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  • 1
    Electronic Resource
    Electronic Resource
    Plasma cortisol levels before and during "low-dose" hydrocortisone therapy and their relationship to hemodynamic improvement in patients with septic shock (2000)
    Springer
    Intensive care medicine 26 (2000), S. 1747-1755 
    Details
    ISSN: 1432-1238
    Keywords: Shock Sepsis Septic shock Cortisol Adrenocorticotropic hormone Hydrocortisone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objectives: To compare cortisol levels during "low-dose" hydrocortisone therapy to basal and ACTH-stimulated endogenous levels and to assess whether clinical course and the need for catecholamines depend on cortisol levels and/or pretreatment adrenocortical responsiveness. Design and setting: Prospective observational study in a medical ICU of a university hospital. Patients: Twenty consecutive patients with septic shock and a cardiac index of 3.5 l/min or higher, started on "low-dose" hydrocortisone therapy (100 mg bolus, 10 mg/h for 7 days and subsequent tapering) within 72 h of the onset of shock. Measurements and results: Basal total and free plasma cortisol levels ranged from 203 to 2169 and from 17 to 372 nmol/l. In 11 patients cortisol production was considered "inadequate" because there was neither a response to ACTH of at least 200 nmol/l nor a baseline level of at least 1000 nmol/l. Following the initiation of hydrocortisone therapy total and free cortisol levels increased 4.2- and 8.5-fold to median levels of 3587 (interquartile range 2679–5220) and 1210 (interquartile range 750–1846) nmol/l on day 1, and thereafter declined to median levels of 1310 nmol/l and 345 nmol/l on day 7. Patients with "inadequate" steroid production could be weaned from vasopressor therapy significantly faster, although their plasma free cortisol concentrations during the hydrocortisone treatment period did not differ. Conclusions: (a) During proposed regimens of "low-dose" hydrocortisone therapy, initially achieved plasma cortisol concentrations considerably exceed basal and ACTH stimulated levels. (b) Cortisol concentrations decline subsequently, despite continuous application of a constant dose. (c) "Inadequate" endogenous steroid production appears to sensitize patients to the hemodynamic effects of a "therapeutic rise" in plasma cortisol levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340000685
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  • 2
    Electronic Resource
    Electronic Resource
    Contribution of color and power Doppler sonography to the differential diagnosis of acute and chronic rejection, and tacrolimus nephrotoxicity in renal allografts (1999)
    Springer
    Transplant international 12 (1999), S. 127-134 
    Details
    ISSN: 1432-2277
    Keywords: Key words Doppler sonography ; Acute rejection ; Chronic rejection ; Tacrolimus ; Kidney transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present study was to differentiate acute rejection, chronic rejection, and tacrolimus nephrotoxicity with color and power Doppler imaging of renal transplants. One hundred examinations were obtained from 45 patients. Pulsatility and resistive indices were calculated from color Doppler images. The grade of renal vascularization was quantified using computer-assisted pixel analysis in a rectangular region-of-interest. The percentage of vessel-covered renal parenchyma (POV) was calculated using a histogram that discriminated renal vessels from renal parenchyma via power Doppler images. Furthermore, the distance from the most peripherally located vessels to the renal capsule (PVD) was measured. A reduced POV K 55 % proved to be the best discriminator when chronic rejection was suspected (sensitivity 79 %, specificity 87 %). Tacrolimus nephrotoxicity showed not only a moderate elevation of the Doppler signal but also an increased PVD L 3.9 mm and a normal POV. We conclude that the evaluation of renal vessels by power Doppler images improves diagnostic accuracy for patients with renal allografts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001470050197
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  • 3
    Electronic Resource
    Electronic Resource
    Impact of long-term immunosuppression with cyclosporin A on serum lipids in stable renal transplant recipients (1991)
    Springer
    Transplant international 4 (1991), S. 92-95 
    Details
    ISSN: 1432-2277
    Keywords: Serum lipids, cyclosporin A ; Cyclosporin A, serum lipids ; Kidney transplantation, serum lipids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine the impact of long-term immunosuppression on serum lipids in stable renal graft recipients we measured serum lipids and apolipoprotein B concentrations in 20 patients receiving therapy with cyclosporin (CsA) and low-dose prednisolone (CsA/P) and in 18 patients on therapy with azathioprine and maintenance steroids (Aza/P). The patients were matched for age, body mass index, primary renal disease and dose of prednisolone, but not for the duration in transplantation and serum creatinine concentration. Triglyceride concentrations were significantly higher in the CsA/P group than in Aza/P-treated patients: 2.62±0.35 vs 1.62±0.23 mmol/l (P〈0.05). Similarly, total cholesterol (C) levels were significantly more elevated in the CsA/P recipients than in the other group: 7.44±0.32 vs 5.84±0.25 (P〈0.02). CsA/P patients had higher serum levels of LDL-C (4.79±0.20 vs 3.43±0.19 mmol/l P〈0.001) and apolipoprotein B concentrations (191±13 vs 128±9 mg/dl; P〈0.001). CsA/P and Aza/P recipients had similar concentrations of HDL-C (1.73±0.13 vs 1.52±0.09 mmol/l; NS). We conclude that in stable renal graft recipients with good transplant function long-term immunosuppression with CsA/P is associated with a more atherogenic lipid status than therapy with Aza/P.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00336404
