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Journal articles on the topic 'Hyperlipoproteinaemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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1

Sniderman, Allan D., Jean-Charles Hogue, Jean Bergeron, Claude Gagné, and Patrick Couture. "Non-HDL cholesterol and apoB in dyslipidaemia." Clinical Science 114, no. 2 (December 11, 2007): 149–55. http://dx.doi.org/10.1042/cs20070265.

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On the basis of a high correlation, non-HDL-C (non-high-density lipoprotein cholesterol) and apoB (apolipoprotein B) have been suggested to be of equivalent value for clinical practice; however, the strength of this relationship has not been examined in detail in patients with dyslipidaemia. The present study examines the variance of non-HDL-C compared with apoB in 1771 consecutive patients evaluated in a lipid clinic. These patients were divided into normolipidaemic subjects (n=407), type I hyperlipoproteinaemia (n=16), type IIa (n=736) and IIb (n=231) hyperlipoproteinaemia, type III hyperlipoproteinaemia (n=38), type IV hyperlipoproteinaemia (n=509) and type V hyperlipoproteinaemia (n=101). The relationship between non-HDL-C and apoB was examined both in terms of correlation and concordance. Correlation was high, but concordance was only moderate in the normolipidaemic subjects and in those with type IIa and type IIb hyperlipoproteinaemia. Correlation and concordance were both low in the subgroups with type III and type V hyperlipoproteinaemia. In those with type IV hyper-lipoproteinaemia, correlation was moderately high (r=0.74), but concordance was only fair. In conclusion, our results indicate that there is substantial variance of apoB for given values of non-HDL-C in many dyslipidaemic subjects. It follows that correlation is not adequate as a sole judge of equivalence of laboratory parameters.

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2

Crispin, S. M. "Ocular manifestations of hyperlipoproteinaemia." Journal of Small Animal Practice 34, no. 10 (October 1993): 500–506. http://dx.doi.org/10.1111/j.1748-5827.1993.tb03522.x.

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3

Jiao, S., K. Kameda, Y. Matsuzawa, and S. Tarui. "Hyperlipoproteinaemia in primary gout: hyperlipoproteinaemic phenotype and influence of alcohol intake and obesity in Japan." Annals of the Rheumatic Diseases 45, no. 4 (April 1, 1986): 308–13. http://dx.doi.org/10.1136/ard.45.4.308.

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4

Thompson, G. N., A. J. Knight, I. H. Craig, and J. L. Bresson. "Type V hyperlipoproteinaemia in neonates." Archives of Disease in Childhood 62, no. 9 (September 1, 1987): 967–69. http://dx.doi.org/10.1136/adc.62.9.967.

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5

Crispin, Sheila. "Ocular lipid deposition and hyperlipoproteinaemia." Progress in Retinal and Eye Research 21, no. 2 (March 2002): 169–224. http://dx.doi.org/10.1016/s1350-9462(02)00004-6.

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6

&NA;. "Simvastatin or gemfibrozil for combined hyperlipoproteinaemia?" Inpharma Weekly &NA;, no. 1087 (May 1997): 15. http://dx.doi.org/10.2165/00128413-199710870-00034.

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7

GILLETT, MICHAEL P. T., MOHAMMED S. LAKHANI, and GUY NATION. "Spontaneous hyperlipoproteinaemia in the Arabian dromedary." Biochemical Society Transactions 23, no. 2 (May 1, 1995): 281S. http://dx.doi.org/10.1042/bst023281s.

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8

&NA;. "Pravastatin has therapeutic potential in hyperlipoproteinaemia." Inpharma Weekly &NA;, no. 758 (October 1990): 17. http://dx.doi.org/10.2165/00128413-199007580-00045.

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9

Gaw, Allan, and Dzifa Wosornu. "Simvastatin during warfarin therapy in hyperlipoproteinaemia." Lancet 340, no. 8825 (October 1992): 979–80. http://dx.doi.org/10.1016/0140-6736(92)92872-d.

