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Biomedical subjects

P H Plotz

Publications and source records attributed to P H Plotz.

At least 109 records · Page 6Linked to original sources
PubMed1979

Bladder complications in patients receiving cyclophosphamide for systemic lupus erythematosus or rheumatoid arthritis.

The bladder complications of 54 patients treated with oral cyclophosphamide for systemic lupus erythematosus (43) or rheumatoid arthritis (11) were reviewed. During an observation period of 241 patient years, we saw seven cases of acute hemorrhagic cystitis and two cases of transitional cell carcinoma of the bladder. Bladder carcinoma was identified 28 and 60 months after withdrawal of the drug and resulted in the death of one patient. The late-occurring serious toxicities of cyclophosphamide should limit the use of the drug in the treatment of nonmalignant inflammatory rheumatic conditions.

Administration, Oral↗
PubMed1979

NIH conference. Systemic lupus erythematosus: evolving concepts.

Systemic lupus erythematosus, a disease of unknown cause and protean manifestations, continues to excite substantial investigational interest. These papers bring together recent advances in concepts of its immunopathogenesis, evidence for a major genetic role in the causation of the process, developing systems for the morphologic assessment of its often fatal nephritis, and data from ongoing trials of cytotoxic drugs in its management.

Adolescent↗
PubMed1979

Studies of reticuloendothelial function in the mouse with model immune complexes. II. Serum clearance, tissue uptake, and reticuloendothelial saturation in NZB/W mice.

We have extended the findings in the accompanying paper by characterizing the serum clearance and tissue uptake of model soluble immune complexes and the saturation of the reticuloendothelial system (RES) by these complexes in normal mice and in mice with murine lupus (NZB/W F1 females). Adult NZB/W or young C3H mice were injected with radiolabeled stable site-specifically cross-linked mouse anti-DNP oligomers as model immune complexes to probe RES function. Blood clearance and uptake by liver, spleen, and kidney were unimpaired in NZB/W mice. To determine if the RES exhibits partial saturation in the NZB/W mice, we deliberately induced a state of RES blockade with heat-aggregated human gamma-glubulin (HAG). With increasing doses of HAG (1 to 4 mg/20 g body weight) both strains similarly showed a progressive increase in RES saturation as measured by reduced liver uptake of model oligomers. Recovery from saturation was complete by 120 min in both strains. At maximal liver saturation there was only a small increase in oligomer uptake by kidney or spleen, the majority of complexes remaining within the circulation. Thus, RES capacity for handling soluble model immune complexes appears unimpaired in NZB/W mice.

Animals↗
PubMed1978

Reduction of renal function by newer nonsteroidal anti-inflammatory drugs.

Because aspirin and indomethacin, two structurally dissimilar anti-inflammatory agents which reduce prostaglandin synthesis, both alter renal function, we studied the effect on renal function of three new nonsteroidal anti-inflammatory drugs which also reduce prostaglandin synthesis. We have shown that ibuprofen, naproxen, and fenoprofen are able to reduce renal function in patients with systemic lupus erythematosus and that such changes are associated with reduced excretion of urinary prostaglandin E (PGE)-like compounds. The changes may attenuate despite continued drug administration. These findings emphasize that renal function must be assessed with caution in patients taking these and perhaps other drugs which inhibit prostaglandin synthesis.

Adult↗
PubMed1978

Elevated urinary prostaglandins and the effects of aspirin on renal function in lupus erythematosus.

We studied the urinary excretion of immunoreactive prostaglandin E-like material (iPGE) and renal function in seven women with systemic lupus erythematosus to evaluate the relation between urinary iPGE and the increase in serum creatinine in patients taking aspirin. The mean pretreatment excretion of urinary iPGE in patients with lupus erythematosus, 42.7 +/- 6.4 ng/h, was significantly higher than the value of 29.0 +/- 1.9 ng/h for normal subjects (P less than 0.02). With aspirin, the urinary iPGE decreased an average of 45% (P less than 0.001). Increases in serum creatinine and blood urea nitrogen confirmed our previous clinical observations. The concomitant mean fall in creatinine clearance of 18% (P less than 0.001) was accompanied by a 14% decrease in inulin clearance (P less than 0.005); p-aminohippurate clearance fell 29% (P less than 0.005). The decline in urinary iPGE preceded the fall in creatinine clearance but was significantly correlated with it (r = 0.78; P less than 0.001). The observed changes reversed rapidly when aspirin was stopped. These data show that, in these patients with high urinary iPGE excretion, aspirin causes significant changes in renal function that may be mediated by the inhibition of prostaglandin synthesis.

Adult↗
PubMed1977

Aspirin-induced depression of renal function.

