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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of corticosteroids on beta cell function and humoral immune response in type 1 diabetes was tested in a 2-month trial conducted on 32 newly diagnosed patients (age 22.8 +/- 1.4 years, mean +/- S.E.M.). Prednisone was administered at immunosuppressive dosage (1 mg.kg-1.day-1) during the initial 10 days and at a maintenance dosage (0.3 mg.kg-1.day-1) for 50 days. Patients (n = 32) were enrolled within 6 weeks after diagnosis and matched in pairs for age, sex, presence of islet cell antibodies (ICA) and glucagon stimulated C-peptide levels. Insulin discontinuation was not contemplated. All the patients who received prednisone became ICA during treatment but in some (4 out of 10) this effect was only transient. Insulin antibodies (IA) were significantly lower in the prednisone group at second and third month (P < 0.05). No patient experienced complete remission but in 10 prednisone and 4 control patients the insulin requirements were below 0.3 IU/kg (P < 0.05). With similar glycemia the fasting C-peptide levels were higher in the treated patients. The profile of the insulin requirements during the follow-up was different in the two groups and at 9 months the prednisone group needed less insulin than the control (P < 0.05). Interestingly, within the prednisone-treated group and after 6 months, the levels of stimulated C-peptide improved significantly among the ICA+ patients while they were steady or declined in ICA- (P < 0.01). The analysis of variance covariance confirmed a positive interaction between ICA and the administration of prednisone on the outcome of beta cell function.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res Clin Pract 1993 Apr
PMID:Effects of a short prednisone regime at clinical onset of type 1 diabetes. 834 27

We prospectively withdrew prednisone in 28 adult patients who had stable graft function more than 2 years after orthotopic liver transplantation (OLTx) and had been on 5 mg/d prednisone for at least 6 months. Prednisone was decreased from 5 mg/d to 2.5 mg/d for 1 month then stopped completely. Cyclosporine monotherapy was maintained at a level of approximately 200 ng/mL (TDX). Nineteen patients had prednisone withdrawn without complications. Four (14.2%) had modest elevations in liver function tests (two biopsy proven mild rejections and two were not biopsied). These four were treated with methylprednisolone boluses and then withdrawal of steroids again. Prednisone was restarted in five patients because of generalized fatigue and body aches (n = 4) and colitis (n = 1). Steroids later were successfully withdrawn in two of these patients. After prednisone withdrawal, three of five insulin-dependent diabetic patients were able to discontinue insulin therapy and their glycosylated hemoglobin levels improved. Four of fourteen hypertensive patients were able to discontinue antihypertensive medicines. Mean serum cholesterol decreased from 222.6 +/- 43.3 to 188.3 +/- 33.3 mg/dL (P < .001). The number of patients with serum cholesterol levels > 220 mg/dL decreased from 13 to 4. A control group of 24 patients maintained on 5 mg/d prednisone at least 2 years after liver transplantation also was studied. In this group during the study period, no diabetic became normoglycemic, no patient decreased their antihypertensive medicine, and the mean serum cholesterol levels did not change significantly. We conclude that prednisone withdrawal using cyclosporine monotherapy late after liver transplantation does not lead to graft loss and decreases the prevalence of diabetes, hypertension, and hypercholesterolemia. Symptoms occurring during withdrawal may be minimized by earlier or slower tapering.
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PMID:Prednisone withdrawal late after adult liver transplantation reduces diabetes, hypertension, and hypercholesterolemia without causing graft loss. 898 86

Diabetes mellitus with preexisting end-organ damage (EOD) is considered a contraindication for heart transplantation. The outcome of such patients has not been well characterized. Among 138 patients transplanted between 12/88 and 7/94, 29 were diabetic (11 insulin-dependent); of these, 12 had preexisting EOD, defined as a creatinine clearance < or = 50 ml/min, a 24-hour urine protein concentration > or = 500 mg/L or typical symptoms of peripheral or autonomic polyneuropathy, and 17 had no EOD. We compared diabetics with and without EOD and non-diabetics (n = 109) for operative mortality, length of stay, serum creatinine, fasting glucose levels, and postoperative prednisone doses at 1,6, and 12 months. Actuarial survival and freedom from rejection and infection were analyzed. Both diabetic groups were significantly older than nondiabetics, Ischemic time, operative mortality, surgical technique, ICU- and total length of stay were similar. Actuarial survival and freedom from rejection were similar among the three groups. Infection rates including CMV did not differ. Serum creatinine levels increased in all groups compared to pretransplant levels (p = 0.001), but without significant differences among the groups. Post-transplant glucose levels at 6 and 12 months were higher for diabetic patients with EOD than for those without or for nondiabetics (183, 153, and 94 mg/dl at 6 months, p = 0.01; 202, 161, and 102 mg/dl at 12 months, p = 0.0001). Prednisone dosage was lower in diabetics with EOD at 6 months, but did not differ among the three groups at 12 months. The incidence of angiographically proven transplant vasculopathy did not differ at 1 and 2 years. Diabetics with preexisting EOD undergoing heart transplantation experience similar short- and intermediate-term results when compared to diabetics without EOD and nondiabetics. Metabolic control is more difficult to achieve, as indicated by higher fasting glucose levels. Larger and longer-term prospective studies have to confirm our findings, since the shortage of donor organs would increase if such patients were transplanted routinely.
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PMID:Heart transplantation in patients with diabetic end-organ damage before transplantation. 902 4

