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SCLEROSING PERITONITIS AFTER PERITONEAL DIALYSIS
1080 DRUG SENSITIVITY PATTERNS OF M LEPRAE FOOTPAD
(3651) IN MOUSE
INFECTIONS*
investigators found peritoneal sclerosis in 2 of their CAPD patients who had had repeated episodes of septic and "aseptic" peritonitis. After repeated attempts, a fungus (Rhodotorula rubra) was cultured from the peritoneal effluent. On the other hand, peritoneal clearance is not decreased in CAPD patients who have had multiple peritonitis episodes.4Since peritoneal clearance can be reduced as a result of peritoneal sclerosis,the reported patients with repeated peritonitis episodes and normal clearances presumably have not developed sclerosis to a substantial degree. In 1 CAPD patient with frequent peritonitis could be directly examined, no episodes in whom the peritoneum evidence of sclerosis was found.5 Because of such divergent observations, we agree with Dr Oreopoulos and colleagues (Aug 13, p 409) that, even though repeated episodes of peritonitis may lead to sclerosing peritonitis, These
we
should continue
to
search for other causative factors. T. S. ING
J. T. DAUGIRDAS Hines-Loyola Medical Center, Hines, Illinois 60141, USA *Each BALB/c mouse, 6-8 weeks ofage, was inoculated with 5000 M leprae prepared from the skin biopsy on day 0. Harvests of control ammals were made on days 191-197. Drug treated groups were harvested on day 200. Drug-containing diets were fed continuously from day 0. Inoculation, harvesting, and counting were done by standard methods.°>‘ The limit of detectability is 1 -6x )0* acid-fast bacilli per footpad.
ansamycin (see table). The results of harvests from the first strain are given in the table. An additional two strains have been harvested and both show no growth in animals fed ansamycin at a concentration of 03parts per million w/w in the diet, as well as the higher concentrations. Mice have been inoculated with a rifampicin-resistant strain of M leprae to test cross-resistance to ansamycin, but results are not yet available. Thus ansamycin shows anti-M leprae activity in mouse footpad infections with a minimum effective dose of about 0 -3ppm in the diet. Clinical trials in leprosy are indicated. Laboratory Research Branch and Clinical Branch, National Hansen’s Disease Center, Carville, Louisiana 70721, USA
ROBERT C. HASTINGS ROBERT R. JACOBSON
SCLEROSING PERITONITIS AFTER PERITONEAL DIALYSIS
StR,—Dr Bradley and colleagues (Sept 3, p 572) suggested that sclerosing peritonitis (peritoneal sclerosisl) might be a sequela of recurrent peritonitis in patients on continuous ambulatory peritoneal dialysis (CAPD). Over the past seven years, among 125 intermittent peritoneal dialysis patients, we have encountered 7 cases of peritoneal sclerosis.l°2 All of the affected patients had experienced prior episodes of peritonitis, which apparently responded adequately, both clinically and bacteriologically, to intraperitoneal and/or systemic antibiotic therapy. We wonder how far infection may have been responsible for their sclerotic lesions. Despite standard, prolonged antibiotic therapy the peritonitis may sometimes have been treated inadequately so that a smouldering, subclinical infection persisted. Other patients with peritoneal sclerosis may have had a low-grade, subclinical peritonitis to begin with, so that their peritonitis escaped diagnosis and treatment for a long time. The organisms responsible for peritonitis in such patients might be fastidious bacteria or fungi, which are difficult or even impossible to detect using current techniques. A report by Eisenberg and colleagues3lends support to the possible association between peritoneal sclerosis and peritoneal infection by organisms whose importance in this area has been previously unrecognised. 5.
Shepard CC, McRae DH. A method for counting acid-fast bacteria. Int J Lepr 1968; 36: 78-82.
1. Gandhi VC,
Ing TS, Daugirdas JT, et al. Failure of peritoneal dialysis due to peritoneal
sclerosis. Int J Artif Organs 1983; 6: 97. 2. Gandhi VC, Humayun HM, Ing TS, et al. Sclerotic thickening of the peritoneal membrane in maintenance peritoneal dialysis patients. Arch Intern Med 1980, 140: 1201-03. 3. Eisenbery ES, Alpert BE, Weiss RA, et al. Rhodotorula rubra peritonitis in patients undergoing continuous ambulatory peritoneal dialysis. Am J Med 1983; 75: 349-52.
