Type III hyperlipoproteinemia with xanthomas and multiple myeloma

Burnside, Nancy J.; Alberta, Lauren; Robinson‐Bostom, Leslie; Bostom, Andrew G.

doi:10.1016/j.jaad.2005.04.009

Cited by 24 publications

(9 citation statements)

References 18 publications

(12 reference statements)

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“…However, hyperlipidemia may also occur. A case of type III hyperlipoproteinemia with xanthomas has been reported in a patient with multiple myeloma (MM) [21]. Furthermore, severe secondary hypercholesterolemia due to cholestasis in a patient who had obstructive jaundice as the initial presentation of non-Hodgkin's lymphoma (NHL) has been reported [22].…”

Section: Pseudohyponatremiamentioning

confidence: 99%

Hyponatremia in Patients with Hematologic Diseases

Koumpis

Florentin

Hatzimichael

et al. 2020

JCM

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Hyponatremia is the most common electrolyte disorder in clinical practice and is associated with increased morbidity and mortality. It is frequently encountered in hematologic patients with either benign or malignant diseases. Several underlying mechanisms, such as hypovolemia, infections, toxins, renal, endocrine, cardiac, and liver disorders, as well as the use of certain drugs appear to be involved in the development or the persistence of hyponatremia. This review describes the pathophysiology of hyponatremia and discusses thoroughly the contributing factors and mechanisms that may be encountered specifically in patients with hematologic disorders. The involvement of the syndrome of inappropriate antidiuretic hormone (SIADH) secretion and renal salt wasting syndrome (RSWS) in the development of hyponatremia in such patients, as well as their differential diagnosis and management, are also presented. Furthermore, the distinction between true hyponatremia and pseudohyponatremia is explained. Finally, a practical algorithm for the evaluation of hyponatremia in hematologic patients, as well as the principles of hyponatremia management, are included in this review.

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Section: Pseudohyponatremiamentioning

confidence: 99%

Hyponatremia in Patients with Hematologic Diseases

Koumpis

Florentin

Hatzimichael

et al. 2020

JCM

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“…Such antibodies have been reported in multiple myeloma, but not yet in patients with auto-immune diseases. Burnside 42 reported the case of a 72-year-old man with an IgA myeloma who developed dysbetalipoproteinaemia on the background of an apoE 2/3 genotype. Immunostaining showed that the monoclonal IgA antibody was complexed to VLDL.…”

Section: Pathogenesis Of Dysbetalipoproteinaemiamentioning

confidence: 99%

Dysbetalipoproteinaemia: A mixed hyperlipidaemia of remnant lipoproteins due to mutations in apolipoprotein E

Marais

Solomon

Blom

2014

Critical Reviews in Clinical Laboratory Sciences

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Atherosclerosis is strongly associated with dyslipoproteinaemia, and especially with increasing concentrations of low-density lipoprotein and decreasing concentrations of high-density lipoproteins. Its association with increasing concentrations of plasma triglyceride is less clear but, within the mixed hyperlipidaemias, dysbetalipoproteinaemia (Fredrickson type III hyperlipidaemia) has been identified as a very atherogenic entity associated with both premature ischaemic heart disease and peripheral arterial disease. Dysbetalipoproteinaemia is characterized by the accumulation of remnants of chylomicrons and of very low-density lipoproteins. The onset occurs after childhood and usually requires an additional metabolic stressor. In women, onset is typically delayed until menopause. Clinical manifestations may vary from no physical signs to severe cutaneous and tendinous xanthomata, atherosclerosis of coronary and peripheral arteries, and pancreatitis when severe hypertriglyceridaemia is present. Rarely, mutations in apolipoprotein E are associated with lipoprotein glomerulopathy, a condition characterized by progressive proteinuria and renal failure with varying degrees of plasma remnant accumulation. Interestingly, predisposing genetic causes paradoxically result in lower than average cholesterol concentration for most affected persons, but severe dyslipidaemia develops in a minority of patients. The disorder stems from dysfunctional apolipoprotein E in which mutations result in impaired binding to low-density lipoprotein (LDL) receptors and/or heparin sulphate proteoglycans. Apolipoprotein E deficiency may cause a similar phenotype. Making a diagnosis of dysbetalipoproteinaemia aids in assessing cardiovascular risk correctly and allows for genetic counseling. However, the diagnostic work-up may present some challenges. Diagnosis of dysbetalipoproteinaemia should be considered in mixed hyperlipidaemias for which the apolipoprotein B concentration is relatively low in relation to the total cholesterol concentration or when there is significant disparity between the calculated LDL and directly measured LDL cholesterol concentrations. Genetic tests are informative in predicting the risk of developing the disease phenotype and are diagnostic only in the context of hyperlipidaemia. Specialised lipoprotein studies in reference laboratory centres can also assist in diagnosis. Fibrates and statins, or even combination treatment, may be required to control the dyslipidaemia.

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“…Om lipidseinkande medikasjon åleine ville hatt saerleg effekt hjå henne er usikkert, då det er rapportert om behandlingsresistens for lipidsenkande medikasjon ved denne tilstanden (7). Ho starta med cellegift kort tid etter at diagnosen myelomatose vart stilt, og totalkolesterol-og triglyseridnivå fell parallelt med reduksjonen i den monoklonale komponenten.…”

Section: Diskusjonunclassified

“…Dette kunne tyde på at hyperlipidemien skuldast manglande opptak av triglyseridrike lipoprotein i levra. Monoklonalt immunglobulin kan via binding til lipoproteinpartiklar hindre binding til reseptor på levercellene (7,15). Alternativt kan ein tenkje seg at antistoffa kan binde seg til reseptoren på levercellene og blokkere denne.…”

Section: Diskusjonunclassified