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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Large numbers of diabetics with renal failure have been treated by continuous ambulatory peritoneal dialysis (CAPD). Overall 1-year patient survival varies from 51% to 87%. Mortality is due to cardiovascular disease in more than 50% of the cases. Young diabetics with good blood pressure control and without cardiac disease have a chance at long survival on CAPD. In comparison to hemodialysis, CAPD yields better patient survival for young diabetics and worse for old diabetics, worse technique survival, probably greater overall morbidity, and similar rates of progression of retinopathy, neuropathy and peripheral vascular disease. Adequacy of peritoneal clearance and peritoneal ultrafiltration characteristics are similar between diabetics and non-diabetics on CAPD. CAPD is associated with better preservation of renal function than hemodialysis in diabetics. The rates of CAPD peritonitis do not differ substantially between diabetics and non-diabetics. However, diabetes appears to be associated with higher incidence of tunnel infection. Hyperlipidemia is generally less severe in diabetics than non-diabetics on CAPD, but malnutrition is more frequent in diabetics. CAPD has many attractive features and several drawbacks for the management of diabetics with end stage renal failure (ESRF). Its ultimate success will depend on the outcome of efforts to improve cardiovascular mortality, malnutrition, hyperlipidemia and catheter-related infections.
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PMID:CAPD in end stage patients with renal disease due to diabetes mellitus--an update. 136 83

A prospective study of 150 diabetic patients was undertaken with the aim of determining the factors associated with the development of foot ulcerations. Seventy five patients had foot ulceration and 75 had no foot lesions. Peripheral (78.7%) and autonomic (38.7%) neuropathy were more commonly found in the "ulcer" group, as were vascular insufficiency (49.3%) and hyperlipidaemia (60%). Renal failure (9.3%) and ketoacidosis (20%) were also commoner in patients with foot ulceration. Most, if not all, of the aetiological factors are related to prolonged uncontrolled hyperglycaemia.
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PMID:Aetiology of diabetic foot ulceration. 207 69

The initial treatment in the past of diabetes was one "of trial and error" as easily understandable. Carbohydrate restriction and their replacement by fats was followed, happily, last century already, by global caloric restriction. Around the fourties, after the introduction of insulin in 1922, the principle of the carbohydrate tolerance was introduced as an objective+ measure, followed by the proposal of "bread equivalencies" in the dietetic practice, assuring in this manner a figured evaluation. Around the seventies years the diet fiber came into its own and seemed very important for the evolution of the postprandial glycemia and insulinemia. Next to this, complex polysaccharides looked also of prime impact on this two biochemical parameters. The nature of this complex character is due to their liaison with other diet components (lectins, phytins, tannins etc.). So the concept of the glycemic index was born which explains why next to the presence of a given carbohydrate quantity the evolution of the glycemia is different from what is expected, just because the absorption is accelerated or retarded by the structure or the manipulation of these polysaccharides. This novel data are so much the more important because actually the hyperglycemia on the long run seems so important for the development of micro-angiopathy, at the base of the famous diabetic triad (nephropathy, retinopathy, neuropathy). The hyperlipemia is also beneficially influenced by the diet fiber and at the same level by the complex polysaccharides. All this statements are at the base of novel ways for the dietetic treatment of diabetes, as well on the quantitative as on the qualitative level and equally so for the diabetes of type I as of type II.
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PMID:[Diet treatment of the diabetic patient: yesterday and today. What has changed? What can be learned from it?]. 208 51

Abnormalities of Zn metabolism are well documented in patients with chronic renal disease, especially those with nephrotic disease and uremia. The causes of Zn deficiency in kidney disease are not clear. Decreased dietary Zn intake and intestinal absorption, increased endogenous Zn secretion, and increased urinary Zn excretion (as in the nephrotic syndrome and in renal transplant recipients) all may contribute to altered Zn metabolism. Zn depletion may account for decreased taste, sexual and gonadal dysfunction, hyperprolactinemia, glucose intolerance, hyperlipidemia, growth retardation in children, neuropathy, anemia, abnormalities of neutrophil and lymphocyte function, and delayed wound healing. The benefit of pharmacologic doses of Zn, in the treatment of such manifestations, requires further evaluation under controlled conditions. Before use of Zn routinely for therapeutic purposes in uremic subjects, the cause(s) of abnormal Zn metabolism should be identified.
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PMID:Zinc in kidney disease. 267 56

