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The edematogenic properties of insulin have long been documented, although they have been underestimated despite current trends toward intensive insulin therapy. Insulin treatment has been associated with weight gain, mild or moderate edema, and, rarely, generalized edema and cardiopulmonary congestion. In addition, the use in recent years of thiazolidinediones, which improve insulin sensitivity, has been associated with weight gain and peripheral edema, which can progress to pulmonary edema, particularly when thiazolidinediones are used in combination with insulin. This article attempts to raise awareness about the overlooked edematogenic action of insulin. In addition, the potential role of edema-provoking properties of insulin in the development of vascular complications in patients with diabetes is discussed.
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PMID:The edematogenic properties of insulin. 1538 8

We previously found that contrast-induced nephropathy (CIN) complicating percutaneous coronary intervention adversely affects patients with chronic kidney disease (CKD). Therefore, we further investigated whether the predictors and outcome of CIN after percutaneous coronary intervention differ among patients with versus without CKD. Among 7,230 consecutive patients, CIN (>or=25% or >or=0.5 mg/dl increase in preprocedure serum creatinine 48 hours after the procedure) developed in 381 of 1,980 patients (19.2%) with baseline CKD (estimated glomerular filtration rate [eGFR] <60 ml/min/1.73 m(2)) and in 688 of 5,250 patients (13.1%) without CKD. Decreased eGFRs, periprocedural hypotension, higher contrast media volumes, lower baseline hematocrit, diabetes, pulmonary edema at presentation, intra-aortic balloon pump use, and ejection fraction <40% were the most significant predictors of CIN in patients with CKD. Apart from intra-aortic balloon pump use, predictors of CIN in patients without CKD were the same as mentioned, plus older age and type of contrast media. Regardless of baseline renal function, CIN correlated with longer in-hospital stay and higher rates of in-hospital complications and 1-year mortality compared with patients without CIN. By multivariate analysis, CIN was 1 of the most powerful predictors of 1-year mortality in patients with preexisting CKD (odds ratio 2.37, 95% confidence interval 1.63 to 3.44) or preserved eGFR (odds ratio 1.78; 95% confidence interval 1.22 to 2.60). Thus, regardless of the presence of CKD, baseline characteristics and periprocedural hemodynamic parameters predict CIN, and this complication is associated with worse in-hospital and 1-year outcomes.
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PMID:Contrast-induced nephropathy after percutaneous coronary interventions in relation to chronic kidney disease and hemodynamic variables. 1561 87

We defined the prevalence and impact on survival of clinical bedside variables in 385 patients with symptomatic congestive heart failure (CHF), of whom there were 176 with and 209 without diabetes mellitus. Patients were consecutively hospitalized and admitted for various acute conditions. Following discharge all-cause mortality was recorded. Prevalence and association of various variables with mortality were statistically analyzed. Prevailing in the diabetics versus nondiabetics were younger age (p < 0.05), pulmonary edema on admission (p = 0.002), using furosemide > 80 mg/day (p < 0.01) for > 1 year (p < 0.01) and hyponatremia (p = 0.01). Less prevalent were chronic lung disease (p < 0.01) and cardiac arrhythmias (p = 0.001). On follow-up extending up to 60 months, diabetic patients, especially those with fasting blood glucose levels on admission > or = 180 mg/dl, survived for a shorter period of time than nondiabetics (p = 0.02). Associated with increased mortality in the diabetic group were female gender (p = 0.04), furosemide > or = 80 mg/day (p < 0.001) and renal dysfunction (RD; p = 0.04). The respective variables in the nondiabetics were advanced age (p < 0.001) and RD (p = 0.002). Although they were younger, diabetic patients presented more severe CHF. It is recommended that special attention should be given to diabetic females, those using higher furosemide dosages and those suffering from RD.
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PMID:Heart failure in diabetes mellitus: clinical features and prognostic implications. 1578 22

Renal artery stenosis (RAS) is a common cause of secondary hypertension, with the activation of the renin-angiotensin-aldosterone system being the pathophysiologic hallmark of the disease. Renovascular hypertension, ischemic nephropathy, proteinuria, and flash pulmonary edema are the main clinical syndromes associated with RAS. The prevalence of RAS is on the rise, owing to an increasing prevalence of diabetes and atherosclerotic disease among our aging population. This rise in RAS prevalence poses major challenges for clinicians making diagnostic and treatment decisions. Although renal angioplasty is of proven benefit in fibromuscular dysplasia, randomized trials in atherosclerotic RAS have not shown any advantage for revascularization over medical therapy in terms of blood pressure control or renal function preservation. Angioplasty and surgical interventions should be reserved for patients with preserved kidney size and hemodynamically significant stenosis.
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PMID:Challenges in the diagnosis and management of renal artery stenosis. 1591 98

We present a case of a 29-year-old woman with known Type 1 diabetes who presented with diabetic ketoacidosis (DKA). Despite appropriate treatment and initial improvement, 12 h after initiation of treatment she deteriorated rapidly and developed pulmonary oedema, cerebral oedema and multiple infarctions of the brain and cervical spinal cord. This resulted in spastic quadraparesis and she has remained wheelchair-bound. These complications of DKA are rare and unpredictable. In this case report we discuss the proposed aetiologies of these complications with reference to our case report and highlight the importance of vigilance for early signs of these complications during the treatment of all patients with DKA.
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PMID:Simultaneous pulmonary and cerebral oedema, and multiple CNS infarctions as complications of diabetic ketoacidosis: a case report. 1711 96

Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.
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PMID:Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus. 1669 44

