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Query: UMLS:C0020473 (hyperlipidemia)
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A new system is proposed for treating the spectrum of patients with high blood pressure. It is based on studies of the renin axis using renin profiling, pharmacologic probes and our bipolar vasoconstriction-volume hypothesis. The new system does not require renin profiling, pharmacologic testing or a vasoconstriction-volume analysis for widespread application. But these procedures, whenever available, will make treatment more efficient and more certain, and at the same time provide better base line definition. In the new system, all patients, except the elderly and those with congestive heart failure, bradycardia or a history of asthma, are treated first with propranolol alone, a procedure which will diminish or normalize blood pressure in many patients with high and noraml renin levels. For nonresponders, diuretic therapy is then superimposed. Subsequently, a propranolol subtraction trial picks out the low-renin patients who will usually respond to a diuretic alone. This program is likely to be fully effective in possible up to 85 per cent of patients. For the residual smaller fraction, drugs such as hydralazine, methyl DOPA, clonidine, reserpine or guanethidine are then added in traditional trial and error fashion. The proposed system has the theoretic attraction for long-term commitment, implicit in antihypertensive therapy, of achieving blood pressure control in large fractions with one drug instead of two or with two drugs instead of three or more. Moreover, the large groups who respond to therapy with propranolol alone (most high-renin and normal-renin patients) or to diuretics alone (most low-renin patients) gain the advantage of simple, more specific, long-term (i.e., antirenin or antivolume) therapy. The use of propranolol alone has practical and theoretic advantages over diuretics. Control may be achieved with even fewer side effects and without hypokalemia and chronic dehydration with its possibly adverse consequences (hyperuricemia, azotemia, hyperlipidemia, hyperreninemia, increased blood viscosity). Also, propranolol provides more direct control of the increased peripheral resistance and of neurogenically-induced swings in blood pressure. At the same time, the new system efficiently exploits the long-term use of diuretic therapy alone in low-renin patients in whom volume excess seems a causal factor. And it tends to avoid the use of diuretics in high-renin patients and of beta-blockers in low-renin patients in whom these drug types may be contraindicated.
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PMID:Modern system for treating high blood pressure based on renin profiling and vasoconstriction-volume analysis: a primary role for beta blocking drugs such as propranolol. 1 Jul 30

Type II diabetes mellitus may affect as many as 20% of the elderly US population. In the absence of data to support the need to maintain a specific level of glucose beyond that necessary to relieve symptoms, choice of therapy is problematic. Clearly, supervised dietary therapy for the obese type II diabetic patient represents a safe and cost-effective treatment. For those patients who fail dietary therapy because they fail to lose weight or regain lost weight, or because blood glucose levels remain high despite weight loss, further therapy must be individualized. The only rational criteria for drug treatment supportable by currently available data are (1) persistent symptoms associated with hyperglycemia, (2) ketonuria in the unstressed state, and (3) certain cases of hyperlipidemia, especially with triglyceride levels greater than 1000 mg/dl. In these clinical settings, drug therapy is necessary to eliminate symptoms, prevent development of ketoacidosis, and reduce the risk of pancreatitis, respectively. Consideration of drug therapy should also be made in the case of very elevated blood glucose levels, even in the absence of symptoms, when dehydration and risk of severe hyperosmolarity exist. The issues regarding insulin versus sulfonylureas have not been examined specifically in the elderly population. Extrapolating from published studies that generally include patients older than 65 years leads to the following conclusions: Caution regarding adverse side effects of insulin (hypoglycemia, theoretic risk of hyperinsulinemia) and sulfonylureas (hypoglycemia, drug interactions, increased risk of cardiovascular death) must be balanced against the theoretic benefit of treatment in the absence of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin treatment in the elderly diabetic patient. 222 55