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  • 4
    Electronic Resource
    Electronic Resource
    High mortality from urothelial carcinoma despite regular tumor screening in patients with analgesic nephropathy after renal transplantation (1996)
    Springer
    Transplant international 9 (1996), S. 231-235 
    Details
    ISSN: 1432-2277
    Keywords: Analgesic nephropathy, urothelial carcinoma, kidney transplantation ; Kidney transplantation, urothelial carcinoma ; Urothelial carcinoma, kidney transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Patients with end-stage renal failure due to analgesic nephropathy have an increased risk of developing a urothelial carcinoma. To determine the impact of renal transplantation on the frequency of urothelial carcinomas, we analyzed 2072 patients who underwent 2371 renal transplantations between 1968 and 1993, including 78 (3.8%) with clinically proven analgesic nephropathy. Before and after transplantation a regular tumor screening was performed in patients with analgesic nephropathy by urine cytology and abdominal sonography. In 11 of the 78 patients with analgesic nephropathy (14.1%; age 51–66 years, 40–108 months after initiation of dialysis treatment, 5–77 months after transplantation), a urothelial carcinoma of the native urinary tract, especially the kidneys, was diagnosed. Therapy comprised nephroureterectomy (n=6), transurethral resection (n=6) and/or cystectomy (n=2). Seven patients died due to tumor progression 16.3 (4–33) months postoperatively and one patient died due to a perioperative complication. Despite regular tumor screening after transplantation, the diagnosis of a urothelial carcinoma was made very late, leading to a high tumor-related mortality. As a consequence, we suggest that a bilateral nephroureterectomy should be performed prophylactically in patients with proven analgesic nephropathy. In addition, a cystoscopy with lavage cytology testing of the bladder should be performed twice a year.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00335391
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  • 5
    Electronic Resource
    Electronic Resource
    Left ventricular hypertrophy and diastolic dysfunction: Their relation to coronary heart disease (1995)
    Springer
    Cardiovascular drugs and therapy 9 (1995), S. 533-537 
    Details
    ISSN: 1573-7241
    Keywords: coronary artery disease ; left ventricular hypertrophy ; diastolic dysfunction ; echocardiography ; Doppler
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diastolic dysfunction is an early sign in the temporal sequence of ischemic events in coronary heart disease. The ischemic cascade, beginning with an oxygen demand supply imbalance and metabolic alterations, identifies diastolic disorders of the left ventricle (LV) as an early phenomenon, sometimes before systolic dysfunction, electrocardiographic changes, or chest pain occur. Although the physiology of diastolic function is complex, the factors contributing to diastolic disturbances can be differentiated intointrinsic andextrinsic LV abnormalities. Intrinsic mechanisms include (a) impaired LV relaxation, (b) the complex of LV hypertrophy, and (c) increased LV asynchrony. Myocardial hypertrophy leads to an increase of the myocardial mass/volume ratio, and the degree of hypertrophy is the main determinant of chamber stiffness. The main, if not unique, determinant of myocardial diastolic tissue distensibility is the structure and concentration of the collagen. Consequently, tissue stiffness is increased in coronary disease by reparative interstitial fibrosis or scar following myocardial infarction. In myocardial hypertrophy the LV collagen concentration is elevated due to reactive fibrosis. An increase in regional asynchrony of LV contraction and relaxation is a result of regional ischemia as well as of LV hypertrophy and tissue fibrosis. Factors extrinsic to the LV causing diastolic disorders include (a) increased central blood volume, which will increase left ventricular pressure without altering the LV pressure-volume relation, and (b) ventricular interaction mediated by pericardial restraint, which may cause a parallel upward shift of the diastolic LV pressure-volume relation. Improved insight into the mechanisms of LV relaxation and filling characteristics help in the treatment of LV diastolic dysfunction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00877866
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