Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Definite inherited defect in hereditary pancreatitis (HP) is not known. A new kindred with 3 definite and 6 suspected cases of HP was investigated for possible inherited abnormalities. No aminoaciduria (except for a slight rise in urinary histidine in one patient) and no hyperparathyroidism, hyperlipidemia, or chromosomal abnormality was present. An increase in serum IgM level of a polyclonal type was noted in 3 definitely affected sisters and also in 2 nonaffected members. Serum alpha-1-antitrypsin and serum trypsin inhibition were normal. However, very marked dilatation and ectasia of the pancreatic duct were found in the propositus. Reviewing the data from this family and previously described kindreds, it is postulated that the genetic abnormality in HP encompasses a wide variety of structural and anatomical defects in the sphincter of Oddi or the pancreatic ductal system. These predispose to intermittent obstruction of the duct with concomitant activation of enzymes and ductal metaplasia. In suspected cases an early effort should be made to outline the pancreatic duct as the defect may be amenable to surgery.
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PMID:Inherited defect in hereditary pancreatitis. 30 62

Pancreatitis has been described previously following renal transplantation, but not in association with chronic renal failure. Analysis of 168 patients with renal transplants revealed five who developed pancreatitis, three of whom died. All five were on treatment with prednisone and azathioprine. Four patients were seen with definite attacks of pancreatitis and chronic, stable renal failure from a variety of causes. None had received immunosuppressive agents, prednisone nor thiazide diuretics, but two were on regular frusemide. One patient was on maintenance dialysis, which could not be related directly to the pancreatitis. In either group alcohol ingestion, cholethiathiasis, or hypercalcaemia was not a factor. This diagnosis of pancreatitis was established on clinical grounds and serum amylast levels of greater than 900 iu/1. Similar serum amylast elevation was not found ina random group of patients with chronic renal failure. Hyperlipidaemia was not present in any patient with pancreatitis. Although hypercalcaemia and primary hyperparathyroidism was not found in the transplant and non-transplant subjects, elevated serum parathormone levels have been described in uraemic patients with normocalcaemia. Hyperparathyroidism may be a factor in the development of pancreatitis in reanl failure. Pancreatitis carries a significant mortality risk in renal transplantation. The four non-transplanted patients have survived, despite recurrent attacks of pancreatitis.
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PMID:Pancreatitis and renal disease. 31 21

Dyslipidemia of chronic renal failure is of multifactorial origin. Decreased activity of lipoprotein lipase and hepatic triglyceride lipase, peripheral insulin resistance, hyperparathyroidism and L-carnitine deficiency are the contributing factors. This results in a disturbed catabolism of chylomicron, accumulation of very-low-density (VLDL) and intermediate-density (IDL) lipoproteins as well as incompletely cleared remnant particles, whereas low-density lipoprotein (LDL) levels are diminished. There is current debate as to whether cardiovascular disease is accelerated and whether hyperlipidemia should specifically be treated. In addition, there have been few means of influencing these metabolic alterations. Drug incompatibility and consequently side effects render treatment difficult. The drugs that have been most tested for lipid lowering in chronic renal failure are the fibric acids. By their mode of action, they are the logical choice. Dose reduction overcomes major side effects such as myopathy and rhabdomyolysis. The second generation of fibric acid derivatives (gemfibrozil and beclobrate) show several advantages over formerly used derivatives. Treatment with lovastatin and simvastatin appears to be safe and is recommended in a minority of patients with predominantly elevations of LDL. HMG-CoA reductase inhibitors also lower remnant particles effectively in hemodialysis (HD) patients. L-Carnitine and low-molecular-weight heparin have been shown to influence VLDL rich in triglycerides in a subset of patients on HD. In posttransplant hyperlipidemia, diet remains the first course of action in all patients. When this approach fails, the new lipid-lowering agents, especially fibric acids, appear to be safe in short-term studies in azathioprine- and ciclosporin-treated patients. Lovastatin has been shown to be safe in stable renal transplant patients. Its toxicity seems to depend mainly on high ciclosporin whole blood through or plasma levels.
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PMID:Hyperlipoproteinemia in chronic renal failure: pathophysiological and therapeutic aspects. 186 98