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10

CARELESS, D. J., M. G. COHEN, and F. LEPRE. "Mosculoskeletal Complaints in Patients with Hyperlipoproteinaemia." Rheumatology 34, no. 4 (1995): 393–94. http://dx.doi.org/10.1093/rheumatology/34.4.393.

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11

Vogt, Anja. "Hyperlipoproteinaemia(a) – apheresis and emerging therapies." Clinical Research in Cardiology Supplements 12, S1 (February 9, 2017): 12–17. http://dx.doi.org/10.1007/s11789-017-0083-2.

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12

Bogner, U., H.-R. Arntz, H. Peters, and H. Schleusener. "Subclinical hypothyroidism and hyperlipoproteinaemia: indiscriminate L-thyroxine treatment not justified." Acta Endocrinologica 128, no. 3 (March 1993): 202–6. http://dx.doi.org/10.1530/acta.0.1280202.

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It is still under discussion whether subclinical hypothyroidism is a biochemical syndrome or a disease associated with an increased risk for development of vascular diseases due to lipid elevation. Therefore, we investigated lipid values in 40 patients with subclinical hypothyroidism, which is defined in terms of normal (N =26) or slightly increased (N= 14) basal TSH values and/or an exaggerated TSH response (N=34) to TRH (>25 mU/l). Patients with increased lipid values were treated with L-thyroxine and reanalysed three months later. Mean levels of total cholesterol, LDL- and HDL-cholesterol and triglycerides in patients with subclinical hypothyroidism were comparable with those in normal subjects. Individual analysis, however, revealed hyperlipoproteinaemia (HL) in 22.5% of the patients investigated (HL type Ila in seven, type IV in two patients). Thyroid function was the same in affected patients as in those with normal lipid values, whereas higher age was significantly more often associated with this syndrome (p <0.01). Treatment with L-thyroxine resulted in a significant decrease in total and LDL-cholesterol (p<0.05), although a normalization of their lipid values could be obtained only in half of the patients. None of the subjects with hyperlipoproteinaemia had a history or clinical signs of actual vascular disease. Although the incidence of hyperlipoproteinaemia in our study group of patients with mild subclinical hypothyroidism (22.5%) is comparable to that of the normal population (21.5%), it is more severe in the former group (LDL-cholesterol in patients 5.26±0.58 vs 4.8±0.56 mmol/l in controls: p<0.05). Formally, approximately half of the patients with this syndrome benefit from L-thyroxine treatment with a normalization of their total and LDL-cholesterol. In the remaining patients with hyperlipoproteinaemia, elevated lipid levels do not seem to be associated with borderline thyroid dysfunction. We conclude that indiscriminate L-thyroxine treatment is not justified in subclinical hypothyroidism.

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13

Umeki, S., Y. Niki, and R. Soejima. "Sarcoidosis and acquired type II-b hyperlipoproteinaemia." European Respiratory Journal 1, no. 6 (June 1, 1988): 558–59. http://dx.doi.org/10.1183/09031936.93.01060558.

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In four of eleven patients with histologically-proven sarcoidosis (stage II or III), type II-b hyperlipoproteinaemia (HLP) with increased levels of total cholesterol, triglycerides and low density lipoprotein, and a decreased level of high density lipoprotein was observed. These results suggest that type II-b HLP may be associated with sarcoidosis with systemic sarcoid infiltration (stage II or III).

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14

&NA;. "Combination therapy needed for type III hyperlipoproteinaemia." Inpharma Weekly &NA;, no. 1202 (August 1999): 11. http://dx.doi.org/10.2165/00128413-199912020-00022.

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15

KUTTY, K. MADHAVAN, VARAGUR M. PRABHAKARAN, and RONALD H. PAYNE. "Relationship between pseudocholinesterase and lipids in hyperlipoproteinaemia." Biochemical Society Transactions 15, no. 3 (June 1, 1987): 421–22. http://dx.doi.org/10.1042/bst0150421.

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16

Crispin, Sheila. "Erratum to “Ocular lipid deposition and hyperlipoproteinaemia”." Progress in Retinal and Eye Research 22, no. 4 (July 2003): 563–64. http://dx.doi.org/10.1016/s1350-9462(03)00037-5.

