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

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

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a "uremic toxin" responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant "uremic toxin."
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PMID:Parathyroid hormone metabolism and its potential as a uremic toxin. 699 9

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

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44

Patients with primary hyperparathyroidism (PHPT) have an increased cardiovascular morbidity and mortality. Elevated serum calcium and/or PTH may directly contribute to vascular tissue damage, but the role of classic factors for atherosclerosis has not fully been evaluated in this disease. The aim of our study was to dissect the potential effect of hypercalcemia and/or high PTH from that of major cardiovascular risk factors (i.e. diabetes mellitus, hyperlipidemia, hypertension, obesity, smoking habit) on the carotid artery structure of patients with PHPT. Twenty-six consecutive patients with PHPT [subdivided into two groups according to the absence (n = 10) or the presence (n = 16) of one or more risk factors] and 15 normocalcemic healthy subjects as controls were studied. At ultrasonography, a significant increase (P < 0.001) of carotid mean and maximum intima-media thickness, as well as a significant reduction of lumen diameter (P < 0.05) were found in the PHPT group with risk factors, compared with the other two groups. This suggests that hypercalcemia and/or PTH elevation per se are not determinant of carotid atherosclerosis in PHPT, and that increased cardiovascular mortality and morbility in this disease is attributable to the combined presence of classic cardiovascular risk factors.
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PMID:Ultrasound evaluation of carotid artery in primary hyperparathyroidism. 1272 60

When primary hyperparathyroidism was a more symptomatic disease, it was often associated with increased cardiovascular risk. As the clinical manifestations of the disease have changed to a milder, more asymptomatic disorder, investigation is shifting to more subtle cardiovascular abnormalities. We measured arterial stiffness in 39 patients with mild primary hyperparathyroidism [serum calcium, 2.66 +/- 0.2 mmol/liter (10.7 +/- 0.6 mg/dl); PTH, 21.7 +/- 9.5 pmol/liter (89 +/- 39 pg/ml)] and in 134 controls. Arterial stiffness was measured mathematically at the radial artery with a noninvasive device as the "augmentation index" (AIx). The AIx measures the difference between the second and first systolic peaks in the pressure waveform and correlates with increased cardiovascular risk. When physiological variables affecting augmentation index and potentially confounding cardiovascular risk factors (age, gender, heart rate, height, blood pressure, diabetes mellitus, smoking, and hyperlipidemia) were adjusted for, primary hyperparathyroidism was an independent predictor of increased augmentation index (B = 3.37; P < 0.03). A matched-pair analysis showed that 15% of the variance in AIx was uniquely accounted for by the presence of primary hyperparathyroidism. The presence of primary hyperparathyroidism was a stronger predictor of elevated AIx than age, gender, smoking, hypertension, hyperlipidemia, or diabetes mellitus. AIx was also directly correlated with evidence of more active parathyroid disease, including higher PTH levels (r = +0.42; P < 0.05) and lower bone mineral density at the distal one-third radius (r = -0.33; P < 0.05). The diagnosis of primary hyperparathyroidism was therefore an independent predictor of increased AIx, an early measure of arterial stiffness, and the increase was associated with evidence of more active parathyroid disease.
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PMID:Arterial stiffness in mild primary hyperparathyroidism. 1576 95

Cardiovacular disease is the main cause of morbidity and mortality in hemodialysis (HD) patients. However, there are no reliable data neither on the prevalence of cardiovacular disease nor its risk factors in Spain. The Morbidity and mortality Anemia Renal study (MAR) is a two-year multicenter, open-label, prospective cohorts study. Its main objective is to assess the general morbidity and mortality, particularly of a cardiovascular cause, and its relationship with the degree of anemia. Secondary objectives are: a/ the description of current clinical practices in anemia, dialysis, vascular access, and CV risk factor management; and b/ the description of hospitalization and mortality causes. This paper describes the prevalence of cardiovascular disease and risk factors of the HD population in Spain. A total of 1.710 patients were included (60% male, aged 64.4 years, 16.2 months on HD). The mean co-morbidity Charlson index was 6.5 +/- 2.3. Cardiovascular disease was the most prevalent comorbidity, 16.7% had a coronary disease, and 13.9% had different degrees of heart failure, while 11.6% had arrhythmia, 1.7% stroke and 5.5% peripheral artery disease. The prevalence of hypertension was 75.8%, 74.4% of patients received antihypertensive drugs, and still 40% of patients had an inadequate blood pressure control. The investigators considered as dyslipidemic 34.1% of patients, and prescribed treatment to 69.5% of them, while the remaining 30.5% (10.4% of the total) had hyperlipidemia with no drug therapy. Eleven percent was active smoker, and 26.6% former smoker. There was 47.4% of patients with a corporal mass index above 25. Secondary hyperparathyroidism with PTH above of 300 pg/ml was present in 22.2% of patients. Despite the EBPG and K-DOQI recommendations, only 68.8% of prevalent hemodialysis patients attained a hemoglobin (Hb) above 11 g/dl, 89.4% ferritin levels above 100 ng/ml, 66.5 degrees/a a transferrin saturation index (TSI) above 20%, and 61.1% met all three objectives. In summary, this first cross-sectional analysis has allowed us to know in detail the standard practice in multiple aspects of management of HD population in Spain. It has also established clear differences in the prevalence of cardiovascular disease and risk factors from the US registries. Last but not least we have identified therapeutic opportunities to improve the course and prognosis of our patients.
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PMID:[Cardiovascular risk in hemodialysis in Spain: prevalence, management and target results (MAR study)]. 1605 11