We observed elevation of serum creatinine and blood urea nitrogen and decrease in creatine clearance in patients taking anti-inflammatory doses of aspirin. In 13 of 23 patients with systemic lupus erythematosus increases in serum creatinine ranged from 27 to 163 per cent, and those in urea nitrogen from 42 to 270 per cent. Sequential creatinine-clearance studies, available in 11 of the 13 patients, demonstrated decreases up to 58 per cent. Patients with aspirin-induced changes in renal function were more likely to have active renal disease (P =0.035) or hypocomplementemia (P =0.030). Four of 22 patients with rheumatoid arthritis and two of three normal volunteers also demonstrated biochemical changes. The rate of aspirin-induced alterations was significantly higher in systemic lupus erythematosus (P =0.007) than in rheumatoid arthritis. Aspirin, and other nonsteroidal anti-inflammatory agents, can have a major reversible effect on renal function that may influence the interpretation of clinical data.

Adult↗
PubMed1977

Hemoperfusion through albumin-conjugated agarose gel for the treatment of neonatal jaundice in premature rhesus monkeys.

Hemoperfusion through albumin-conjugated agarose gel (AAG) effectively removes bilirubin (BR) and other albumin-bound materials from whole blood or plasma. We have used this technique to treat neonatal jaundice in premature rhesus monkeys with a specially designated apparatus which permits continuous perfusion through one of four columns arranged in parallel while the others are sequentially washed with saline and regenerated with ethanol. Less than 15 per cent of the animal's blood volume is required in the extracorporeal circuit at any time. Results indicate that (1) compared with five control monkeys which had a peak BR concentration ([BR]) averaging approximately 4 mg./100 ml., six experimental monkeys showed a significant (p less than 0.01) reduction, averaging 60 per cent, in [BR] after each of two perfusions at approximately 20 and 26 hours of age; (2) AAG hemoperfusion was even more effective in lowering [BR] in monkeys with higher preperfusion concentrations produced by BR infusion (average reduction = 68 and 87 per cent at preperfusion concentrations of 11.9 and 24.2 mg./100 ml., respectively); and (3) overall, BR eluted from the column averaged 93 per cent of the estimated preperfusion plasma BR pool. Unlike previous studies in rats, perfused monkeys showed significant platelet losses, although it was possible to prevent these losses by the use of "regional citrate" during perfusion. These studies suggest that AAG hemoperfusion is effective in the treatment of neonatal jaundice, although potential problems such as sterility and platelet loss need further evaluation before it can be considered for human use.

Albumins↗
PubMed1977

The use of calcium chelating agents and prostaglandin E to eliminate platelet and white blood cell losses resulting from hemoperfusion through uncoated charcoal, albumin-agarose gel, and neutral and cation exchange resins.

Hemoperfusion through adsorbents such as charcoal, cation exchange (e.g., AG 50W-X8) and uncharged (e.g., XAD-2) resins, and albumin-agarose gel (AAG) has been proposed for use in patients with hepatic failure. However, the loss of white blood cells and, particularly, platelets caused by each of these adsorbents remains a major deterrent to their clinical use. In vitro studies demonstrate that addition of citrate, ethylenediamine tetraacetate (EDTA), or oxalate to heparinized human blood eliminated this loss of formed blood elements during hemoperfusion. The improvement in postperfusion platelet counts (per cent of preperfusion values) produced by citrate were XAD-2, 13 leads to 95 per cent; AG 50W-X8, 10 leads to 94 per cent; AAG, 17 leads to 94 per cent; and charcoal, 44 leads to 96 per cent. Prostaglandin E1 in high doses (5 mug/ml.) markedly reduced platelet losses. Lower doses were less uniformly effective. Three young rhesus monkeys were hemoperfused for 160 minutes with columns containing AAG, XAD-2, and charcoal. During the first 80 minutes, citrate and calcium were infused into the column inflow and outflow lines respectively. For all three adsorbents, average platelet counts in the monkeys (115 per cent) and column effluent (95 per cent) were unchanged from preperfusion control values during the first 80 minutes but fell promptly to 13 and 7 per cent, respectively, after the citrate infusion was stopped. Each of the monkeys tolerated the procedure without ill effects. Use of a system analogous to that described here may facilitate clinical application of the technique of hemoperfusion through a variety of adsorbents.

Albumins↗
PubMed1975

Health-care workers positive for hepatitis B surface antigen. Are their contacts at risk?

To assess the hepatitis risk to patients exposed to HBs AG-positive health-care workers, 228 contacts were followed prospectively for six to nine months. Health workers included two physicians with chronic hepatitis, a chronic asymptomatic carrier nurse, a food handler with acute HBs Ag-positive hepatitis and a physician who was HBs Ag-positive for 25 days before the onset of acute hepatitis. Controls (167) consisted of identically followed patients who had not been exposed to an HBs Ag-positive health worker. No exposed or control patient acquired clinical hepatitis or HBs Ag. Isolated elevations in serum glutamic pyruvic transaminase occurred equally in both groups and did not correlate with serologic evidence for hepatitis B infection. One exposed patient demonstrated antibody seroconversion (anti-HBs), as did two of the controls. These data do not demonstrate hepatitis B transmission from HBs Ag-positive health workers to their patients. Restriction of such carriers is not warranted at present.

Acute Disease↗