PubMed · 14126167
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I MACHTEY. 1964-02-01. [DERMATOMYOSITIS].. https://pubmed.ncbi.nlm.nih.gov/14126167/
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UNLABELLED: Steroid withdrawal from patients taking prednisone for their renal allograft at the time of reinduction of immunosuppression for subsequent pancreas after kidney (PAK) transplantation has not been explored. Our expectation was that lymphocyte depletion, in conjunction with an augmentation of immunosuppression at the time of pancreas transplantation would protect the recipient from rejection of the renal allograft when chronic maintenance steroids are withdrawn. METHODS: Pancreas transplantation was performed using systemic venous drainage and enteric exocrine drainage. Regardless of preoperative immunosuppression, all patients received induction with antithymocyte globulin, a brief taper of intravenous solumedrol over four to five days, maintenance therapy with tacrolimus and sirolimus and either resumption of chronic maintenance steroids or complete withdrawal of steroids. RESULTS: A total of 30 PAK transplants were performed in 29 recipients and divided into two groups: continuation of chronic steroids (n = 10) or steroid-free (n = 19). One pancreas allograft was lost and there was a single mortality in the steroid free group. There was no significant difference in renal function or incidence of infections. CONCLUSION: Steroids can be safely withdrawn following pancreas after kidney transplantation for recipients already on maintenance prednisone in the setting of rabbit antithymocyte globulin induction and tacrolimus and sirolimus maintenance immunosuppression.
BACKGROUND: Mitochondrial respiratory chain disorders are the most prevalent group of inherited neurometabolic diseases. They present with central and peripheral neurological features usually in association with other organ involvement including the eye, the heart, the liver, and kidneys, diabetes mellitus and sensorineural deafness. Current treatment is largely supportive and the disorders progress relentlessly causing significant morbidity and premature death. Vitamin supplements, pharmacological agents and exercise therapy have been used in isolated cases and small clinical trials, but the efficacy of these interventions is unclear. OBJECTIVES: To determine whether there is objective evidence to support the use of current treatments for mitochondrial disease. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group trials register (searched September 2003), the Cochrane Central Register of Controlled Trials, MEDLINE (January 1966 to October 3 2003), EMBASE (January 1980 to October 3 2003) and the European Neuromuscular Centre (ENMC) clinical trials register, and contacted experts in the field. SELECTION CRITERIA: We included randomised controlled trials (including crossover studies) and quasi-randomised trials comparing pharmacological treatments, and non-pharmacological treatments (vitamins and food supplements), and physical training in individuals with mitochondrial disorders. The primary outcome measures included an improvement in muscle strength and/or endurance, or neurological clinical features. Secondary outcome measures included quality of life assessments, biochemical markers of disease and negative outcomes. DATA COLLECTION AND ANALYSIS: Details of the number of randomised patients, treatment, study design, study category, allocation concealment and patient characteristics were extracted. Analysis was based on intention to treat data. We planned to use meta-analysis, but this did not prove necessary. MAIN RESULTS: Six hundred and seventy-eight abstracts were reviewed, and six fulfilled the entry criteria. Two trials studied the effects of co-enzyme Q10 (ubiquinone), one reporting a subjective improvement and a significant increase in a global scale of muscle strength, but the other trial did not show any benefit. Two trials used creatine, with one reporting improved measures of muscle strength and post-exercise lactate, but the other reported no benefit. One trial of dichloroacetate showed an improvement in secondary outcome measures of mitochondrial metabolism, and one trial using dimethylglycine showed no significant effect. AUTHORS' CONCLUSIONS: There is currently no clear evidence supporting the use of any intervention in mitochondrial disorders. Further research is needed to establish the role of a wide range of therapeutic approaches.
Guanidinoacetic acid (GAA) measurement has recently become of great interest for the diagnosis of creatine (Cn) metabolism disorders, and research calls for rapid and inexpensive methods for its detection in plasma and urine in order to assess a large number of patients. We propose a new assay for the measurement of GAA by a simple CZE UV-detection without previous sample derivatization. Plasma samples were filtered by Microcon-10 microconcentrators and directly injected into the capillary, while for urine specimens a simple water dilution before injection was needed. A baseline separation was obtained in less than 8 min using a 60.2 cm x 75 microm uncoated silica capillary, 75 mmol/L Tris-phosphate buffer pH 2.25 at 15 degrees C. The performance of the developed method was assessed by measuring plasma creatinine and Cn in 32 normal subjects and comparing the data obtained by the new method with those found with the previous CE assay. Our new method seems to be an inexpensive, fast and specific tool to assess a large number of patients both in clinical and in research laboratories.