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17

Pasquale, M., A. Bruzzese, V. Bruzzese, and F. Nasso. "[75] HYPERLIPOPROTEINAEMIA TYPE III, A DIFFICULT DIAGNOSIS." Nutrition, Metabolism and Cardiovascular Diseases 19 (November 2009): S19. http://dx.doi.org/10.1016/s0939-4753(09)70076-6.

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18

Carr, D., H. M. Thornes, A. C. Rutter, R. D. Finney, and P. R. Turner. "Sheehan's syndrome presenting with type III hyperlipoproteinaemia." Postgraduate Medical Journal 63, no. 746 (December 1, 1987): 1099–100. http://dx.doi.org/10.1136/pgmj.63.746.1099.

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19

Schmidt, Hartmut H.-J., Georg Behrens, Janine Genschel, Matthias Stoll, André Dejam, Regina Haas, Michael P. Manns, and Reinhold E. Schmidt. "Lipid Evaluation in HIV-1-Positive Patients Treated with Protease Inhibitors." Antiviral Therapy 4, no. 3 (April 1, 1998): 163–70. http://dx.doi.org/10.1177/135965359900400305.

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There is accumulating evidence that human immunodeficiency virus type 1 (HIV-1) protease inhibitors (PIs) can induce hyperlipidaemia. To evaluate the frequency and type of hyperlipidaemia in PI-treated patients, 98 outpatients were prospectively analysed for their lipoprotein characteristics at the Medizinische Hochschule in Hannover, Germany. Fifty-seven percent of the patients studied presented with hyperlipidaemia. Both hypertrigylceridaemia (type IV and V hyperlipoproteinaemia, 33%) and hypercholesterolaemia (type IIa hyperlipoproteinaemia, 6%) were detectable. The remaining 18% had a type IIb hyperlipoproteinaemia. Increased lipid levels were highly statistically significant compared to a control group of PI-naive HIV-1-infected patients [low-density lipoprotein (LDL) 146 mg/dl (range, 53–274 mg/dl) versus 105 mg/dl (range, 22–188 mg/dl; P=0.0006); very-low-density lipoprotein (VLDL) 35.5 mg/dl (5–253 mg/dl) versus 18 mg/dl (range, 3–94 mg/dl; P=0.0002)]. All PIs used (saquinavir, indinavir, nelfinavir and ritonavir) were associated with this variable form of hyperlipidaemia according to the Fredrickson classification. There was no significant correlation of any determined lipid value with the duration of treatment. A higher frequency of the apolipoprotein E2 allele and E4 allele was observed in the hyperlipidaemic subjects. Patients with excessive hypertriglyceridaemia showed a reduced lipoprotein lipase activity. Lipodystrophy was observed especially in hyperlipidaemic patients and to a lesser extent in normolipidaemic subjects. The frequency of hyperlipidaemic risk factors was surprisingly high in the group studied, which in turn may explain the proposed increased risk of atherogenesis in HIV-1 PI-treated patients. Therefore, PI-treated subjects should also be evaluated for their lipoprotein pattern, which may require antihyperlipidaemic interventions.

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20

&NA;. "Long-term fenofibrate + ezetimibe in type V hyperlipoproteinaemia." Inpharma Weekly &NA;, no. 1537 (May 2006): 14. http://dx.doi.org/10.2165/00128413-200615370-00035.

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21

JONES, B. R., A. C. JOHNSTONE, and W. S. HANCOCK. "Tyzzer's disease in kittens with familial primary hyperlipoproteinaemia." Journal of Small Animal Practice 26, no. 7 (July 1985): 411–19. http://dx.doi.org/10.1111/j.1748-5827.1985.tb02217.x.

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22

Dallongeville, Jean. "Apolipoprotein E mutations, type V hyperlipoproteinaemia and diet." British Journal of Nutrition 83, no. 6 (June 2000): 573–74. http://dx.doi.org/10.1017/s0007114500000738.

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23

Johnstone, A. C., B. R. Jones, J. C. Thompson, and W. S. Hancock. "The pathology of an inherited hyperlipoproteinaemia of cats." Journal of Comparative Pathology 102, no. 2 (February 1990): 125–37. http://dx.doi.org/10.1016/s0021-9975(08)80118-1.