A case of acute intestinal vascular necrosis in a 19-year-old user of oral contraceptives (OCs) is described, and hypotheses explaining the digestive complications of synthetic estrogens are reviewed. The patient had originally presented with a violent gastric pain that subsequently spread to the entire abdomen. An abrupt worsening of her condition involved cardiovascular collapse associated with a peritoneal syndrome, vomiting and dehydration, and hyperleukocytosis. Emergency opening of the peritoneum was followed by evacuation of a large quantity of fetid gas and alimentary debris, and observation of a completely necrosed stomach. A careful lavage of the entire intestinal cavity led to temporary improvement, but it became clear during an attempt at gastrectomy that further treatment would be unavailing and the patient died shortly thereafter. Estrogens were believed to be responsible for the digestive necrosis because it occurred in a young woman who had used an estrogen-rich OC for 3 years and who smoked; a hapatic biopsy confirmed the diagnosis. No traces of other risk factors such as hypertension, hyperlipidemia, diabetes, neoplasia, or obesity were observed. Recent publications indicate that OCs are responsible for a certain number of digestive problems, which may include acceleration of intestinal transit, severe diarrhea, rectorrhagia, ischemic or ulcerative colitis, intestinal infarct which is usually localized, and hepatocellular problems ranging from moderate hepatic insufficiency to malignant tumor and Budd-Chiari syndrome. OCs do not modify hemodynamic regimes, but they may cause elevation of fibrinogen and thrombin, diminution of antithrombin III acitivty, increased platelet adhesivity, and decreased fibrinolysis leading to hypercoagulability. These modifications in hemostasis occur in all OC users and are not statistically correlated with occurence of thrombotic accidents. OCs are probably responsible for parietal vascular lesions; experimental injection of synthetic estrogens is associated with both arterial and venous lesions. The most characteristic anomaly is at the level of the intima, with proliferation of smooth muscle cells and increased conjunctive tissue fibers associated with proliferation of the media or the endothelium. The absence of lipid deposits, the simultaneous appearance of arterial and venous lesions, and other evidence argues against and atheromatous origin of parietal lesions. A significant correlation has been found between high levels of anti-synthetic ethinyl estradiol antibodies and the presence of vascular lesions. It is hypothesized that these circulating immune complexes penetrate the vascular walls of OC users and produce lesions, which may depend on factors such as smoking.
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PMID:[Digestive complications of oral contraceptives: a case of extensive digestive necrosis in a young woman]. 647 54

The effect of weight loss produced by gastric exclusion on the metabolism of previously morbidly obese persons was examined. A standardized gastric exclusion procedure was performed in 150 morbidly obese patients during a 6 year period. These patients were followed for from 6 to 60 months (mean 27.8 months). The mean excess weight loss was 75 percent and was maintained from 2 to 5 years. A small but significant decrease was noted during the first 3 to 6 postoperative months in the parameters of protein metabolism examined. Although this may reflect mild depletion in protein stores, of greater importance was the demonstration that these parameters spontaneously corrected themselves by 12 months. Mild abnormalities in serum electrolyte concentrations were noted in the postoperative period. They appeared to be related to dehydration, were not clinically significant, and also resolved spontaneously. Clinically significant abnormalities in divalent ions were absent. Significant and sustained reductions in blood pressure, fasting glucose concentration, serum triglyceride values, and uric acid and hepatic enzyme concentrations were demonstrated in the entire population. A small and non-sustained decrease in cholesterol was seen. Hypertension was eliminated in 96 percent of the affected subpopulation, diabetes in 100 percent, gout in 100 percent, hyperlipidemia in 92 percent, and improved hepatic function was found in 95 percent. These changes should reduce the overall morbidity and mortality of the patient population in the future.
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PMID:Prospective metabolic evaluation of 150 consecutive patients who underwent gastric exclusion. 671 48

