Cases reported "Hyperlipidemias"

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1/125. The evaluation of lipoprotein changes during gemfibrozil treatment.

    During treatment with gemfibrozil, 1200 mg daily, total serum triglyceride levels were reduced in 7 of the 11 patients, owing chiefly to a fall in VLDL triglyceride levels. Total serum cholesterol responded variably, falling in a majority of patients with hypercholesterolaemia. High density lipoprotein cholesterol rose during treatment in patients who had either hypertriglyceridaemia or hypercholesterolaemia.
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keywords = lipoprotein
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2/125. Identification of compound heterozygous mutations (G188E/W382X) of lipoprotein lipase gene in a Japanese infant with hyperchylomicronemia: the G188E mutation was newly identified in Japanese.

    We herein report a case of a 5-month-old Japanese female (patient AN) with fasting hyperchylomicronemia due to a primary lipoprotein lipase (LPL) deficiency. Patient AN was compound heterozygous for a missense mutation (GG818G-->GAG/Gly188-->Glu; G188E) in exon 5 and a nonsense mutation (TGG1401-->TGA/Trp382-->Stop; W382X) in exon 8 of the LPL gene. This resulted in less than 10% of the control levels for both the LPL activity and immunoreactive LPL mass in the postheparin plasma. A G188E mutation was thus identified for the first time in a Japanese, and the haplotype of this G188E allele was different from that of the G188E alleles identified in other ethnic groups. This additional mutation might be useful for early diagnosis of LPL gene aberrations in Japanese patients with fasting hyperchylomicronemia.
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ranking = 1.0002310913745
keywords = lipoprotein, deficiency
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3/125. A novel frameshift mutation in exon 6 (the site of Asn 291) of the lipoprotein lipase gene in type I hyperlipidemia.

    A new heterozygous lipoprotein lipase gene defect has been identified in a type I hyperlipidemic patient at the position of notable amino acid Asn 291. The patient is a 33-year-old male. His body mass index (BMI) was 18.5 kg/m2. The total cholesterol (TC), triglycerides (TG) and high density lipoprotein-cholesterol (HDL-C) concentration from his fasting plasma were 4.8, 11.9 and 0.4 mmol/l, respectively. The lipoprotein lipase (LPL) activity and mass in the postheparin plasma (PHP) from the patient were 0.58 mmol/ml/h (normal range: 7.7 /-2.6) and 244 ng/ml (normal range: 192 /-30), respectively. The hepatic lipase activity of the PHP from the patient was 10.6 mmol/ml/h (normal range: 9.9 /-3.6). dna analysis of the LPL gene revealed that this patient had a heterozygous one nucleotide deletion of A coding Asn 291, resulting in a premature termination of the LPL protein at amino acid residue 303. The other abnormality in the LPL gene of the proband was an amino acid residue 194 defect (Ile194-->Thr), which is known to cause a defective enzyme. A medium-chain triglyceride (MCT) loading test was conducted to find how this triglyceride affects plasma lipoprotein metabolism in this patient in a short term (Fig. 3). The plasma total cholesterol (TC) or high density lipoprotein (HDL)-C levels did not change significantly after oral administration of a fatty meal containing long chain triglycerides (LCT) or MCT. The plasma TG level, on the other hand, increased from 11.9 to 19.2 mmol/l ( 61%) at 6 h after loading a fatty meal containing LCT, whereas the plasma TG levels tended to even decrease at 6 h after oral administration of an MCT, tricaprin (from 11.6 to 10.5 mmol/l (-9.4%)). These results suggest that MCT, as opposed to LCT, is useful for treatment of type I hyperlipidemia with a novel mutation at the notable amino acid Asn 291 of the LPL gene.
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keywords = lipoprotein
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4/125. Oxcarbazepine versus carbamazepine treatment and induction of serum lipid abnormalities.

    Long-term treatment with carbamazepine is associated with many metabolic changes, including elevations in serum cholesterol, high-density lipoprotein, low-density lipoprotein, and triglyceride levels. Oxcarbazepine has been reported to be a preferable antiepileptic drug, when compared to carbamazepine with respect to its effects on lipid metabolism, especially cholesterol, high-density lipoproteins, and low-density lipoproteins. The case of a 16-year-old girl who developed high serum cholesterol and low-density lipoprotein levels on both of these medications successively, while triglyceride and high-density lipoprotein levels were unaffected, is reported.
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keywords = lipoprotein
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5/125. leptin deficiency due to lipid apheresis: a possible reason for ravenous hunger and weight gain.

    OBJECTIVE: To investigate how extracorporal cholesterol lowering therapy affects circulating leptin levels in patients with ravenous hunger after treatment and permanent weight gain. DESIGN: A case report. SUBJECT: 51 y old caucasian male patient with moderate chronic renal failure. MEASUREMENTS: serum leptin concentration (RIA, Linco research Inc, St. Louis, MO, USA), total cholesterol, low density lipoprotein cholesterol, blood glucose levels, calorie intake by food records. RESULTS: During treatment total cholesterol was reduced by 50%. serum leptin levels showed a 42% reduction at the end of treatment, that by far exceeds the physiological diurnal variation. Calorie intake was significantly increased on days of treatment. CONCLUSION: We conclude that this artificial reduction in circulating leptin plays an important role in the pathogenesis of ravenous hunger and weight gain under extracorporal cholesterol lowering therapy in this case.
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ranking = 0.20092436549794
keywords = lipoprotein, deficiency
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6/125. diabetic retinopathy and serum lipids.