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24

François, J., F. Lentini, P. Hose, and R. Rottiers. "Genetic study of hyperlipoproteinaemia types IV and V." Clinical Genetics 12, no. 4 (April 23, 2008): 202–7. http://dx.doi.org/10.1111/j.1399-0004.1977.tb00927.x.

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25

Bröijersén, Anders, Anders Hamsten, Angela Silveira, Kamaran Fatah, Alison H. Goodall, Sabina Eriksson, Bo Angelin, and Paul Hjemdahl. "Gemfibrozil Reduces Thrombin Generation in Patients with Combined Hyperlipidaemia, without Influencing Plasma Fibrinogen, Fibrin Gel Structure or Coagulation Factor VII." Thrombosis and Haemostasis 76, no. 02 (1996): 171–76. http://dx.doi.org/10.1055/s-0038-1650548.

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SummaryA double-blind, placebo-controlled, cross-over study was conducted in 21 men with combined hyperlipoproteinaemia to examine if lipid-lowering treatment with gemfibrozil (10-12 weeks) affects blood coagulation and fibrin gel structure at rest or during mental stress. Gemfibrozil lowered plasma triglycerides by 57 ± 4%, whereas high density lipoprotein (HDL) cholesterol increased by 22 ± 5%. Gemfibrozil lowered the triglyceride content of low density lipoprotein (LDL). Gemfibrozil reduced the plasma concentrations of thrombin-antithrombin complex (TAT) and prothrombin fragment F1+2 (F1+2), both at rest and during mental stress. However, there were no effects of gemfibrozil treatment on the plasma concentrations of fibrinogen, factor VII antigen, activated factor VII (Vila) or activated factor XII (XIIa), or on fibrin gel structure. Acute mental stress per se did not influence coagulation factors, reaction products or fibrin gel structure, or their responses to the study drug. Thus, gemfibrozil reduces thrombin generation in men with combined hyperlipoproteinaemia, without influencing the plasma levels of fibrinogen, Vila and XIIa, or fibrin gel structure. Attenuation of thrombin generation may contribute to the primary-preventive effects of gemfibrozil on coronary heart disease.

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26

Yuan, Yvonne V., David D. Kitts, and David V. Godin. "Interactive effects of increased intake of saturated fat and cholesterol on atherosclerosis in the Japanese quail (Coturnix japonica)." British Journal of Nutrition 80, no. 1 (July 1998): 89–100. http://dx.doi.org/10.1017/s0007114598001810.

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Increasing the energy value of diets with dietary fat, particularly fats rich in saturated fatty acids, can result in the elevation of plasma total and lipoprotein cholesterol. In the present study, experimental diets were designed to examine the effects of increasing the energy content of diets with a saturated fat source and cholesterol in a non-purified diet on hyperlipoproteinaemia and aortic plaque composition in the atherosclerosis-susceptible Japanese quail (Coturnix japonica) model of human atherosclerosis. Commercial poultry diets containing two levels (i.e. 60 or 120 g/kg) of beef tallow as the primary source of saturated fat were balanced for endogenous cholesterol or supplemented with cholesterol (i.e. 0·5 or 5·0 g/kg) and fed to quail for 9 weeks to examine the effects on whole plasma, lipoprotein and aortic plaque lipid composition in relation to aortic plaque formation. Hypercholesterolaemia (P<0·001) was confirmed in birds fed on high-cholesterol (HC) diets only. An interaction (P=0·05) between dietary cholesterol and fat intake level was observed for plasma triacylglycerols (TG) and was specific to changes observed in VLDL composition. Diet-induced changes in lipoprotein total cholesterol, TG and phospholipid composition were greatest in the portomicron and VLDL fractions in birds fed on atherogenic diets. Hyperlipoproteinaemia induced by the 60 g/kg added beef tallow–HC diet resulted in significant (P<0·001) aortic plaque deposition, which was further enhanced in birds fed on the 120 g/kg beef tallow–HC diet. Quail fed on 120 g/kg beef tallow-HC diets exhibited the most severe aortic plaque formation, with marked increases in aortic tissue cholesterol content and quantifiable amounts of several cholesterol oxides (5,6α-epoxy-5α-cholesterol, 7β-hydroxycholesterol, cholestanetriol, 7-ketocholesterol and 25-hydroxycholesterol). In summary, hyperlipoproteinaemia associated with HC diets with a greater proportion of energy from saturated fat produced a combined effect in altering plasma and lipoprotein lipid composition as well as aortic tissue cholesterol and cholesterol oxide content in the Japanese quail.