The topographic diagnosis of facial nerve lesions is based on the symptoms that accompany paralysis, allowing lesions to be located in the protuberance, pontocerebellar angle, facial channel or trajectory distal to the stylomastoid foramen. Most cases of peripheral facial palsy have no apparent cause (idiopathic, or Bell's, peripheral facial palsy). However, facial palsy can sometimes be a manifestation of neuroborreliosis, multiple sclerosis, diabetes, HIV infection or neurinoma. Neurophysiologic studies complement physical examination to establish a prognosis; after the fifth day axonal degeneration related to incomplete recovery can be recognized. Magnetic resonance identifies nerve lesions but is useful only in atypical cases. Prednisone 1 mg/kg over 5 days, with gradual weaning, is the most widely accepted treatment for Bell's palsy. Acyclovir is indicated in Ramsay-Hunt syndrome. Early surgical decompression in cases with poor prognosis is not generally considered beneficial. Cases of permanent facial palsy have serious consequences, particularly because facial expression is altered.
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PMID:[Diagnosis and treatment of facial palsy]. 913 9

This study, a retrospective view of 34 patients with myasthenia gravis, compared the course of the disease for patients with onset before 65 and after 65 years. 70% of those under 65 were female while 55.8% of those over 65 were male. Bulbar symptoms were more frequent in older patients. Only 3 patients had another immune disease (rheumatoid arthritis, diabetes mellitus, thyroid pathology), and two a thymoma. All patients were treated with anticholinesterases. Prednisone was used in 44% of cases and rarely Azathioprine. In our cases and in the review of the literature there is no significant difference between age groups except for the sex ratio and the outcome in the older group in case of thymoma or respiratory failure.
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PMID:[Late onset myasthenia: 34 cases in patients over 65 years of age]. 929 25

Treatment of chronic inflammatory demyelinating polyneuropathy (CIDP) requires long-term immunomodulatory therapy, which has potential side effects. Before such therapy is instituted, a firm diagnosis of CIDP must be established. Prednisone, plasma exchange (PE), and intravenous immunoglobulin (IVIG) are all proven first-line therapies for CIDP that are of similar efficacy. The choice of treatment should be individualized based on costs, availability, and potential adverse effects. Except in the elderly and in those with complicating medical illnesses, IVIG is well tolerated and easy to administer; hence, it should be the initial therapy for most patients with CIDP. Because of its prohibitive costs and limited availability, however, it is not ideal for long-term administration. In the elderly and in those with complicating medical illnesses (eg, diabetes, obesity, or hypertension), PE may be used as the first-line therapy. Because the effects of PE are transient and because it is expensive, requires vascular access, and can only be performed in specialized centers, long-term therapy with PE alone is problematic. Prednisone is inexpensive, easily available, and of proven efficacy. It is the preferred treatment in young, otherwise healthy persons either as a first-line therapy or in association with IVIG or PE. Patients who require repeated treatment with IVIG or PE and cannot tolerate prednisone or those who require high-dose prednisone should be administered azathioprine, cyclosporin A, or cyclophosphamide, usually in combination with one of the first-line therapies.
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PMID:Chronic Inflammatory Demyelinating Polyneuropathy. 1109 13