    The association between serum lipid levels and diabetic retinopathy has been investigated in many studies. Some studies show a positive relationship between serum cholesterol and low-density lipoprotein levels and retinal hard exudation. Other studies show serum triglyceride levels as being important in the progression of retinopathy. Certain other studies show no relationship between serum lipid levels and diabetic retinopathy. We review the literature on this subject and illustrate this report with an example of a diabetic with severe diabetic maculopathy and high serum lipid levels.
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7/125. A clinical feature of hyperlipidemia in patients with central diabetes insipidus.

    In this study, we analyzed plasma lipid and lipoprotein levels before and after treatment with 1-desamino-8-D-arginine vasopressin (DDAVP) in subjects with partial and complete central diabetes insipidus (DI) in order to determine how a shortage and supplement of this hormone affect plasma lipid metabolism. The subjects consisted of 6 patients with partial and 6 with complete central DI. After treatment with DDAVP through nasal cavity, plasma total cholesterol (TC) level did not decrease either in complete or partial form. plasma triglyceride (TG) levels decreased from 306 /-175 mg/dl to 198 /-91 (35% decrease, p=0.027) in complete form, while TG did not change significantly in partial form. A detailed investigation of plasma lipoprotein metabolism during treatment with DDAVP was carried out in 3 of the 6 subjects with complete form of DI. lipoprotein lipase activity and mass in post-heparin plasma from those three subjects tended to increase after treatment with DDAVP, along with the complete disappearance of an unusual lipoprotein between low density lipoprotein (LDL) and very low density lipoprotein (VLDL) as analyzed by polyacrylamide gel electrophoresis. These results suggest that the DDAVP treatment has a favorable effect on lipid and lipoprotein metabolism, especially triglyceride-rich lipoproteins, either directly or through modifying factors contributing to lipid metabolism.
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ranking = 1.4
keywords = lipoprotein
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8/125. Impressive lipid changes following hypolipidaemic drug administration can unveil subclinical hyperthyroidism.

    It is well known that thyroid hormones modulate lipoprotein metabolism. Thus, the presence of clinical or subclinical hyperthyroidism may influence lipid parameters of dyslipidaemic patients and the efficacy of hypolipidaemic therapy. Here we present a patient with mixed hyperlipidaemia whose impressive improvement of his lipid profile following ciprofibrate administration pointed towards the diagnosis of asymptomatic underlying subclinical hyperthyroidism.
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keywords = lipoprotein
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9/125. Dyslipemia in familial partial lipodystrophy caused by an R482W mutation in the LMNA gene.

    Lipatrophic diabetes, also referred to as familial partial lipodystrophy, is a rare disease that is metabolically characterized by hypertriglyceridemia and insulin resistance. Affected patients typically present with regional loss of body fat and muscular hypertrophic appearance. Variable symptoms may comprise pancreatitis and/or eruptive xanthomas due to severe hypertriglyceridemia, acanthosis nigricans, polycystic ovaria, and carpal tunnel syndrome. Mutations within the LMNA gene on chromosome 1q21.2 were recently reported to result in the phenotype of familial partial lipodystrophy. The genetic trait is autosomal dominant. We identified a family with partial lipodystrophy carrying the R482W (Arg(482)Trp) missense mutation within LMNA. Here we present the lipoprotein characteristics in this family in detail. Clinically, the loss of sc fat and muscular hypertrophy especially of the lower extremities started as early as in childhood. Acanthosis and severe hypertriglyceridemia developed later in life, followed by diabetes. The characterization of the lipoprotein subfractions revealed that affected children present with hyperlipidemia. The presence and severity of hyperlipidemia seem to be influenced by age, apolipoprotein E genotype, and the coexistence of diabetes mellitus. In conclusion, dyslipemia is an early and prominent feature in the presented lipodystrophic family carrying the R482W mutation within LMNA.
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ranking = 0.6
keywords = lipoprotein
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10/125. Enhanced intra-abdominal visceral fat accumulation in patients with Werner's syndrome.

    OBJECTIVE: Studies were made on the abnormality of glucose and lipid metabolism and its cause in four patients with Werner's syndrome to infer the reason for accelerated atherogenesis in this syndrome. RESULTS: Of these four patients, hypercholesterolemia was found in three, hypertriglyceridemia in four, hypoalphalipoproteinemia in two and hypertension in two. All the patients had insulin-resistant diabetes mellitus and three of them had apparent hyperinsulinemia. Abdominal computed tomography revealed that all of them had visceral fat obesity, namely augumented intra-abdominal adipose tissue. CONCLUSION: The clinical features of these patients resemble those recently designated as insulin resistant syndrome (syndrome X) or visceral fat syndrome. The metabolic abnormality may be one of important factors in the accelerated atherogenesis in this syndrome.
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ranking = 0.2
keywords = lipoprotein
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