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27

Miller, George J. "Coronary Heart Disease Prevention in Type II Primary Hyperlipoproteinaemia." Journal of the Royal Society of Medicine 78, no. 3 (March 1985): 262. http://dx.doi.org/10.1177/014107688507800320.

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28

Smud, R., and B. Sermukslis. "Bezafibrate and fenofibrate in Type II diabetics with hyperlipoproteinaemia." Current Medical Research and Opinion 10, no. 9 (January 1987): 612–24. http://dx.doi.org/10.1185/03007998709112415.

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29

RUHN, G., U. ERIKSON, and A. G. OLSSON. "Prevalence of femoral atherosclerosis in asymptomatic men with hyperlipoproteinaemia." Journal of Internal Medicine 225, no. 5 (May 1989): 317–23. http://dx.doi.org/10.1111/j.1365-2796.1989.tb00088.x.

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30

Fung, Michelle, Richard Bebb, and Jiri Frohlich. "Follow-up of type III hyperlipoproteinaemia in a child." Lancet 358, no. 9299 (December 2001): 2171. http://dx.doi.org/10.1016/s0140-6736(01)07205-1.

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31

Zulewski, H., A. R. Miserez, C. C. Sieber, N. Chiodetti, and U. Keller. "Acquired type III hyperlipoproteinaemia in recipient of liver transplant." Lancet 343, no. 8903 (April 1994): 971. http://dx.doi.org/10.1016/s0140-6736(94)90091-4.

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32

Richard, Pascale, Isabelle Beucler, Maria Pascual De Zulueta, Nicolas Biteau, Jean-Luc De Gennes, and Albert Iron. "Compound Heterozygote for Both Rare Apolipoprotein E1(Gly127→Asp, Arg158→Cys) and E3(Cys112 → Arg, Arg251 → Gly) Alleles in a Multigeneration Pedigree with Hyperlipoproteinaemia." Clinical Science 93, no. 1 (July 1, 1997): 89–95. http://dx.doi.org/10.1042/cs0930089.

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1. A French multigeneration pedigree with hyperlipoproteinaemia was investigated for the transmission of the rare apolipoprotein E1(Gly127 → Asp, Arg158 → Cys) variant. The proband, a 46-year-old male carrying the rare apoE1 variant, presented a severe type III hyperlipoproteinaemia like his three brothers and his sister. 2. ApoE phenotyping and genotyping showed a discrepancy in the second allele carried by the proband's wife and two of her children, thus suggesting another apoE gene mutation. Cloning and sequencing of the entire exon 4 demonstrated a point mutation at codon 251, leading to an apoE3(Cys112 → Arg, Arg251 → Gly) allele. The proband's wife was normolipaemic and heterozygous for this rare isoform and the common apoE3 protein. The rare apoE3(Cys112 → Arg, Arg251 → Gly) allele has been transmitted to her two daughters. The first, aged 19, was normolipaemic and heterozygous for this allele and the common apoE2 allele. The second, carrying both the rare isoforms apoE1(Gly127 → Asp, Arg158 → Cys) and apoE3(Cys112 → Arg, Arg251 → Gly), presented a hypertriglyceridaemia at the age of 10. 3. The exploration of apoE status associated with plasma lipid levels and lipoprotein profiles in this three-generation pedigree made it possible to describe a compound heterozygote for two mutated alleles, one mutation being located in the N-terminal domain of the apoE protein and the other arising in the C-terminal domain.