V. C. GANDHI D. J. LEEHEY
CYCLOSPORIN AND GLUCOSE TOLERANCE IN PANCREAS ALLOTRANSPLANTATION
;)iR,—Ur (junnarson and colleagues reported (Sept 3, p 571) that the use of cyclosporin in pancreas transplant recipients led to a deterioration in glucose metabolism. In the past two years we have used this drug to treat twelve diabetic patientsgiven segmental pancreatic and renal transplants. We investigated the response to stimulatory tests (oral and intravenous glucose tolerance tests, and arginine and tolbutamide tests), the 24 h metabolic profile for blood and 24 h glucose, free insulin, and lactate and 0-hydroxybutyrate, 7 and urinary glucose C-peptide profiles. Blood glucose and serum free-insulin response to insulinogenic stimuli showed no great differences between patients treated with cyclosporin alone and patients treated with steroids plus azathioprine.8In one patient oral glucose tolerance improved after the suppression of steroid administration and the introduction of cyclosporin. The 24 h metabolic profiles showed no great differences in the free insulin and intermediary metabolites patterns between the two groups, although the blood glucose values were closer to normal in patients treated with cyclosporin alone.99 Evaluation of glucose homoeostasis showed, in two patients switched from azathioprine and steroids to cyclosporin, a progressive reduction of the urinary levels ofC-peptide, without the appearance of glycosuria, indicating a reduction of the hyperinsulinaemia related to the peripheral insulin resistance due to steroid administration. It seems that in our patients cyclosporin has not led to a deterioration of the endocrine function of the grafted pancreas. Medical Clinic VIII, Istituto San Raffaele, 20132 Milan,
Italy; Nephrology and Metabolic Diseases Clinic (INSERM U80), Hôpital E. Herriot, Lyon, France and
G. POZZA
J. TRAEGER J. M. DUBERNARD A. SECCHI E. BOSI A. E. PONTIROLI
4. Rubin
J, Nolph K, Arfania D, et al. Follow-up of peritoneal clearances in patients undergoing continuous ambulatory peritoneal dialysis. Kidney Int 1979; 16:
-
619-23
5. Sorkin
MI, Luger AM, Prowant B, et al Histologic and functional characteristics of the peritoneal membrane of adiabetic patient after 34 months of CAPD. Peritoneal Dial Bull 1982; 2: 24-27. 6. Traeger J, Dubernard JM, Bosi E, Gelet A, El-Yafi S, Secchi A, Pozza G, Touraine JL. Cyclosporin in clinical pancreatic transplantation. Transplant Proc (in press). 7. Secchi A, Pontiroli AE, Traeger J, Dubernard JM, Touraine JL, Ruitton A, Blanc N, Pozza G. A method for early detection of graft failure in pancreas transplantation Transplantation 1983, 35: 344-48. 8. Pozza G, Traeger J, Dubernard JM, Secchi A, Pontiroli AE, Bosi E, Mahk MC, Ruitton A, Blanc N. Endocrine responses of type I (insulin-dependent) diabetic patients following successful pancreas transplantation. Diabetologia 1983, 24: 244-48.
A, Pontiroli AE, Bosi E, Traeger J, Dubernard JM, Gelet A, Touraine JL Influence of steroid administration on the endocrine function in neopreneinjected segmental pancreas allotransplantation. Transplant Proc (in press).
9. Pozza G, Secchi
(3651) IN MOUSE
INFECTIONS*
investigators found peritoneal sclerosis in 2 of their CAPD patients who had had repeated episodes of septic and "aseptic" peritonitis. After repeated attempts, a fungus (Rhodotorula rubra) was cultured from the peritoneal effluent. On the other hand, peritoneal clearance is not decreased in CAPD patients who have had multiple peritonitis episodes.4Since peritoneal clearance can be reduced as a result of peritoneal sclerosis,the reported patients with repeated peritonitis episodes and normal clearances presumably have not developed sclerosis to a substantial degree. In 1 CAPD patient with frequent peritonitis could be directly examined, no episodes in whom the peritoneum evidence of sclerosis was found.5 Because of such divergent observations, we agree with Dr Oreopoulos and colleagues (Aug 13, p 409) that, even though repeated episodes of peritonitis may lead to sclerosing peritonitis, These
we
should continue
to
search for other causative factors. T. S. ING
J. T. DAUGIRDAS Hines-Loyola Medical Center, Hines, Illinois 60141, USA *Each BALB/c mouse, 6-8 weeks ofage, was inoculated with 5000 M leprae prepared from the skin biopsy on day 0. Harvests of control ammals were made on days 191-197. Drug treated groups were harvested on day 200. Drug-containing diets were fed continuously from day 0. Inoculation, harvesting, and counting were done by standard methods.°>‘ The limit of detectability is 1 -6x )0* acid-fast bacilli per footpad.