The need for treatment of mild and apparently asymptomatic primary hyperparathyroidism (HPT) is questioned, but a raised incidence of cardiovascular disease has been regarded as evidence in favour of surgery. While it is well known that several risk factors for cardiovascular disease (hypertension, hyperlipidaemia and diabetes mellitus/impaired glucose tolerance) are overrepresented in HPT, it is not known whether surgery provides long-term normalization in these respects and reduces the risk of premature death. In a 15-year follow-up of a cohort of 172 subjects in whom mild hypercalcaemia was initially detected during a health screening, it was found that 56 subjects had died. 17 individuals had been operated on for HPT, 47 individuals were persistently hypercalcaemic, while 45 subjects had serum calcium within the normal range (seven individuals were lost to follow-up). There had been no significant differences in blood pressure between these groups of mildly hypercalcaemic patients and age- and sex-matched controls at the initial screening, but at follow-up blood pressure was significantly higher not only in subjects with persistent hypercalcaemia, but also in those who had been successfully operated on for HPT. Neither of the hypercalcaemic groups showed any significant deviations from the controls with regard to indices of lipid or glucose metabolism. These findings suggest that there is no simple cause-and-effect relationship to account for the propensity toward high blood pressure in primary HPT. Consequently it cannot be assumed that surgery for HPT will eliminate the increased risk of cardiovascular disease in patients with mild HPT.
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PMID:Cardiovascular risk factors in primary hyperparathyroidism: a 15-year follow-up of operated and unoperated cases. 206 9

Little notice has been paid in the surgical literature to problems with psychoeffective lithium, which by interfering with adenylate cyclase affects thyroid and parathyroid function, causing hypercalcemia, hyperparathyroidism, and hypothyroidism. Seven patients with lithiumogenic hyperparathyroidism occurring after years of lithium therapy underwent treatment and manifested osteoporosis (n = 2), hypertension (n = 2), nephrolithiasis (n = 1), coma (n = 1), rising hypercalcemia (n = 1), goitrous myxedema (n = 4), nephrogenic diabetes insipidus (n = 2), renal failure (n = 2), and hyperlipidemia (n = 1). Disease-directed parathyroidectomy (without morbidity) was curative. Unique laboratory findings included normal serum phosphorus and reduced urinary calcium and cyclic adenosine monophosphate values. Three separate cases of thyroid carcinoma after long-term lithium therapy were also treated, being preceded by myxedema (n = 2) and concurrent with hyperparathyroidism (n = 1). There has been only one previous report of lithium-associated thyroid carcinoma. All patients taking lithium should undergo surveillance for thyroid and parathyroid dysfunction and neoplasia, and appropriate surgical and medical treatment should be considered in each situation. Although hyperparathyroidism may be reversible with lithium discontinuance, such therapy may be obligatory for patient well-being, thus dictating parathyroidectomy.
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PMID:Lithiumogenic disorders of the thyroid and parathyroid glands as surgical disease. 224 24

In a Chinese family with hereditary pancreatitis, two members are proven to have chronic pancreatitis. The propositus, a 31-year-old man, had epigastric pain since the age of 18. Multiple calcifications in the region of the pancreas were seen on plain film of the abdomen, ultrasonography, computed tomography, and endoscopic retrograde pancreatography. Pancreatolithotomy and side-to-side pancreatojejunostomy gave symptomatic improvement. His 60-year-old mother also had pancreatic calcifications in addition to diabetes. Known causes of secondary pancreatitis, such as hyperlipidemia, hyperparathyroidism, and amino aciduria, were ruled out in both patients.
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PMID:Hereditary pancreatitis in a Chinese family. 230 90