The pathogenic basis and treatment of diabetic polyradiculoneuropathy is a source of recent controversy as there may be two or more distinct forms of diabetic polyradiculoplexopathy. We believe that the following two categories of diabetic polyradiculoneuropathy can be made on the basis of clinically differences: 1) the more common asymmetric, painful polyradiculoneuropathy; and 2) the rare symmetric, painless, polyradiculoneuropathy. The asymmetric, painful form (also known as diabetic amyotrophy) may have an autoimmune basis, but the etiology is not clear. The natural history for diabetic amyotrophy is spontaneous improvement. Nevertheless, various immunotherapies (eg, corticosteroids and intravenous immunoglobulin (IVIg) have been tried with subsequent improvement in symptoms. Treatment is reserved only for patients with severe ongoing pain, given the significant side effects of these medications in those patients with diabetes. Prednisone and IVIg may help alleviate the pain associated with diabetic amyotrophy. Relief of pain can help patients begin physical therapy earlier, however, there are no prospective, blinded, controlled studies that demonstrate that these treatments lead to an earlier and better recovery of muscle strength compared with the natural history of the disorder. The symmetric, painless form of diabetic polyradiculoneuropathy may in fact represent chronic inflammatory demyelinating polyneuropathy (CIDP) occurring in a patient with diabetes mellitus (DM). Patients with idiopathic CIDP may improve various immunomodulating therapies, including corticosteroid treatment, plasma exchange (PE), and IVIg. In this regard, patients with the symmetric, painless, proximal diabetic polyradiculoneuropathy may also respond to corticosteroids, plasma exchange, IVIg, azathioprine, or cyclophosphamide. However, as with diabetic amyotrophy, some patients improve spontaneously without treatment. In still other patients, the neuropathy appears unresponsive to immunotherapy. In such patients, this polyradiculoneuropathy might be caused by metabolic dysfunction associated with DM. Unfortunately, from a clinical, laboratory, and electrophysiologic standpoint, it is impossible to distinguish the patients with a symmetric, painless diabetic polyradiculoneuropathy who might respond to therapy. A trial of PE can be useful in identifying patients who might have a polyradiculoplexopathy that is responsive to immunotherapy. If patients respond to PE, they may continue to receive intermittent exchanges or be switched over to prednisone or IVIg.
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PMID:Diabetic Lumbosacral Polyradiculoneuropathies. 1118 Jul 51

The treatment of patients with autoimmune pancreatitis poses a challenge to the clinician. Prednisone, in an initial dosage of 30 to 40 mg/d, is used in patients with moderate abdominal and back pain, obstructive jaundice, or sclerosing cholangitis. Antacid or anticholinergic agents may be used to minimize stimulation of pancreatic exocrine function. Patients with quiescent disease may not need pharmacologic medication. In patients with complications such as obstructive jaundice and infection, biliary drainage and administration of antibiotics are recommended prior to steroid therapy. Steroid therapy occasionally ameliorates diabetes mellitus associated with autoimmune pancreatitis.
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PMID:Autoimmune-related Pancreatitis. 1156 Jul 84

Statins have anti-inflammatory effects, modify endothelial function and improve peripheral insulin resistance. We hypothesized that statins influence the development of new-onset diabetes mellitus in renal transplant recipients. The records of all previously non-diabetic adults who received an allograft in Toronto between January 1, 1999 and December 31, 2001 were reviewed with follow-up through December 31, 2002. All patients receiving cyclosporine or tacrolimus, mycophenolate mofetil and prednisone were included. New-onset diabetes was diagnosed by the Canadian Diabetic Association criteria: fasting plasma glucose > or =7.0 mmol/L or 2-h postprandial glucose > or =11.1 mmol/L on more than two occasions. Statin use prior to diabetes development was recorded along with other variables. Cox proportional hazards models analyzing statin use as a time-dependent covariate were performed. Three hundred fourteen recipients met study criteria, of whom 129 received statins. New-onset diabetes incidence was 16% (n = 49). Statins (p = 0.0004, HR 0.238[0.109-0.524]) and ACE inhibitors/ARB (p = 0.01, HR 0.309[0.127-0.750]) were associated with decreased risk. Prednisone dose (p = 0.0001, HR 1.007[1.003-1.010] per 1 mg/d at 3 months), weight at transplant (p = 0.02, HR 1.022[1.003-1.042] per 1 kg), black ethnicity (p = 0.02, HR 1.230[1.023-1.480]) and age > or =45 years (p = 0.01, HR 2.226[1.162-4.261]) were associated with increased diabetes. Statin use is associated with reduced new-onset diabetes development after renal transplantation.
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PMID:Reduced incidence of new-onset diabetes mellitus after renal transplantation with 3-hydroxy-3-methylglutaryl-coenzyme a reductase inhibitors (statins). 1547 92

We examined short-term outcomes and posttransplant medical complications under three different immunosuppressive regimens at a single center. The study design was a randomized, prospective, open-label trial comparing a calcineurin inhibitor-free (CNI) protocol to standard triple therapy with tacrolimus, prednisone, and mycophenolate mofetil. They were also compared to a concurrent but nonrandomized third cohort treated with a prednisone-free protocol. All three groups had excellent early outcomes with no significant difference in patient or graft survival or biopsy-proven acute rejection. Serum creatinine was significantly lower in the CNI-free recipients. Lipid panels and posttransplant diabetes mellitus were significantly lower in the prednisone-free patients. Prednisone-free kidney transplant recipients have improved early glucose metabolism and hyperlipidemia compared to CNI-free or standard triple therapy recipients with comparable rejection and graft survival rates.
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PMID:Short-term results under three different immunosuppressive regimens at one center. 1717 5


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