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33

Lerique, Brice, Bruno Moulin, Claude Delpero, Rajsingh Purgus, Michel Olmer, and Jean Boyer. "High-Affinity Interaction of Long-Chain Fatty Acids with Serum Albumin in Nephrotic Syndrome." Clinical Science 89, no. 4 (October 1, 1995): 417–20. http://dx.doi.org/10.1042/cs0890417.

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1. We have examined the effect of hypoalbuminaemia, a hallmark of nephrotic syndrome, on the albumin—fatty acid equilibrium in the plasma of 11 adult patients with nephrosis compared with 12 healthy subjects and six subjects with normoalbuminaemic hyperlipoproteinaemia. 2. We used a dialysis exchange rate method which allows the evaluation in relative terms of the binding affinity of albumin for plasma fatty acid and the fatty acid availability, tentatively equated with the unbound fatty acid fraction. 3. In nephrotic patients, an increase (P < 0.001) in albumin affinity for fatty acid was seen compared with healthy subjects, which was negatively correlated with albuminaemia (r = −0.69, P < 0.02). No change in fatty acid availability was seen for the group as a whole, but individual values showed a wide scatter, with the highest values in four patients with the highest fatty acid-albumin molar ratios. The increase in albumin affinity for fatty acid was specific to nephrotic syndrome since no such effect was seen in subjects with hyperlipoproteinaemia, who only showed a moderate increase (P < 0.01) in fatty acid availability. 4. The increased albumin affinity for fatty acid in nephrotic syndrome supports the hypothesis that an albumin component with lower affinity for fatty acid might filter out through the diseased glomerular membrane and leave the high-affinity albumin in plasma.

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34

Angelin, B., K. Einarsson, B. Leijd, and L. Wallentin. "Plasma cholesterol esterification rate in hyperlipoproteinaemia: Relation to cholesterol elimination." Scandinavian Journal of Clinical and Laboratory Investigation 48, no. 5 (September 1, 1988): 481–87. http://dx.doi.org/10.3109/00365518809085761.

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35

van der Kolk, J. H., and Th Wensing. "Urinary concentration of corticoids in ponies with hyperlipoproteinaemia or hyperadrenocorticism." Veterinary Quarterly 22, no. 1 (January 2000): 55–57. http://dx.doi.org/10.1080/01652176.2000.9695024.

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36

Vermeer, Bert Jan. "Hyperlipoproteinaemia and Xanthomatosis as a Model of Cholesterol Ester Accumulation." Journal of Dermatology 13, no. 1 (February 1986): 2–9. http://dx.doi.org/10.1111/j.1346-8138.1986.tb02892.x.

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37

Kršek, M., R. Češka, A. Hořinek, B. Hořrejši, and V. Weiss. "Type III hyperlipoproteinaemia and primary amenorrhoea associated with severe hypothyroidism." Acta Paediatrica 89, no. 8 (January 2, 2007): 1023–24. http://dx.doi.org/10.1111/j.1651-2227.2000.tb00429.x.

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38

Angelin, B., K. Einarsson, B. Leijd, and L. Wallentin. "Plasma cholesterol esterification rate in hyperlipoproteinaemia: Relation to cholesterol elimination." Scandinavian Journal of Clinical and Laboratory Investigation 48, no. 5 (September 1988): 481–87. http://dx.doi.org/10.1080/00365518809085761.

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39

HAFFNER, S. M., R. S. KUSHWAHA, and W. R. HAZZARD. "Metabolism of chylomicrons in subjects with dysbetalipoproteinaemia (type III hyperlipoproteinaemia)." European Journal of Clinical Investigation 19, no. 5 (October 1989): 486–90. http://dx.doi.org/10.1111/j.1365-2362.1989.tb00264.x.

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40

Wisselink, M. A., J. P. Koeman, Th Wensing, J. de Bruijne, and T. Willemse. "Hyperlipoproteinaemia associated with atherosclerosis and cutaneous xanthomatosis in a cat." Veterinary Quarterly 16, no. 4 (December 1994): 199–202. http://dx.doi.org/10.1080/01652176.1994.9694448.

