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Biomedical subjects

E V Hess

Publications and source records attributed to E V Hess.

At least 55 records · Page 3Linked to original sources
PubMed1991

NSAID induction of interleukin 1/catabolin inhibitor production by osteoarthritic synovial tissue.

Select classes of nonsteroidal antiinflammatory drugs (NSAID), independent of their cyclooxygenase suppressing property, may potentially regulate pathophysiologic mechanisms operative in accelerated cartilage catabolism occurring in osteoarthritis (OA). Piroxicam has been shown to downregulate the expression of interleukin 1 (IL-1) associated chondrocyte enzyme inducing activity (catabolin) produced by OA synovium. In situ membrane synthesis of catabolin/IL-1 inhibitors functioning at various levels in thymocyte and catabolin bioassay systems is currently shown. The piroxicam effect appears due to a selective increase in production of a naturally occurring inhibitor(s) and/or induction of new inhibitor formation acting on chondrocytes at a post-IL-1 receptor level.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Induction of autoantibodies by human immunodeficiency virus infection and their significance.

Although many of the changes in HIV and AIDS appear to be global, on closer investigation the defects are specific and can be explained by recognized mechanisms. Despite a demonstrated concurrent polyclonal B-cell activation, studies fail to show any evidence to date of significant dysregulation of the immune system leading to serologic or clinical autoimmunity.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Effects of procainamide hydroxylamine on generation of reactive oxygen species by macrophages and production of cytokines.

A series of experiments was conducted to examine the effects of the N-oxidized metabolite of procainamide, procainamide hydroxylamine (PAHA), on reactive oxygen species (ROS) production by macrophages in vitro, as well as on the release of the cytokine interleukin-1 (IL-1). Results with PAHA were compared with those from the parent compound, procainamide, and in some cases with other procainamide metabolites such as N-acetylprocainamide or nitrosoprocainamide. The effects of PAHA on ROS production by mouse and rat macrophages were complex, resulting in both stimulatory and inhibitory activity depending upon the PAHA concentration and whether macrophages were resting or elicited. The primary effect of PAHA appeared to be a stimulation of ROS production. Monocytes pretreated with PAHA (20 microM) depressed the responsiveness of lymphocytes in co-culture to a T-cell mitogen (conconavalin A) but not a B-cell mitogen (lipopolysaccharide). This effect was inhibited when monocyte pretreatment with PAHA was accompanied by the antioxidants, catalase or superoxide dismutase. IL-1 production by rat adherent splenocytes was unaffected by PAHA in concentrations that were not cytotoxic. These observations suggest that the oxidative metabolism of procainamide to PAHA may result in enhanced production of ROS by macrophages contributing its toxicity to lymphocytes.

Animals↗
PubMed1990

HIV and arthritis.

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Arthritis, Infectious↗
PubMed1989

Procainamide hydroxylamine lymphocyte toxicity--I. Evidence for participation by hemoglobin.

A number of lines of evidence suggest that the lupus-like symptoms associated with procainamide therapy may be caused by products of metabolic N-oxidation. In the present study, the perfusion of the isolated rat liver with a hemoglobin-free solution containing procainamide (100 microM) resulted in the rapid appearance of the N-oxidation metabolite procainamide hydroxylamine in the perfusate. Addition of procainamide hydroxylamine in vitro to whole rat blood (1-40 microM) resulted in a concentration-dependent loss of proliferative response among mononuclear cells isolated from the treated blood and cultured with mitogens (phytohemagglutinin, PHA-P: concanavalin A, Con A; and pokeweed mitogen, PWM), as well as a loss of viability. Similar effects on lymphocyte mitogen responsiveness were observed when procainamide hydroxylamine (1-40 microM) was added to rat whole splenic cell populations. Carbon monoxide or ascorbic acid pretreatment inhibited the toxicity of procainamide hydroxylamine to lymphocytes in whole blood, but only carbon monoxide pretreatment inhibited procainamide hydroxylamine-induced methemoglobin formation. These observations are consistent with the participation of hemoglobin in a redox cycle with procainamide hydroxylamine, generating products which are primarily responsible for its cytotoxicity in blood.

Acecainide↗
PubMed1989

Drug-related lupus.

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Drug-Related Side Effects and Adverse Reactions↗
PubMed1989

Immunomodulatory effects of procainamide metabolites: their implications in drug-related lupus.

Evidence suggests that N-oxidized metabolites of procainamide may be responsible for the development of lupus-like symptoms associated with procainamide therapy. The human hepatic microsomal metabolism of procainamide has been previously reported to result in formation of the N-hydroxylamine derivative of procainamide (procainamide hydroxylamine [PAHA]). The objective of this study was to examine the effects of PAHA on human lymphocytes and adherent cells (monocytes and macrophages). When incubated with lymphocytes in whole blood, PAHA enhanced the response to mitogen and immunoglobulin secretion at lower concentrations (less than or equal to 4 mumol/L) but suppressed these functions at higher concentrations. The cytotoxic effects were nonselective for T lymphocytes and B lymphocytes and appeared to involve an interaction between PAHA and hemoglobin. When erythrocytes were removed or when hemoglobin was converted to carboxyhemoglobin, the suppressive effects of PAHA on lymphocytes were reduced. PAHA stimulated interleukin-1 production by adherent cells at 25 mumol/L but had no effect at lower concentrations. Superoxide anion release was unaffected by PAHA in "resting" adherent cells. Pretreatment with PAHA (2 mumol/L) diminished superoxide release in response to stimulation by phorbol myristate acetate (PMA) or latex bead phagocytosis but augmented superoxide release when coincubated with PMA or latex. These observations indicate that PAHA produces complex, concentration-dependent interactions with human immunoregulatory cells, and they suggest that the effects of PAHA on lymphocyte function may result from the further oxidation of PAHA by hemoglobin, perhaps to the nitroso form.

