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Query: UMLS:C0020473 (hyperlipidemia)
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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

Male and female, arteriosclerotic and nonarteriosclerotic rats were subjected to acute myocardial infarction by two, subcutaneous injections (spaced 24 hr apart) of isoproterenol. During the immediate postinfarct repair phase all of the experimental animals were made severely diabetic with alloxan. Two weeks later the animals were sacrificed and their blood and pertinent organs analyzed for biochemical and pathologic changes. Females survived the myocardial infarct with superimposed diabetes in significantly greater than males. In addition to marked loss in body weight all of the experimental animals developed marked adrenal hypertrophy and thymus gland involution, cardiac hypertrophy, and unusual increase in ovarian or testicular size and weight. The combined conditions of myocardial infarction + diabetes led to substantial increases in serum creatine phosphokinase (CPK) and glutamic oxaloacetic transaminase (SGOT) whereas the enzymes glutamic pyruvic transaminase (SGPT) and lactic dehydrogenase (LDH) were reduced. Although serum triglyceride levels were greatly elevated, total cholesterol and free fatty acids were reduced. All of the animals were severely hyperglycemic and had greatly increased B.U.N. levels. Diabetes caused hypercalcemia but diabetes + myocardial infarction was associated with a definite reduction of this hypercalcemia. Despite marked adrenal hypertrophy, circulating Cmpd. B levels were subnormal. The diabetic condition and its attendant hyperlipidemia did not alter the morphologic nature of the arterial lesions in the breeder rats but the diabetes did cause definite impairment of the usual myocardial repair process observed in these rats with a particularly high incidence of left ventricular aneurysms in males.
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PMID:Metabolic and histopathologic changes in arteriosclerotic versus nonarteriosclerotic rats following isoproterenol-induced myocardial infarction with superimposed diabetes. 119 29

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

Chronic "idiopathic" pancreatitis (CP) in a 7 year-old-boy, whose father has suffered from CP, and whose former grandfather had suffered from pains possibly of pancreatic origin, led us suspect a hereditary etiology. An analysis, extended in a control fashion to the relatives of the healthy spouse of the affected grandfather, surprisingly revealed 2 more proven and 3 more suspected CP, giving the overall number of 8 affected members in this 35-member 3 generation kindred and revealed a maternal heredity instead of paternal heredity (which was first thought to be apparent). We therefore recommend that in a family suspected to suffer from hereditary CP (HCP), a screening should be extended to cover even the unaffected spouse's family--the present extended study revealed for 23 new members them to belong in an affected family. Without an extensive screening advises for family planning, alcohol consumption etc. can not be given. Plain abdominal X-ray accompanied with epigastric ultrasonographic are suitable for screening, which might be extended to every individual in smaller families, but may be safely restricted to the members ever suffered from epigastric pains in the case of a huge family. Pancreatic duct anomalies, hyperlipidaemia, hypercalcaemia, aminoaciduria or hyperimmunoglobulinaemia, all of which have been seen to accompany HCP, were not present in this family. Neither was any linkage found between the penetrance of HCP and ABO/Rh blood groups or HLA haplotypes.
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PMID:Screening a family for hereditary chronic pancreatitis. 226 97

The majority (about 75%) of patients who suffer from acute pancreatitis do so as a consequence of gallstones or alcohol abuse. The other 25% of patients often present difficult diagnostic problems. Over several years the author has accumulated a series of patients with remedial causes of pancreatitis. They include a group of congenital conditions such as pancreas divisum, choledochal cysts and congenital abnormalities of the pancreatic ductal system. Patients who have had pancreatitis and who have an intact gallbladder often have stones that are difficult to identify. Repeated attacks of pancreatitis in the absence of any other apparent cause justifies cholecystectomy, which will often identify the cause so that recurrence can be prevented. A group of nonanatomic causes are also known. They include hyperlipidemia, drugs and toxins, certain systemic illnesses such as systemic lupus erythematosus, pregnancy, hypercalcemia, hereditary causes and occasionally cancer. In his lecture the author reviews the various etiologies of acute pancreatitis and describes an algorithm that can be used when the diagnosis is difficult.
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PMID:Recurrent acute pancreatitis--rarely idiopathic: 1989 Du Pont lecture. 226 8

A long-term hemodialysis patient with a giant intracranial vascular channel, which has been called a giant serpentine aneurysm, is presented. A 50-year-old man with an eight-year history of hemodialysis treatment was admitted because of headache, nausea and double vision. Computed tomographic scans and nuclear magnetic resonance revealed intracranial abnormal shadow. The left vertebral arteriography showed that the distal portion of the left vertebral artery was dilated to 17 mm in diameter. The basilar artery showed a large tortuous vascular channel and globular aneurysms over 25 mm in diameter. This giant serpentine aneurysm is a rather rare disease. To our knowledge, it has not been reported as a complication in a hemodialysis patient, although fourteen cases have been reported in the literature. In our case, several conditions such as long-term hypertension, hyperlipidemia, hypercalcemia, atherosclerosis and abnormal blood flow due to arteriovenous fistula for hemodialysis treatment might be considered to play a role in the formation of the giant serpentine aneurysms.
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PMID:Giant serpentine aneurysm in a long-term hemodialysis patient. 318 May 24

Acute recurrent pancreatitis in the absence of alcoholism and gallstones is a frustrating illness for both the patient and the physician. Over a 10 year period, 33 patients were operated on and found to have a duct of Wirsung entering the duodenum through the fibers of the sphincter of Oddi. Recurrent pancreatitis of sufficient intensity to require hospitalization had occurred an average of 4.2 times per patient, and each had experienced numerous episodes of abdominal pain of lesser severity. At least two attacks of pancreatitis that required hospitalization had occurred in all patients. All known causes of pancreatitis, including alcoholism, gallstones, hypercalcemia, hyperlipidemia, drug reactions, and pancreas divisum were excluded. Endoscopic retrograde cholangiopancreatography showed no ductal abnormalities. Twenty-eight of the patients had previously undergone cholecystectomy 8 months to 20 years before operation. A sphinteroplasty of the common bile duct and duct of Wirsung resulted in elimination of attacks of pancreatitis in all except two patients. Follow-up has been more than 5 years in 16 patients, more than 4 years in 10 patients, and more than 1 year in 5 patients. There have been no deaths. It appears that the entrance of the duct of Wirsung into the duodenum through a separate orifice through the fibers of the sphincter of Oddi causes recurrent acute pancreatitis. It seems likely that the problem is one of intermittent pancreatic duct obstruction. Normal pancreatic duct caliber is attributed to the intermittent nature of the obstruction. Enlargement of the orifice of the duct of Wirsung and division of the sphincter of Oddi relieved attacks of recurrent pancreatitis.
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PMID:Misplaced pancreatic duct orifice as a cause of recurrent acute pancreatitis. 381 90

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

A case of subcutaneous fat necrosis (S.F.N.) with hypercalcemia and hyperlipemia in a newborn infant is reported. On the basis of previous reports it is impossible to definite the pathogenesis of hypercalcemia and hyperlipemia in subcutaneous fat necrosis. Moreover the Authors point out that in a newborn with S.F.N. plasma levels of calcium and lipids and, if it is possible, urinary prostaglandin E and serum PTH and 250HD3 should be determined.
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PMID:[Fat necrosis in the newborn infant associated with hypercalcemia and dyslipidemia (description of a case)]. 692 59


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