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41

Lehtonen, A., and J. Viikari. "Effect of Clofibrate and Calcium in Type II A Hyperlipoproteinaemia." Acta Medica Scandinavica 202, no. 1-6 (April 24, 2009): 179–81. http://dx.doi.org/10.1111/j.0954-6820.1977.tb16808.x.

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42

ILLINGWORTH, D. R., W. E. CONNOR, L. F. HATCHER, and W. S. HARRIS. "Hypolipidaemic effects of n-3 fatty acids in primary hyperlipoproteinaemia." Journal of Internal Medicine 225, S731 (December 1989): 91–97. http://dx.doi.org/10.1111/j.1365-2796.1989.tb01441.x.

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43

Groudeva, Janet, Maria G. Kratchanova, Ivan N. Panchev, and C. G. Kratchanova. "Application of granulated apple pectin in the treatment of hyperlipoproteinaemia." Zeitschrift f�r Lebensmitteluntersuchung und -Forschung A 204, no. 5 (May 7, 1997): 374–78. http://dx.doi.org/10.1007/s002170050093.

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44

Olsson, Anders G., P. Dieter Lang, and Joachim Vollmar. "Effect of bezafibrate during 4.5 years of treatment of hyperlipoproteinaemia." Atherosclerosis 55, no. 2 (May 1985): 195–203. http://dx.doi.org/10.1016/0021-9150(85)90098-x.

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45

VERRILLO, A., A. DETERESA, P. CARANDENTEGIARRUSSO, and S. LAROCCA. "Soybean protein diets in the management of type II hyperlipoproteinaemia." Atherosclerosis 54, no. 3 (March 1985): 321–31. http://dx.doi.org/10.1016/0021-9150(85)90125-x.

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46

Rotchford, Alan P., Douglas K. Newman, Anthony T. Moore, Declan W. Flanagan, and Richard Miles. "Lipaemia retinalis in a premature infant with type I hyperlipoproteinaemia." Eye 11, no. 6 (November 1997): 940–41. http://dx.doi.org/10.1038/eye.1997.235.

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47

Mirzaee, S., P. Thein, A. Nasis, and J. Cameron. "Cardiac Manifestations of Type V Hyperlipoproteinaemia: A Lipid Clinic Experience." Heart, Lung and Circulation 27 (2018): S304. http://dx.doi.org/10.1016/j.hlc.2018.06.582.

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48

Meriño-Ibarra, E., J. Puzo, E. Jarauta, A. Cenarro, D. Recalde, Á. L. García-Otín, E. Ros, et al. "Hyperlipoproteinaemia(a) is a common cause of autosomal dominant hypercholesterolaemia." Journal of Inherited Metabolic Disease 30, no. 6 (October 20, 2007): 970–77. http://dx.doi.org/10.1007/s10545-007-0585-z.

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Hoffer, M. J. V., S. Niththyananthan, R. P. Naoumova, L. M. Havekes, and G. R. Thompson. "A novel mutation causing dominant type III hyperlipoproteinaemia: APOEI Hammersmith." Atherosclerosis 115 (June 1995): S4. http://dx.doi.org/10.1016/0021-9150(95)96269-x.

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50

Houlston, R., J. Quiney, G. F. Watts, and B. Lewis. "Gemfibrozil in the Treatment of Resistant Familial Hypercholesterolemia and Type III Hyperlipoproteinaemia." Journal of the Royal Society of Medicine 81, no. 5 (May 1988): 274–76. http://dx.doi.org/10.1177/014107688808100512.

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Abstract:

The efficacy of gemfibrozil in the treatment of resistant familial hypercholesterolaemia and type III hyperlipoproteinaemia was evaluated in 26 individuals over a mean period of 16 months. In the untreated state both disorders are associated with a high frequency of coronary heart disease. In the former, gemfibrozil with a bile acid sequestrant reduced plasma cholesterol by 32%, an incremental decrease of 17% compared with sequestrant therapy alone. In type III, plasma cholesterol was reduced by 40% and plasma triglyceride by 70%, while high-density lipoprotein cholesterol increased by 45%. In none of the patients studied did clinical or biochemical side effects occur.

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