We investigated the patients who underwent operation for cholelithiasis and the diabetic patients at our clinic in order to determine whether there was a significant relationship between the occurrence of cholesterol gallbladder stone and age, obesity, hyperlipidemia, diabetes mellitus and neuropathy. In 647 patients undergoing surgery, cholesterol gallstones were not highly associated with diabetes mellitus or hyperlipidemia, compared with calcium bilirubinate and black stones. Eighty-seven percent of the male operated patients and 88% of the female patients were over 40 years old of age. Of the female patients in whom gallstones were detected at surgery, 36% were obese. We found cholesterol gallbladder stone in 11.5% (males 11%, females 12%) of 208 diabetic patients at our clinic. All of them were over 40 years old. The prevalence of cholesterol gallbladder stones was related to the decrease in motor nerve conduction velocity in the male diabetic patients (p less than 0.05). We observed that method of treatment had no definite effect on the prevalence of gallbladder stones. Fifty-four percent of the diabetic patients was normolipidemic in both sexes. Obesity was present in 64% of the female cholesterol gallbladder stone patients. Our data suggest that age, obesity and poor contraction of the gallbladder could be high risk factors for cholesterol gallstone formation.
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PMID:The relationship between cholelithiasis and diabetes mellitus: discussion of age, obesity, hyperlipidemia and neuropathy. 336 60

Iatrogenic pathology of the optic nerve is examined according to a framework which distinguishes direct and indirect effects on the optic nerve. Direct effects due to toxic drugs should be suspected when unexplained, usually bilateral loss of visual acuity occurs. The 3 clinical stages of classical optic toxic neuropathy are 1) anomalies of color vision, 2) loss of visual acuity and narrowing field of vision, and 3) papillary palor corresponding to irreversible optic atrophy. Usually only the 1st stages are reversible, but the reversibility may be incomplete. The list of drugs which can cause such effects is lengthy and includes antiinfectious drugs such as sulfamides and derivatives of hydroxyquinoleins, chloramphenicol especially when used to treat cystic fibrosis of the pancreas in children, the antituberculins ethambutol in high doses and isoniazide, which occasion particular risks when combined; antiparasitics such as quinine and its derivatives chloroquine and hydroxychloroquine, which cause optic neuropathy through their effect on the retina; arsenic pentavalents such as tryparsamide, quinacrine, trecator and mystatin; drugs affecting the central nervous system such as monoamineoxydase inhibitors, laroxyl, phenothiazine and the barbituates; anticonvulsants such as phenytoin; antimitotics such as vincristine; digitalics, disulfiram; penicillamines, and pexid. The action of lasers on the optic nerve can have a similar effect. The optic nerve may be indirectly damaged during surgical procedures leading to hypotonia, acute ischemia of the head of the optic nerve or embolic accident after a local or regional injection. Damage may also be caused by radiotherapy of intracranial tumors and certain drugs which cause isolated papillary edema or edema associated with headaches, such as Tetracycline, large doses of vitamin A or D, corticoids, and oral contraceptive (OC) pills, which may cause papillary edema through cerebral pseudo-tumors that regress with discontinuation of treatment. This condition has been observed in women with uncontrolled hyperlipidemia. It is probable that an alteration ofaxonal transport is at the basis of the neuropathic mechanisms. The 1st step in therapy is the suppression of the toxin, or at least its discontinuation. Some success has been obtained with vitamin B therapy, corticotherapy, zinc, or isaxonine, depending on the specific condition.
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PMID:[Iatrogenic pathology of the optic nerve]. 676 92

We describe six patients with painful polyneuropathy associated with hyperlipidemia. Each had mild, slowly progressive neuropathy characterized by pain in feet, without proximal extension or involvement of hands. Weakness and autonomic symptoms and signs were absent. Three patients had normal tendon reflexes; three others had decreased ankle reflexes. Serum cholesterol levels were moderately increased; serum triglyceride levels were exceedingly high. In one patient, symptoms resolved with correction of hypertriglyceridemia. No other cause of peripheral neuropathy was found. Marked increases in serum triglycerides may cause painful small-fiber neuropathy.
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PMID:Neuropathy associated with hyperlipidemia. 750 Nov 85

