psoriasis patients and were highest in the psoriatic arthritis group. No increase in cell counts was found for mononuclear leukocytes. PMN adherence was not increased in lithium-treated patients or a nonpsoriatic patient control group although such patients did have significant granulocytosis. PMN's are frequently present in lesions of psoriasis as are activated complement components and abnormal keratinocyte cyclic nucleotide levels. These factors or others may cause a generalized activation of PMN's in psoriasis leading to migration of neutrophils into the skin lesion. The present study demonstrates a systemic effector cell alteration in psoriasis and contradicts the general concept that uncomplicated psoriasis is limited to the skin.

Arthritis↗
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↗