Adult↗
PubMed1989

Nonsteroidal antiinflammatory drugs in rheumatoid arthritis: duration of use as a measure of relative value.

To determine if any nonsteroidal antiinflammatory drug (NSAID) was superior in the treatment of rheumatoid arthritis, duration of use of each drug was employed as a measure of combined efficacy and tolerability. Duration was treated as survival data and a proportional hazards model utilized to adjust for differences in disease severity and concomitant antirheumatic therapy. One hundred and sixteen patients took 188 courses of nonsalicylate NSAID during the 3-year study period. The NSAID prescribed included naproxen, ibuprofen, sulindac, indomethacin, piroxicam, and tolmetin. Naproxen was used significantly longer than any other NSAID (p less than 0.001).

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1989

In vitro effect of select nonsteroidal antiinflammatory drugs on the synthesis and activity of anabolic regulatory factors produced by osteoarthritic and rheumatoid synovial tissue.

Nutriment replenished conditioned media derived from cultures of osteoarthritic and rheumatoid synovial tissue contain factors of variable molecular weight, independent of prostaglandin activity, which are capable of reversibly down-regulating cartilage matrix proteoglycan synthesis. Piroxicam significantly reduced anabolic suppressant factor production on an apparent selective basis. It could be shown to partially modify the chromatographic profile of newly synthesized osteoarthritic synovial tissue protein fractions containing suppressant activity. Dependent on experimental design, piroxicam also partially blocked inhibitory activity at a chondrocyte level. Indomethacin and sodium salicylate were essentially without effect.

Animals↗
PubMed1988

Acquired immune deficiency syndrome (AIDS) and autoimmunity--mutually exclusive entities?

Loss of normal immune homeostasis occurs in acquired immune deficiency syndrome (AIDS). We evaluated patients at the University of Cincinnati and New York University Medical Centers for serologic evidence of autoimmune changes. Specifically, tests for antinuclear and organ-specific antibodies by immunofluorescence, antisperm and anti-seminal plasma antibodies, rheumatoid factor by latex and sensitized sheep cell agglutination techniques, anti-polyadenosine (poly A), and single-stranded DNA antibodies were performed in human immunodeficiency virus (HIV) antibody-positive sera. A parallel study of mitogen responsiveness was performed and showed inhibition of response by AIDS and AIDS-related complex (ARC) sera. In spite of evidence of polyclonal B-cell activation, hyperglobulinemia, and the presence of antibodies to many infectious agents, as well as the known cellular immune abnormalities, the patients tested had a striking absence of these autoantibodies. The only major difference noted from normal controls, was a low but significant level of antibody binding to poly A. The autoimmune connective tissue diseases were not observed in this group of patients.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Prospective study of the evolution of Raynaud's phenomenon.

Seventy-four patients with Raynaud's phenomenon and no associated illness were followed prospectively to determine whether a secondary disease would develop, and clinical and laboratory assessments were performed at study entry to determine their association with the subsequent development of disease. After an average of 2.7 years of follow-up (range 0.5 to 5.7 years), outcome information was available on 58 persons (78.4 percent). A connective tissue disease developed in 11 (19.0 percent): three systemic sclerosis and eight CREST syndrome. The two variables at entry most strongly associated with the subsequent development of a connective tissue disease were an abnormal nailfold capillary pattern (adjusted odds ratio = 26.82, 95 percent confidence interval = 4.69, 153.2) and an abnormal pulmonary function test result (odds ratio = 4.78, 95 percent confidence interval = 1.02, 22.41). The positive association of an abnormal barium esophagram, presence of antinuclear antibodies, and cutaneous abnormalities did not reach statistical significance. The development of connective tissue diseases in this group of patients is not rare. An abnormal nailfold capillary pattern is strongly associated with the subsequent development of systemic sclerosis or CREST syndrome in patients with Raynaud's phenomenon.

Adolescent↗
PubMed1988

Sperm and seminal plasma antibodies in acquired immune deficiency (AIDS) and other associated syndromes.

Although HIV has been established as the etiologic agent in AIDS, other contributory cofactors may be responsible for selective clinical manifestations of the syndrome. While the pathogenesis remains unclear, the development of immunologic abnormalities observed in some homosexual males with AIDS and AIDS-related complex may be attributed to repeated exposure to allogeneic sperm and seminal plasma components. Accordingly, antibody levels to semen fractions were measured in sera from 338 individuals (295 AIDS, 36 ARC, 16 randomly selected homosexuals, 29 patients with infectious hepatitis, 12 hemophiliacs, 20 rheumatic disease patients, and 24 healthy heterosexual adults). The methods were (i) passive hemagglutination for antibodies to human seminal plasma (HuSePl), and (ii) indirect immunofluorescence (IF) assay on methanol-fixed human sperm noting staining of acrosomal, equatorial, postnuclear, and tail main-piece regions. HuSePl was positive in 31% AIDS sera, while 39% were positive by IF. ARC sera were 30% positive for HuSePl and 38% positive IF. No control sera were positive. Results reveal a significant incidence of antibody to sperm and seminal plasma components in ARC and AIDS patients. Because of the known immunomodulating properties of both, it is possible that these responses may indicate risk factors for disease progression and severity.

AIDS-Related Complex↗