Hyperlipidemia is common in chronic renal failure (CRF), but the underlying mechanisms are not clearly defined. Certain data points toward a potential role for the state of secondary hyperparathyroidism of CRF in its pathogenesis. We examined the effects of parathyroid hormone (PTH) on lipid metabolism utilizing intravenous fat tolerance test (IVFTT) and post-heparin lipolytic activity in five normal dogs, in six animals with CRF and secondary hyperparathyroidism (NPX) and in six normocalcemic-thyroparathyroidectomized dogs (NPX-PTX) with comparable degree and duration of CRF. NPX dogs had fasting hypertriglyceridemia (82 + 6.0 mg/dl vs. 49 +/- 2.7 mg/dl in normal dogs, P less than 0.01), abnormal IVFTT, and reduced post-heparin plasma LPL activity (151 +/- 10 vs. 275 +/- 15 mumol fatty acids/ml/min in normal dogs, P less than 0.01). The NPX-PTX dogs had normal fasting levels of serum triglycerides (42 +/- 0.6 mg/dl), normal IVFTT, and normal post-heparin plasma LPL (317 +/- 19 mumol fatty acids/ml/min) despite CRF. Post-heparin HL activity in plasma was not different between NPX and NPX-TPX dogs. The results show that excess blood levels of PTH and not other consequences of CRF are mainly responsible for the abnormalities in lipid metabolism. The data are consistent with the notion that excess PTH reduces post-heparin LPL activity in plasma, which in turn results in impaired lipid removal from the circulation and consequently hyperlipidemia.
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PMID:Excess parathyroid hormone adversely affects lipid metabolism in chronic renal failure. 231 75

No single pathophysiologic factor has been identified as the cause of recurrent acute pancreatitis. A systematic search should be undertaken in every patient to identify one of a myriad of factors that have been shown to play a part in causing this distressing illness. The abuse of alcohol remains the likeliest cause, and further research may reveal an inborn error of metabolism that jeopardizes some people. Biliary tract disease, gallstones, choledochal cyst, papillary stenosis, and duodenal diverticula show a clear relationship. Metabolic disorders such as hypercalcemia, hyperlipidemia, and hyperparathyroidism remain suspect. Systemic illnesses such as systemic lupus erythematosus and cystic fibrosis must be considered. Development anomalies such as pancreas divisum may precipitate acute pancreatitis through aberrant anatomic structures. Cancer must always be disproved. Not yet firmly established but worthy of thorough investigation are uncommon causes, such as the ingestion of certain drugs or combinations of drugs and trauma, either recent or past. Pancreatitis remains frightening for those with the disease and puzzling and frustrating for the medical people who treat it. A careful history and investigation in accordance with a systematic diagnostic plan that includes many disparate factors will lead to identification of the cause in the majority of patients.
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PMID:Pathophysiologic factors in recurrent acute pancreatitis. 393 40

Out of 512 recipients of kidney allotransplants 36 patients exhibiting cardiovascular complications (coronary artery disease, cerebrovascular accident, aneurysm of aorta, peripheral arterial occlusions) were compared with an age and sex matched group of recipients without cardiovascular problems. The following significant differences were observed in the study group versus the controls: high systolic and diastolic blood pressure, longer duration of hypertension before renal allografting, higher serum concentrations of cholesterol, triglycerides and uric acid, and an increased incidence of left ventricular hypertrophy and preexisting cardiovascular disease. No differences were found between the two groups as regards smoking habits, overweight, hyperparathyroidism, duration of hemodialysis treatment and type of kidney disease. Diabetes mellitus, family history of cardiovascular complications and hypertonic alterations of the eye fundus were more frequent, but not to a statistically significant extent, in the study group as compared to control patients. These findings show the need for regulation of blood pressure, hyperlipemia and hyperuricemia to ensure successful longterm rehabilitation after kidney allografting.
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PMID:[Cardiovascular diseases after kidney transplantation: an analysis of predisposing factors]. 645 62

PTH activates hormone-sensitive lipolysis in adipose tissue by an adenylate cyclase mechanism. Effects on lipoprotein synthesis and catabolism are conceivable, but have not been studied in detail so far. Information on serum lipids in primary and secondary hyperparathyroidism is conflicting. Some authors find an increase of serum lipids upon administration of PTH and in patients with primary hyperparathyroidism, while others find a decrease of serum cholesterol and serum triglycerides which reverts to normal upon parathyroidectomy in patients with primary hyperparathyroidism. In experimental models of uremia, PTH clearly plays a permissive role for the development of uremic hyperlipemia. In PTX uremic animals, hyperlipoproteinemia is less marked than in PT-intact uremic animals, but serum lipids are still higher in PTX uremic animals than in nonuremic PT-intact animals. This would indicate that hyperlipemia is caused by PTH-independent mechanisms but is intensified by the presence of secondary hyperparathyroidism. The role of PTH in the hyperlipoproteinemia of uremic patients has not been clarified so far.
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PMID:Does parathyroid hormone play a role in lipid metabolism? 699 9


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