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 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a six year period twelve patients with insulin dependent diabetes and end-stage renal failure received cadaveric kidney grafts. Eleven of the patients have previous to this been hemodialysed, one patient was transplanted before hemodialysis was necessary. The cumulative two year survival was thirty-seven per cent for the patients, and twenty-nine per cent for the kidney grafts. The average time of observation was eleven months, the motality was fifty per cent. The causes of death were acute myocardial infarction in two cases, sepsis in two cases, severe hypoglycemia in one case and unexpected sudden death in one case. The most prominent problems in the treatment of the diabetic patients after the renal transplantation were difficulties in the regulation of the diabetes, rejections, infections, cardiac failure and aggravation in pre-existing hypertension.
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PMID:Renal transplantation in patients with insulin requiring diabetes and renal failure. 78 7

From August 1974 to January 1985, 53 patients (26 men; seven Maoris) mean age 45 (SD 15) years, with diabetes mellitus for a mean of 12 (SD nine) years had a renal biopsy and were followed. Indications for biopsy were nephrotic syndrome, proteinuria, renal impairment (five) and hematuria (one). Mean plasma creatinine concentration was 0.22 (SD 0.18) mmol/L and protein excretion 3.4 (SD 2.5) g/24 h. Diabetic nephropathy was demonstrated in 39 patients and significantly associated with retinopathy and insulin dependent diabetes mellitus (IDDM). Of the 39 patients followed for 25.7 (SD 22.8) months, 18 had died (nine myocardial infarction, six uremia, two sepsis, one stroke) and nine had begun dialysis. The five-year cumulative renal survival was 28%. The presence of the nephrotic syndrome and the plasma creatinine concentration at presentation were the best predictors of survival. Diabetics with IDDM of 20 years duration, retinopathy and heavy proteinuria, who survive the other complications of their disease, are likely to have diabetic nephropathy requiring renal replacement therapy.
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PMID:Renal disease in diabetics--which patients have diabetic nephropathy and what is their outcome? 324 62

Sixty-four insulin-dependent (Type 1) diabetic patients (IDDM) in Soweto, South Africa were followed over a 10-year period. Patients were assessed in 1982 and again in 1992. There were 10 deaths (16%), half of which were due to renal failure. Ketoacidosis, hypoglycaemia, and sepsis accounted for the rest. At the 10-year follow-up mean age (+/- SD) was 32.4 +/- 5.0 years and diabetes duration 13.6 +/- 2.6 years. Retinopathy affected 52%, peripheral neuropathy 42%, and nephropathy 28% (all significantly increased from the 1982 assessment). Microalbuminuria and autonomic neuropathy were also common. Serum cholesterol was over 6.5 mmol l-1 in 19%, hypertension affected 22%, and 28% were cigarette smokers; though no patient had evidence of macroangiopathy. We conclude that IDDM in South Africa is associated with excess mortality, a significant proportion of which is related to nephropathy. Diabetes of long duration is now not uncommon in South Africa, and although diabetic complications frequently occur, most patients have good life quality and freedom from large vessel disease.
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PMID:Mortality and outcome of insulin-dependent diabetes in Soweto, South Africa. 764 31

A 25-year-old Hispanic female with insulin dependent diabetes mellitus (IDDM) and endstage renal disease on chronic hemodialysis was hospitalized with paroxysms of fever and chills for a day. A day after starting piperacillin for presumed intravascular line infection, she developed a maculopapular dermatitis and abnormal liver function tests, at which point the drug was discontinued. However, the rash persisted for 10 days, after which it progressively worsened. She continued to have high fevers, abnormal liver function tests, and marked leukocytosis, despite multiple negative cultures and other nondiagnostic examinations. She was treated as a patient with sepsis of unknown etiology and received multiple antibiotics on an empiric basis without response. A diagnosis of Stevens-Johnson syndrome was then made based on the triad of cutaneous dermatitis, mucosal, and hepatic involvement. She received high dose corticosteroids and her fever, dermatitis, mucosal lesions, leukocytosis, and abnormal liver function tests improved dramatically.
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PMID:Stevens-Johnson syndrome presenting as intravenous line sepsis. 779 65