Creatinine clearance decreases with age by 1 ml/min/year after 40 years of age, although serum creatinine remains constant because of reduction of muscle mass. Reduction of water intake may occur in the elderly because of a reduced sensation of thirst; this is associated with a tendency to lose water with urine. The capacity to respond to sodium load is impaired in aged kidneys, thereby leading to ECV expansion and hypertension. But there is also, in the elderly, a reduced capacity for retaining sodium (FENa is higher than in young subjects), making old subjects sensitive to salt depletion and ECV contraction. Hypernatraemia (Nas > 150 mmol/l) is not infrequent in the elderly (1%) and is usually due to water deficiency (old subjects should be forced to drink), and rarely to iatrogenic excess of sodium. It is the abrupt occurrence of severe hypernatraemia that causes neurological symptoms due to dehydration and brain shrinking, which may lead to cerebral haemorrhage and death. Hyponatraemia (Nas < 130 mmol/l) is frequent among the elderly (7-11%) and is mainly due to water overload, which is usually iatrogenic. Hypovolaemic hyponatraemia occurs when salt depletion causes ECV contraction > 10%, and is due to water retention in an attempt to normalize ECV. Hypervolaemic hyponatraemia is due to ADH hypersecretion because of a decrease in 'effective' circulating blood volume. 'Pseudohyponatraemia' may occur because of hyperlipidaemia or hyperproteinaemia. It is the abrupt occurrence of severe hyponatraemia that causes neurological symptoms (water intoxication), secondary to the oedomatous swelling of the brain within the skull. While rapidly occurring hyponatraemia may be lethal, slowly occurring hyponatraemia is usually asymptomatic. Rapid correction of hyponatraemia may cause cerebral dehydration and 'osmotic demyelination syndrome' ('central pontine myelinosis'). Decrease (e.g. by diuretics) or increase (e.g. by ACE-inhibitors, non-steroidal anti-inflammatory drugs, beta-blockers) or serum potassium may occur in the elderly. Diuretics should be used with caution in elderly subjects to avoid salt depletion, hypotension and renal function impairment.
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PMID:Some sodium, potassium and water changes in the elderly and their treatment. 905 29

Diabetic ketoacidosis results from insulin deficiency and insulin resistance and is marked by hyperglycaemia, ketoacidosis, dehydration and electrolyte losses. Management includes correction of shock, dehydration, electrolyte deficits, hyperglycaemia, acidosis and sepsis (if present). Warning signs include severe dehydration, shock, pH < 7.0, hypokalaemia, hypernatraemia, hyperosmolality, hyperlipidaemia, deterioration in consciousness and diabetic ketoacidosis in very young patients. The principles of treatment include (i) admission to a unit with paediatric experience, (ii) treatment of shock, (iii) rehydration over 24-36 h, or longer if the osmolality is >360 mmoll(-1), (iv) normal saline for rehydration unless the patient is hypernatraemic, (v) avoidance of bicarbonate unless acidosis is interfering with myocardial contractility, (vi) insulin infusion to achieve a fall in blood glucose levels of 5 mmol h(-1), (vi) potassium, (vii) use of 5% glucose when the blood glucose level falls <12mmoll(-1), (ix) treatment of any complications and (x) change to subcutaneous insulin when diabetic ketoacidosis is controlled.
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PMID:Practical management of diabetic ketoacidosis in childhood and adolescence. 982 96

Nephropathy may develop in patients with type 1 diabetes because poor glycemic control produces effects that eventually lead to glomerular scarring and renal failure. The worse and more prolonged the hyperglycemia, the greater the risk of diabetic nephropathy. In patients with type 2 diabetes, hyperglycemia, as well as insulin resistance and generalized vascular disease, is involved in the pathogenesis of nephropathy. The glomerular changes of early diabetic nephropathy can be identified only by renal biopsy or by testing for microalbuminuria. Once macroalbuminuria occurs (albumin excretion rate, > 300 mg/day), usually after type 1 diabetes has been present for 10 to 15 postpubertal years, end-stage renal disease is almost inevitable. However, aggressive control of hypertension in diabetic patients without microalbuminuria helps avoid nephropathy, and tight glycemic control in those with microalbuminuria can avoid or delay its onset. Even when macroalbuminuria is present, treatment can prolong renal function. Aggressive antihypertensive therapy, especially with ACE inhibitors, can reduce renal decline by half. Avoiding circumstances that may damage the kidneys (e.g., use of radiocontrast materials or nephrotoxic drugs, dehydration, hyperlipidemia, urinary tract infection, buildup of AGEs) is critical. Some treatment methods are controversial (dietary protein restriction) or still under investigation (use of injected or oral heparin) but may help delay renal transplantation or dialysis.
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PMID:Dealing with diabetic nephropathy. 1002 5