Hypertension promotes left ventricular (LV) hypertrophy and myocardial remodeling and is frequently present in patients with systolic or diastolic heart failure. Control of hypertension in both of these settings may attenuate progressive LV hypertrophy and remodeling and improve clinical outcomes. Guidelines for the management of heart failure recommend that hypertension should be treated in all patients with preclinical heart failure as well as in those with heart failure with reduced or preserved LV systolic function. Consistent with national hypertension guidelines, the goal for blood pressure control in hypertensive patients with heart failure is less than 140/90 mm Hg, but lower targets (< 130/80 mm Hg) may be desirable in those with concomitant diabetes mellitus or renal disease. Angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, and beta-adrenoreceptor antagonists are first-line options for hypertension treatment in heart failure. Calcium channel antagonists and the alpha blocker doxazosin should be avoided. Episodes of recurrent pulmonary edema and hypertension may also indicate underlying severe renovascular disease that may respond to percutaneous renal artery intervention.
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PMID:Goals and guidelines for treating hypertension in a patient with heart failure. 1703 73

The impact of gender on the presenting characteristics, management, and outcomes in infective endocarditis (IE) has not been adequately studied. The goal of our study was to better understand differences in management and outcome of IE between genders. Data were obtained prospectively from 439 patients in the Duke Endocarditis Database from 1996 to 2004. Baseline characteristics of patients were examined using univariable analysis. Variables associated with gender, in-hospital surgery and long-term mortality in patients with IE were considered for multivariable analysis. Hemodialysis, diabetes mellitus, and immunosuppression were more frequent in female patients with IE. Intracardiac abscesses and new conduction abnormalities were more common in male patients. The following factors were predictive of short-term mortality through univariable analysis: female gender, age, diabetes mellitus, septic pulmonary infarcts, intracranial hemorrhage, infection with Staphylococcus aureus, and persistently positive blood cultures. Female gender was not associated with mortality in an adjusted analysis of short-term outcome. Age, diabetes mellitus, renal failure requiring hemodialysis, cancer, pulmonary edema, systemic embolization, persistently positive blood cultures, and chronic indwelling central catheters but not female gender were associated with long-term mortality using univariable and an adjusted analysis. In both analyses, surgery was associated with improved mortality. Female gender, a history of diabetes mellitus, hemodialysis, and immunosuppression therapy were predictive of a medical management without the use of surgery, although in the adjusted analysis there was no association between surgery and gender. In conclusion, differences between genders in treatment and outcomes frequently reported in patients with IE most likely result from pre- and co-existing conditions such as diabetes mellitus, renal failure requiring hemodialysis, and chronic immunosuppression.
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PMID:Gender differences in infective endocarditis: pre- and co-morbid conditions lead to different management and outcomes in female patients. 1736 25

Reports of dialysis-associated hyperglycemia (DH) were compared to reports of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH) in patients with preserved renal function. Average serum values in DH (491 observations), DKA (1036 observations), and NKH (403 observations) were as follows, respectively: glucose, 772, 649, and 961 mg/dl; sodium, 127, 134, and 149, mmol/l; and tonicity, 298, 304, and 355 mOsm/kg. Assuming that euglycemic (serum glucose, 90 mg/dl) values were the same (sodium, 140 mmol/l; tonicity, 285 mOsm/kg) for all three states, the hyperglycemic rise in the average serum tonicity value per 100-mg/dl rise in serum glucose concentration was 1.9 mOsm/kg in DH, 3.5 mOsm/kg in DKA, and 8.1 mOsm/kg in NKH. Neurological manifestations in DH patients were caused by coexisting conditions (ketoacidosis, sepsis, and neurological disease) in most instances, and by severe hypertonicity (>320 mOsm/kg), with clearing after insulin administration, in a few instances. In 148 episodes of DH corrected with insulin only, the mean increase in serum sodium per 100-mg/dl decrease in serum glucose (Delta[Na]/Delta[Glu]) was -1.61 mmol/l. In agreement with theoretical predictions, Delta[Na]/Delta[Glu] was numerically smaller in patients with edema than in those with euvolemia. The average hyperglycemic increase in extracellular volume, calculated from changes in serum sodium concentration during correction of DH using insulin alone, was 0.013 l/l per 100-mg/dl increase in serum glucose concentration. A small number of DH patients presented with pulmonary edema rectified by insulin alone. DH causes modest hypertonicity, with few patients having neurological manifestations caused usually by other coexisting conditions. In contrast to DKA or NKH, which usually presents with hypovolemia, DH causes hypervolemia manifested occasionally by pulmonary edema. Insulin is adequate treatment for DH.
J Diabetes Complications
PMID:Body fluid abnormalities in severe hyperglycemia in patients on chronic dialysis: review of published reports. 1819 Oct 75

We report an unusual case of delayed death due to sepsis following closed blunt injury to the neck. The victim was a 71-year-old male with a clinical history of hypertension, diabetes and gout. He was found dead about three weeks after being assaulted. He had not consulted a hospital after the assault. Forensic autopsy demonstrated a large liquefied subcutaneous hematoma on the right side of the neck, peri- and thrombophlebitis of the right internal jugular vein. Otherwise, there was no evidence of trauma. Histological examination showed dermal vesicles in the skin covering the hematoma, accompanied by marked inflammatory cell infiltration phagocytosing gram-positive streptococci, subcutaneous edema, panphlebitis with partially organized thrombi and bacterial colonies, pulmonary edema and multiple pulmonary microthrombi involving bacterial aggregates. Postmortem serum C-reactive protein and neopterin levels were markedly elevated. These findings suggest sepsis as the cause of death, induced by infected internal jugular vein thrombophlebitis following blunt neck injury involving impaired skin barrier.
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PMID:An autopsy case of internal jugular vein thrombophlebitis involving sepsis following blunt neck injury. 1820 29


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