Simultaneous pancreas/kidney transplantation (SPK) has evolved to become a therapeutic option for patients with renal failure resulting from type 1 diabetes mellitus. However, the appropriate route for drainage of the exocrine secretions of the pancreas allograft remains unclear. While bladder drainage (BD) is the current state of the art, it is associated with a high frequency of urologic complications, including urinary tract infections, hematuria, metabolic acidosis, dehydration, and reflux pancreatitis. Although enteric drainage (ED) is the more physiologic route, it has been associated in the past with decreased graft survival and increased infectious complications. In addition, BD offered a technique for detection of rejection through measurement of urinary amylase. However, with the advent of improved immunosuppression and antibiotic therapy, percutaneous pancreas biopsy, improved radiologic imaging, and greater understanding of pancreas transplantation, we hypothesized that ED could be performed without increased morbidity or cost. A group of 23 consecutive SPK was performed with ED during the period from July 1995 to November 1995. Another 23 age- and sex-matched recipients of SPK with BD performed from November 1994 to June 1995 served as a historical control group. Because of the differing lengths of follow-up, data were analyzed with respect to the first six months posttransplant. ED and BD were associated with equivalent actuarial one-year patient and graft survival rates: 100% and 88% for ED, and 96% and 91% for BD, respectively. Hospital charges, length of stay, readmissions, rejection, sepsis-related procedures were also equivalent in ED and BD. However, ED was associated with significantly fewer urinary tract infections and urologic complications. In addition, no grafts were lost as the result of sepsis. In the setting of SPK, ED represents a viable alternative to BD for primary drainage of pancreas exocrine secretions. Further studies with extended lengths of follow-up are necessary to confirm our observations.
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PMID:Simultaneous pancreas/kidney transplantation--a comparison of enteric and bladder drainage of exocrine pancreatic secretions. 902 Mar 24

Among patients hospitalized in 1983-1992 were 416 (239 women) who were immobilized for at least 2 hours due to stroke, orthopedic surgery, or sepsis. 128 (30.8%) had pressure ulcers (PU); 100 (31.2%) had diabetes (DM), including 12 with IDDM and 118 with NIDDM; age (mean +/- SD) was 74.3 +/- 9.5 years. Those with IDDM and NIDDM were younger (70.9 +/- 10.5 and 71.5 +/- 8.4 years, respectively) than the nondiabetic (75.7 +/- 9.6 years; p > 0.05 and < 0.001, respectively). Those with PU were older (76.6 +/- 9.0 vs 73.3 +/- 9.6 years, p < 0.01). Incidence of PU in patients without DM was similar to that in those with NIDDM (30.4 vs 27.1%; no difference even after age-adjustment). However, incidence of PU was significantly higher in those with IDDM than in those without DM (75.0 vs 30.4%, p < 0.01). According to Medline (last 2 years screened), and EBSCO Physician Medline Plus (last 5 years screened), only 5 publications referred to DM as a risk factor for PU. According to our data NIDDM does not appear to be a risk factor for PU, but a causative role for IDDM deserves further study. Increased risk of diabetic foot, infections in ulcers and wounds, and slow healing in DM do not justify considering NIDDM a risk factor for PU.
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PMID:[Is diabetes mellitus a risk factor for pressure ulcers?]. 904 59

In earlier studies it has been shown that prolactin (PRL) is a stimulating factor for the immune system, and it has been suggested that PRL might antagonize immunosuppressive effects of glucocorticoids. PRL has been reported to affect the cytokine secretion pattern, by elevating cytokine gene expression in macrophages, after the onset of sepsis. It also promotes the antibody response in mice where it increases the production of interferon-gamma (IFN-gamma) and inhibits interleukin-1 (IL-1) production. Due to these properties, PRL might influence the development of autoimmune type 1 diabetes. The aim of the present study was to examine the effects of two drugs; PRL and bromocriptine (BC) in vivo on the development of hyperglycemia and pancreatic insulitis in mice treated with multiple doses of streptozotocin (STZ) (40 mg/kg body weight, i.p.). The dopaminergic agonist BC is known to inhibit PRL secretion. In another set of experiments, the direct effects of PRL on the function of pancreatic islets exposed to STZ in vitro were studied. Mice treated with STZ became gradually hyperglycemic, and concomitant treatment with PRL (4 mg/kg body weight) for 21 days significantly reduced the elevation in blood glucose levels from day 10 onwards (P<0.05). Morphologic examinations of the pancreas on day 21 of mice receiving STZ injections revealed a marked insulitis, but only moderate insulitis in the STZ treated animals given PRL. BC administration (10 mg/kg body weight) in combination with STZ did not significantly affect the elevation in blood glucose levels or the insulitis. PRL or BC administration alone did not change the serum glucose concentration. This study indicates that PRL may affect hyperglycemia in the early phase of autoimmune diabetes. We suggest that it might be due to counteraction of autoimmune immunologic mechanisms and/or enhancement of beta-cell regeneration.
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PMID:Prolactin protects against diabetes induced by multiple low doses of streptozotocin in mice. 1055 72

Diabetes mellitus is uncommon in infancy and newborn period. The two common forms seen are the transient and permanent forms of diabetes mellitus of the newborn. They have to be differentiated from the transient hyperglycemic states (Blood sugar > 125 mg/dl) seen in newborns who receive parenteral glucose infusions and in those with septicemia and CNS disorders. Transient diabetes mellitus of the newborn (TDNB) is defined as hyperglycemia occurring within the first month of life lasting at least 2 weeks and requiring insulin therapy. Most of these cases resolve spontaneously by 4 months. It has a reported incidence of 1 in 45,000 to 60,000 live births. The most likely etiology is a maturational delay of cAMP mediated insulin release. The clinical features include small for datedness, proneness for birth asphyxia, open-eye alert facies, dehydration, emaciation, polyuria and poydipsia. These children are prone to septicemia and urinary tract infections. They have hyperglycemia, glucosuria, absent or mild ketonuria, low basal insulin, C-peptide and IGF-1 levels. Treatment consists of hydration and judicious administration of insulin with close monitoring. Thirty percent of these children are likely to develop permanent neonatal diabetes. Compared to transient form, permanent diabetes mellitus is uncommon. It is usually due to pancreatic dysgenesis often associated with other malformations and rarely due to type 1 diabetes mellitus. The diagnosis is based on the demonstration of both exocrine and endocrine pancreatic dysfunction. These children are managed as type 1 diabetes mellitus. They are prone to develop the vascular complications of diabetes at an earlier date.
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PMID:Diabetes mellitus in newborns and infants. 1093 65