We report an 11 month-old infant with severe hypercalcemia associated with hyperlipidemia following bolus vitamin D administration. At the time of admission, serum concentration of calcium was 5.5 mmol/l (22 mg/dl); total cholesterol, high density lipoprotein cholesterol (HDL-C), very low density lipoprotein (VLDL), low density lipoprotein cholesterol (LDL-C), and triglyceride levels were respectively: 6.37 mmol/l (246 mg/dl), 0.77 mmol/l (30 mg/dl), 1.37 mmol/l (54 mg/dl), 4.1 mmol/l (162 mg/dl), 3 mmol/l (271 mg/dl). Physical examination revealed dehydration and irritability that was inappropriately mild according to the serum calcium level. On the 16th day of therapy that consisted of intravenous fluids with furosemide (sodium diuresis), steroid, calcitonin, magnesium sulfate, and phosphorus, serum calcium level declined below 3 mmol/l (12 mg/dl). The hyperlipidemia resolved gradually with a concomitant decline in serum calcium. This report is interesting in that hypercalcemia was associated with transient hyperlipidemia that disappeared with normocalcemia, which might suggest protection against hypercalcemic symptoms.
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PMID:Severe hypercalcemia of an infant due to vitamin D toxicity associated with hypercholesterolemia. 1151 34

Early optimalization of the treatment of patients with chronic renal insufficiency can reduce morbidity and deaths. For each patient with a raised serum creatinine concentration, the creatinine clearance should be measured or calculated. When this is abnormal, the cause thereof should be investigated. Chronic renal insufficiency is often progressive, even when the initiating factors are no longer present. Progression can be delayed by treating the high blood pressure, proteinuria and hyperlipidemia by means of a restricted protein diet and advice not to smoke. Acute deterioration of an existing chronic renal dysfunction through dehydration and underfill or through the use of certain medications or toxic substances such as radio-opaque media should be avoided. In patients with chronic renal insufficiency specific attention should be paid not only to hypertension, lipid disturbances, smoking and weight, but also to the calcium-phosphate balance, anaemia and homocysteine levels. The blood pressure, oedema and weight of patients with a clearance between 30-59 ml/min should be checked 2-3 times a year, in addition to laboratory tests for Hb, Ht, creatinine, urea, potassium, calcium, phosphate, pH, bicarbonate and lipid spectrum. It is recommended that when creatinine clearance (< 50 ml/min) falls a nephrologist should be consulted at least once with respect to the strategy to be followed. Symptoms of chronic renal insufficiency can occur when the creatinine clearance is < 30 ml/min. This relates to: sodium retention, imbalances in the calcium and phosphate levels, anaemia, uraemia, water retention, potassium retention and metabolic acidosis. Referral should take place at a creatinine clearance of < or = 30 ml/min.
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PMID:[Treatment of patients with chronic renal insufficiency; a guideline for internists]. 1511 99

The incidence of diabetes mellitus (DM) is increased in adult organ transplant recipients. As many as 30% to 45% of solid organ adult transplant patients have DM before transplantation or develop posttransplant diabetes mellitus (PTDM). Risk factors for PTDM include family history, ethnic or genetic background, insulin resistance, and diabetogenic effects of immunosuppressive medications. Posttransplant hyperglycemia may result in increased platelet aggregation, increased wound infections, dehydration, and loss of lean body mass. More significantly, long-term complications of DM such as coronary artery disease and peripheral vascular disease may be exacerbated with the use of immunosuppressive medications whose known side effects include hyperglycemia, hyperlipidemia, and hypertension; these effects may lead to premature transplant graft dysfunction. Treatment goals for PTDM reflect those of the American Diabetes Association guidelines; long-term management is linked with early, patient-centered education and optimizing minimally diabetogenic immunosuppressive medication regimens. A multidisciplinary team including the patient, family/support people, transplant surgeon, transplant physician, transplant nurse coordinator, transplant social worker, pharmacist, dietitian, and diabetes educator is crucial to long-term management of PTDM.
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PMID:Posttransplant diabetes mellitus: cause, impact, and treatment options. 1621 4


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