ansamycin (see table). The results of harvests from the first strain are given in the table. An additional two strains have been harvested and both show no growth in animals fed ansamycin at a concentration of 03parts per million w/w in the diet, as well as the higher concentrations. Mice have been inoculated with a rifampicin-resistant strain of M leprae to test cross-resistance to ansamycin, but results are not yet available. Thus ansamycin shows anti-M leprae activity in mouse footpad infections with a minimum effective dose of about 0 -3ppm in the diet. Clinical trials in leprosy are indicated. Laboratory Research Branch and Clinical Branch, National Hansen’s Disease Center, Carville, Louisiana 70721, USA
ROBERT C. HASTINGS ROBERT R. JACOBSON
SCLEROSING PERITONITIS AFTER PERITONEAL DIALYSIS
StR,—Dr Bradley and colleagues (Sept 3, p 572) suggested that sclerosing peritonitis (peritoneal sclerosisl) might be a sequela of recurrent peritonitis in patients on continuous ambulatory peritoneal dialysis (CAPD). Over the past seven years, among 125 intermittent peritoneal dialysis patients, we have encountered 7 cases of peritoneal sclerosis.l°2 All of the affected patients had experienced prior episodes of peritonitis, which apparently responded adequately, both clinically and bacteriologically, to intraperitoneal and/or systemic antibiotic therapy. We wonder how far infection may have been responsible for their sclerotic lesions. Despite standard, prolonged antibiotic therapy the peritonitis may sometimes have been treated inadequately so that a smouldering, subclinical infection persisted. Other patients with peritoneal sclerosis may have had a low-grade, subclinical peritonitis to begin with, so that their peritonitis escaped diagnosis and treatment for a long time. The organisms responsible for peritonitis in such patients might be fastidious bacteria or fungi, which are difficult or even impossible to detect using current techniques. A report by Eisenberg and colleagues3lends support to the possible association between peritoneal sclerosis and peritoneal infection by organisms whose importance in this area has been previously unrecognised. 5.
Shepard CC, McRae DH. A method for counting acid-fast bacteria. Int J Lepr 1968; 36: 78-82.
1. Gandhi VC,
Ing TS, Daugirdas JT, et al. Failure of peritoneal dialysis due to peritoneal
sclerosis. Int J Artif Organs 1983; 6: 97. 2. Gandhi VC, Humayun HM, Ing TS, et al. Sclerotic thickening of the peritoneal membrane in maintenance peritoneal dialysis patients. Arch Intern Med 1980, 140: 1201-03. 3. Eisenbery ES, Alpert BE, Weiss RA, et al. Rhodotorula rubra peritonitis in patients undergoing continuous ambulatory peritoneal dialysis. Am J Med 1983; 75: 349-52.
V. C. GANDHI D. J. LEEHEY
CYCLOSPORIN AND GLUCOSE TOLERANCE IN PANCREAS ALLOTRANSPLANTATION
;)iR,—Ur (junnarson and colleagues reported (Sept 3, p 571) that the use of cyclosporin in pancreas transplant recipients led to a deterioration in glucose metabolism. In the past two years we have used this drug to treat twelve diabetic patientsgiven segmental pancreatic and renal transplants. We investigated the response to stimulatory tests (oral and intravenous glucose tolerance tests, and arginine and tolbutamide tests), the 24 h metabolic profile for blood and 24 h glucose, free insulin, and lactate and 0-hydroxybutyrate, 7 and urinary glucose C-peptide profiles. Blood glucose and serum free-insulin response to insulinogenic stimuli showed no great differences between patients treated with cyclosporin alone and patients treated with steroids plus azathioprine.8In one patient oral glucose tolerance improved after the suppression of steroid administration and the introduction of cyclosporin. The 24 h metabolic profiles showed no great differences in the free insulin and intermediary metabolites patterns between the two groups, although the blood glucose values were closer to normal in patients treated with cyclosporin alone.99 Evaluation of glucose homoeostasis showed, in two patients switched from azathioprine and steroids to cyclosporin, a progressive reduction of the urinary levels ofC-peptide, without the appearance of glycosuria, indicating a reduction of the hyperinsulinaemia related to the peripheral insulin resistance due to steroid administration. It seems that in our patients cyclosporin has not led to a deterioration of the endocrine function of the grafted pancreas. Medical Clinic VIII, Istituto San Raffaele, 20132 Milan,
Italy; Nephrology and Metabolic Diseases Clinic (INSERM U80), Hôpital E. Herriot, Lyon, France and
G. POZZA
J. TRAEGER J. M. DUBERNARD A. SECCHI E. BOSI A. E. PONTIROLI
4. Rubin
J, Nolph K, Arfania D, et al. Follow-up of peritoneal clearances in patients undergoing continuous ambulatory peritoneal dialysis. Kidney Int 1979; 16:
-
619-23
5. Sorkin
MI, Luger AM, Prowant B, et al Histologic and functional characteristics of the peritoneal membrane of adiabetic patient after 34 months of CAPD. Peritoneal Dial Bull 1982; 2: 24-27. 6. Traeger J, Dubernard JM, Bosi E, Gelet A, El-Yafi S, Secchi A, Pozza G, Touraine JL. Cyclosporin in clinical pancreatic transplantation. Transplant Proc (in press). 7. Secchi A, Pontiroli AE, Traeger J, Dubernard JM, Touraine JL, Ruitton A, Blanc N, Pozza G. A method for early detection of graft failure in pancreas transplantation Transplantation 1983, 35: 344-48. 8. Pozza G, Traeger J, Dubernard JM, Secchi A, Pontiroli AE, Bosi E, Mahk MC, Ruitton A, Blanc N. Endocrine responses of type I (insulin-dependent) diabetic patients following successful pancreas transplantation. Diabetologia 1983, 24: 244-48.
A, Pontiroli AE, Bosi E, Traeger J, Dubernard JM, Gelet A, Touraine JL Influence of steroid administration on the endocrine function in neopreneinjected segmental pancreas allotransplantation. Transplant Proc (in press).
9. Pozza G, Secchi