Patients with primary hyperparathyroidism (PHPT) have impaired vasodilation both dependent and independent of endothelium. The aims of our study were to measure three different biochemical markers of endothelial activation, i. e., plasma thrombomodulin, soluble(s) E-selectin, and von Willebrand factor, in PHPT patients before and one year after successful parathyroidectomy, and to distinguish the potential effect of hypercalcemia and/or high parathyroid hormone from that of major cardiovascular risk factors (diabetes mellitus, hyperlipidemia, hypertension, obesity, smoking habit) on endothelial function. Twenty consecutive patients with PHPT subdivided into two groups according to the absence (n = 8) or presence (n = 12) of one or more risk factors, and fifteen healthy normocalcemic subjects were studied. Baseline thrombomodulin levels were similar in the groups with and without risk factors, and in controls. In contrast, sE-selectin and von Willebrand factor were higher in PHPT patients with risk factors than in those without risk factors (p < 0.05 and p < 0.01, respectively) and controls (p < 0.01). Neither thrombomodulin nor sE-selectin changed after parathyroidectomy in either PHPT group. Plasma von Willebrand factor decreased (p < 0.01) in patients without risk factors, while persisting at high levels in patients with risk factors. In conclusion, in spite of a limitation due to the small number of patients, our study suggests that classic cardiovascular risk factors seem to be the main determinants for the high plasma levels of sE-selectin and vWF in PHPT. Together with unaltered thrombomodulin and sE-selectin levels, a plasma vWF decrease after parathyroidectomy might reflect a specific mechanism of its endothelial calcium- and/or PTH-stimulated secretion in some PHPT patients without risk factors. Whether a vWF reduction after parathyroidectomy may be used as a biochemical index for improved endothelial function in PHPT patients without risk factors has yet to be demonstrated in larger studies.
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PMID:Biochemical markers of endothelial activation in primary hyperparathyroidism. 1652 14

Epidemiological and in vitro studies have suggested that hyperlipidemia/oxidized phospholipids adversely affect bone. We recently found that oxidized phospholipids attenuate PTH-induced cAMP and immediate-early gene (IEG) expression in MC3T3-E1 cells, raising concerns that clinical hyperlipidemia may attenuate osteoanabolic effects of PTH in vivo. Thus, we studied whether intermittent PTH treatment has differential osteoanabolic effects in wildtype (C57BL/6) and hyperlipidemic (LDLR(-/-)) mice. Consistent with our previous in vitro studies, induction of IEGs in calvarial tissue, 45 min after a single dose of recombinant hPTH(1-34), was attenuated in LDLR(-/-) mice compared with C57BL/6 mice. Daily hPTH(1-34) injections for 5 wk significantly increased total and cortical BMD and BMC, assessed by pQCT, in C57BL/6 mice. However, this induction was completely abrogated in LDLR(-/-) mice. Similarly, PTH(1-34) failed to increase BMD in another hyperlipidemic mouse model, ApoE(-/-) mice. Histomorphometric analysis showed that trabecular bone of both mice responded similarly to PTH(1-34). Structural parameters improved significantly in response to PTH(1-34) in both mouse strains, although to a lesser degree in LDLR(-/-) mice. With PTH(1-34) treatment, osteoblast surface trended toward an increase in C57BL/6 mice and increased significantly in LDLR(-/-) mice. PTH(1-34) did not alter resorption parameters significantly, except for the eroded surface (ES/BS), which was reduced in the C57BL/6 but not in the LDLR(-/-) mice. These results show that PTH(1-34) has adverse effects on cortical bones of the hyperlipidemic mice, suggesting that the therapeutic effects of PTH may be compromised in the presence of hyperlipidemia.
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PMID:Hyperlipidemia impairs osteoanabolic effects of PTH. 1850 71

Bioactive lipids initiate inflammatory reactions leading to pathogenesis of atherosclerosis. Evidence shows that they also contribute to bone loss by inhibiting parathyroid hormone receptor (PTH1R) expression and differentiation of osteoblasts. We previously demonstrated that bone anabolic effects of PTH(1-34) are blunted in hyperlipidemic mice and that these PTH effects are restored by antioxidants. However, it is not clear which osteoblastic cell developmental stage is targeted by bioactive lipids. To investigate the effects of hyperlipidemia at the cellular level, hyperlipidemic Ldlr(-/-) mice were bred with Col3.6GFPtpz mice, in which preosteoblasts/osteoblasts carry a topaz fluorescent label, and with Col2.3GFPcyan mice, in which more mature osteoblasts/osteocytes carry a cyan fluorescent label. Histological analyses of trabecular bone surfaces in femoral as well as calvarial bones showed that intermittent PTH(1-34) increased fluorescence intensity in WT-Tpz mice, but not in Tpz-Ldlr(-/-) mice. In contrast, PTH(1-34) did not alter fluorescence intensity in femoral cortical envelopes of either WT-Cyan or Ldlr(-/-)-Cyan mice. To test the mechanism of PTH1R downregulation, preosteoblastic MC3T3-E1 cells were treated with bioactive lipids and the antioxidant Trolox. Results showed that inhibitory effects of PTH1R levels by bioactive lipids were rescued by pretreatment with Trolox. The inhibitory effects on expression of PTH1R as well as on PTH-induced osteoblastic genes were mimicked by xanthine/xanthine oxidase, a known generator of reactive oxygen species. These findings suggest an important role of the preosteoblastic development stage as the target and downregulation of PTH receptor expression mediated by intracellular oxidant stress as a mechanism in hyperlipidemia-induced PTH resistance.
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PMID:Roles of parathyroid hormone (PTH) receptor and reactive oxygen species in hyperlipidemia-induced PTH resistance in preosteoblasts. 2403 94


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