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Biomedical subjects

J F Winchester

Publications and source records attributed to J F Winchester.

At least 55 records · Page 3Linked to original sources
PubMed1988

Sclerosing encapsulating peritonitis in rats induced by long-term intraperitoneal administration of antiseptics.

Continuous ambulatory peritoneal dialysis (CAPD) is an effective long-term treatment for renal failure. Sclerosing encapsulating peritonitis (SEP) is a rare but devastating complication of CAPD and may be caused by long-term peritoneal antiseptic exposure. We examined the peritoneal injury resulting from daily inoculations of moderately high concentrations of the following antiseptics: povidone-iodine, Dakin's solution, Amuchina, and Ampercide. After 4, 8, and 12 weeks of daily intraperitoneal injections in rats, a 10% solution of povidone-iodine in dialysis fluid caused a condition that mirrors human SEP. Animals had poor early weight gain, and gross necropsy examination revealed intestinal adhesions and a mesothelium that was sclerotically thickened. From 4 to 8 weeks the 10% povidone-iodine-injected animals showed progressive conditions and the prevalence of multiple encapsulating adhesions increased from 0/6 to 4/4, p = 0.005. Marked visceral mesothelial thickening in the 10% povidone-iodine-injected animals was quantitated after 4, 8, and 12 weeks at 92.0 +/- 11.6, 151.5 +/- 28.8, and 206.0 +/- 36.2 micron, respectively. Rats injected with dialysis fluid (controls) had normal-appearing mesothelial surfaces measured at 1.8 +/- 0.2, 2.4 +/- 0.2, and 2.2 +/- 0.2 micron after 4, 8, and 12 weeks, respectively. The marked thickening of the mesothelium in the 10% povidone-iodine group compared with the controls was highly significant, p less than 10(-8). We conclude that povidone-iodine, the most commonly used antiseptic in CAPD, caused severe tissue injury, whereas other antiseptic solutions, Dakin's, Amuchina, and Ampercide, at the similar dilution did not appear to cause mesothelial injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Management of iron overload in dialysis patients.

Acquired hemosiderosis resulting from massive iron deposits in various organs, including heart, liver, and pancreas, may lead to architectural and functional disturbances of these organs. Even though iron overload can occur in nonuremic as well as in uremic individuals, the dialysis patient is at particular risk for developing hemosiderosis. Many dialysis patients receive exogenous iron from either oral iron therapy or blood transfusions. In addition, these patients seem to be at high risk for retaining iron. A diagnosis of excess iron deposition should be considered if the patient has unexplained cardiomyopathy, hepatic cirrhosis, proximal myopathy, diabetes mellitus, arthropathy, or immune dysfunction such as listeriosis. Several techniques are available for determining iron overload. Diagnostic tests include measuring serum ferritin levels, staining bone marrow preparations for excess iron, measuring tissue hemosiderin concentrations, magnetic resonance imaging, and the deferoxamine (DFO; Desferal) "challenge test." The simplest treatment for iron overload in nonuremic patients is removal of iron by venesection. However, in patients in whom venesection is not feasible, the chelating agent DFO can effectively remove excess iron. In the dialysis patient, DFO therapy can be combined with either dialysis or hemoperfusion to remove the iron-DFO complex that would otherwise be removed by the kidney. DFO therapy in the nondialyzed individual has proven to be successful, but before treatment, the benefits of the treatment must be weighed against possible adverse side effects such as cataracts, changes in color vision, and anaphylaxis. In the dialysis patient, indications for iron removal are less clearly defined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Captopril-associated cholestatic jaundice.

Captopril, the competitive inhibitor of angiotensin-converting enzyme, is of considerable benefit in difficult-to-manage forms of hypertension. Its use has been associated with various untoward effects, but hepatic injury has not been widely reported. We treated a patient with captopril-associated cholestatic jaundice; a review of cases reported to the drug manufacturer and a review of the literature showed 13 additional cases of hepatic injury associated with captopril. In 9 of these the jaundice was categorized as cholestatic, and in 4 of the remaining 5 as mixed cholestatic-hepatocellular. These findings show that jaundice may be an idiosyncratic side effect of captopril, and that captopril-associated jaundice characteristically has strongly cholestatic features.

Adult↗
PubMed1985

Peritonitis, dialysate infusion and lung function in continuous ambulatory peritoneal dialysis (CAPD).

Pulmonary function tests were done in seven CAPD patients with acute peritonitis on the day of admission to the hospital and after recovery. Subsequently, the effect of dialysate infusion alone on lung function was studied in 19 patients initiated on CAPD and nine of these patients were restudied 7.6 +/- 4.1 months later. Peritonitis was associated with a 30% reduction in vital capacity and a significant fall in arterial oxygen tension (7 to 11 mmHg) (p less than 0.01). Dialysate infusion alone decreased functional residual capacity (FRC) and produced small changes in PaO2 which were more pronounced in the supine position. The decrease in PaO2 observed in changing from sitting prior to dialysate infusion, to supine after dialysate infusion was due to the development of airways closure at resting lung volumes. Follow-up studies in nine patients demonstrated a continued and significant fall in FRC with dialysate infusion, without however, any changes in PaO2. We conclude that peritonitis in CAPD patients is accompanied by significant changes in lung function which are probably due to a decrease in diaphragmatic mobility resulting in atelectasis and underventilation of dependent lung zones. In CAPD patients without peritonitis, dialysate infusion in the supine position produces significant changes in PaO2, but with time, compensatory mechanisms develop to abolish the changes in PaO2.

Adult↗
PubMed1983

Analgesic nephropathy. An uncommon cause of end-stage renal disease.

The frequency of analgesic nephropathy as a cause of end-stage renal disease varies considerably, not only between countries but also between different areas in the same country. We questioned 277 hemodialysis patients in the Washington, DC, area regarding the consumption of analgesic preparations. Only eight (2.8%) of the patients consumed excessive quantities of analgesic compounds prior to institution of hemodialysis. In addition, three of the eight patients had other causes for their end-stage renal disease. We conclude that analgesic nephropathy is an unusual cause of end-stage renal disease in the greater Washington, DC, area.

Adult↗
PubMed1981

Urine i-TXB2 in renal allograft rejection.

Immunoreactive thromboxane B2 (i-TXB2) was measured in daily urine samples from twelve patients after renal transplantation. In 21 of 30 rejection episodes, the increase in i-TXB2 preceded both the increase in serum beta 2-microglobulin (beta 2-MG) and the clinical diagnosis of rejection. In 26 of 30 rejection episodes, the increase in urine i-TXB2 preceded the increase in serum creatinine. The degree of change in i-TXB2 is greater than that of either serum beta 2-MG or creatinine. Urinary i-TXB2 was very high in one patient with deep venous thrombosis, but it did not rise in patients with urinary tract infection, pneumonia, or acute tubular necrosis. Thus, urinary i-TXB2 seems to be an early indicator of clinical renal allograft rejection.

Acute Disease↗