Islet transplantation offers patients with type 1 diabetes mellitus freedom from long-term insulin therapy and a degree of metabolic control that is far superior to injected insulin. The hope is that near-perfect glucose control sustained over time will prevent progression of secondary diabetic complications. The selection of optimal immunosuppressive agents for islet transplantation has been a formidable challenge, given the need to overcome both autoimmune and alloimmune barriers, as well as the potential toxicity of immunosuppressive agents on transplanted islets. Early strategies relied on protocols that had proven success in solid organ transplantation and consisted of azathioprine, cyclosporine and corticosteroids. Under these protocols, fewer than 10% of patients were able to achieve insulin independence. The development of the 'Edmonton Protocol' dramatically transformed clinical outcomes in islet transplantation in recent years through the introduction of a more potent, less diabetogenic, and corticosteroid-free immunosuppressive regimen consisting of sirolimus, low-dose tacrolimus, and induction anti-interleukin-2 receptor antibody. While insulin independence rates under this protocol have been highly successful, patients must be maintained on lifelong immunosuppression. While the risk of malignancy, post-transplant lymphoma and sepsis have been low and diminishing in transplanted patients to date, fears of these complications and a host of drug-related adverse effects have precluded broader application. Patients undergoing islet transplantation today must exchange insulin for chronic immunosuppressive therapy, and therefore the procedure can only be justified in patients with very unstable forms of diabetes, or in those with another solid organ allograft who already endure the risks of immunosuppression. Advances in more specific and less toxic immunosuppressive agents together with progress in better understanding the biology of diabetes will lead to more suitable strategies to control both alloimmune and recurrent autoimmune reactions. These protocols, ultimately aimed at establishing tolerance, are an essential pre-requisite to move towards providing islet transplantation earlier in the course of the disease, including transplantation in children. This review addresses the evolution of immunosuppressive strategies in islet transplantation, and highlights some novel agents in pre-clinical development or in early clinical trials that may offer considerable promise in facilitating the induction of tolerance.
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PMID:Islet transplantation in patients with diabetes mellitus: choice of immunosuppression. 1537 74

The object of this review is to provide the definitions and criteria for diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS), and convey current knowledge of the causes of permanent disability or mortality from complications of these conditions, of the risk factors for DKA and HHS, and of early indicators and contemporary treatment of suspected cerebral edema. The frequency of DKA at onset of type 1 diabetes mellitus (DM1) varies from 10-70%, depending on availability of health care and frequency of diabetes. At the onset of type 2 diabetes (DM2), DKA occurs in 5-52%. One study reported HHS in approximately 4% of new patients with DM2. Recurrent DKA rates are equally dependent on variability in medical services and socio-economic circumstances, and are estimated to be eight episodes per 100 patient years, with 20% of patients accounting for 80% of the episodes. Mortality for each episode of DKA internationally varies from 0.15-0.31%, with idiopathic cerebral edema accounting for two-thirds or more of this mortality. Other causes of death or disability include untreated DKA or HHS, hypokalemia, hypophosphatemia, hypoglycemia, other intracerebral complications, peripheral venous thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure, sepsis, aspiration pneumonia, and other pulmonary complications. Population-based studies from the UK, Australia, the USA, and Canada report cerebral edema incidence in DKA of 0.5-2.0%. Published information does not support the notion that treatment factors are causal in cerebral edema. Younger age, greater severity of acidosis, degree of hypocapnia, and severity of dehydration have been suggested as risk factors in several studies. Bimodal distribution of the time of onset of cerebral edema and wide variation in brain imaging findings suggest the variability and likely multiple causation of the clinical picture. Functional brain scanning has indicated that DKA is accompanied by increased cerebral blood flow suggesting that the predominant mechanism of edema formation is a vasogenic process. A method of monitoring for diagnostic and major and minor signs of cerebral edema has been proposed and tested which indicates that intervention will be required in five individuals to provide early intervention for a single case of cerebral edema. The preferred intervention of mannitol infusion has typically been accompanied by intubation and hyperventilation, but recent evidence indicates outcome is adversely affected by aggressive hyperventilation. The prevention of DKA and HHS at the onset of diabetes mellitus requires a high degree of awareness and suspicion by primary care providers; prevention of recurrent DKA necessitates a diligent team effort.
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PMID:Hyperglycemic crises and their complications in children. 1731 23


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