Autonomic and peripheral nerve function was examined in a group of patients with primary biliary cirrhosis using standard cardiovascular reflex tests and peripheral nerve conduction studies. Sixty-three percent had cardiovascular autonomic dysfunction with predominantly parasympathetic abnormalities. Symptoms of peripheral neuropathy were rarely volunteered spontaneously but occurred frequently when specifically sought; 40.7% had definite peripheral neuropathy, with symptoms and/or signs plus peripheral neurophysiological abnormalities. A close association between autonomic and peripheral nerve function was found with correlation between the heart rate variation on deep breathing and both peroneal nerve conduction velocity (r = 0.67, P < 0.001) and sural nerve conduction velocity (r = 0.52, P < 0.008). Correlations were also noted between other autonomic tests and peripheral nerve function. Both autonomic and peripheral nerve function correlated with serum bilirubin and albumin; no significant association was noted with vitamin E deficiency or hyperlipidaemia. A generalised neuropathy with peripheral and autonomic abnormalities is common in primary biliary cirrhosis and could be related to hepatic damage. Although rarely clinically disabling, the autonomic impairment associated with this neuropathy may be of prognostic significance.
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PMID:Autonomic and peripheral neuropathy in primary biliary cirrhosis. 769 49

"Hyperlipidemic crisis" is a term used to describe episodic abdominal pain in patients with hyperlipidemia. The morphologic correlates of this phenomenon have not been investigated and the etiology of the disorder is uncertain. We report a unique histologic finding in the pancreas of a 34-year-old woman with a 17-year history of episodic abdominal pain, sometimes accompanied by hyperamylasemia. At the age of 18 years, grossly elevated cholesterol and triglyceride levels were documented and type V hyperlipidemia was diagnosed. At the age of 34 years, subtotal pancreatectomy was performed for intractable abdominal pain. Histologic examination identified an increased number of enlarged pancreatic nerves that were infiltrated by foamy macrophages and encircled by fibrous tissue; endoneurial infiltration with macrophages occasionally split nerves into individual fascicles. Otherwise, the pancreas had only minimal fibrosis, nesidioblastosis, mucinous metaplasia of some pancreatic ducts, and scattered small collections of chronic inflammatory cells, subtle features suggesting very mild chronic pancreatitis. We propose that this novel xanthomatous neuropathy mimicked pancreatitis and was one of the underlying pathophysiologic mechanisms of abdominal pain in this patient. Further studies are necessary to document the prevalence of this new entity in patients with hyperlipidemia and to correlate its occurrence with "hyperlipidemic crisis" in those individuals.
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PMID:Pancreatic xanthomatous neuropathy associated with hyperlipidemia: a cause of abdominal pain mimicking chronic pancreatitis. 811 25

Non-insulin-dependent diabetes (NIDDM) is a common multimetabolic disorder with potential (and potentially severe) long-term complications affecting large and small blood vessels. Where microvascular complications (retinopathy, nephropathy and neuropathy) are concerned, the Diabetes Control and Complications Trial (DCCT), as well as much circumstantial evidence, suggests that hyperglycaemia is the main aetiological factor and this is likely to apply in NIDDM as well as IDDM. Unfortunately, achieving normoglycaemia in NIDDM is not easy and it is unclear whether insulin has advantages over oral hypoglycaemic agents or vice versa. Turning to macrovascular disease, it is unclear which of the many potentially atherogenic abnormalities-hypertension, hyperinsulinaemia, hyperlipidaemia, etc-are most important. A further problem is that macrovascular disease is already well developed in many patients when NIDDM is diagnosed and we do not know whether secondary prevention is effective. Nevertheless, it is sensible to try to reverse the atherogenic milieu and this should be done in the first instance by lifestyle modification rather than drugs. Even if we cannot manipulate the biochemistry to prevent small or large vessel complications, much can still be done; proactive foot care can prevent ulceration, timely laser treatment can prevent visual loss and thrombolytic therapy is relatively more effective in diabetic patients with myocardial infarction than in their non-diabetic peers. Finally, patients with NIDDM need intensive education and each needs an individualised treatment plan and goals.
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PMID:Targets of therapy for NIDDM. 852 19


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