Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-six patients with xanthomatosis and elevated very low density lipoproteins (VLDL) levels (in different types of hyperlipoproteinaemia) were classified on the basis of the WHO criteria and the cholesterol/triglyceride ratio in VLDL. A large majority (31/46) of the patients referred to the Department of Dermatology could be classified as hyperlipoproteinaemia type III, only 8/46 as type IIB and 7/46 as type IV/V. This distinction seems to be relevant as the xanthomatous lesions differed distinctly between these three types of hyperlipoproteinaemia. Xanthochromia striata palmaris was present in 29/31 cases of hyperlipoproteinaemia type III and was not found in type IV/V patients, who had distinctive papuloeruptive xanthomas. During a follow-up in 35/46 patients all xanthomas disappeared within 2 years except the xanthelasma palpebrarum and tendinous xanthomas. All type IV/V patients (7/7) but only one type III patient (1/31) had abnormal glucose tolerance. Only 2/18 type III patients less than 45 years showed claudication and none of the young type III patients had angina pectoris. In contrast, all four type IIB patients less than 45 years had clinical signs of atherosclerosis. However, angina pectoris and/or claudication were present in 5/13 type III patients over 45 years old. The mean serum cholesterol level was equally elevated in both groups but the cholesterol was mainly present in VLDL in type III and in low density lipoproteins (LDL) in type IIB. In 9/31 type III patients the LDL level was also elevated but was easily normalized by a diet low in carbohydrate, whereas the elevated LDL level in type IIB was therapy-resistant. The recognition of xanthomatous lesions, specifically xanthochromia striata palmaris, as an early sign of type III hyperlipoproteinaemia, can lead to the early diagnosis and successful treatment of these patients, and thus possibly prevent the development of premature atherosclerosis.
Br J Dermatol 1979 Jun
PMID:Xanthomatosis and other clinical findings in patients with elevated levels of very low density lipoproteins. 22 20

We present a normolipaemic young man with extensive facial plane xanthomas and xanthelasmas with a high level of lipoprotein(a) and possibly increased vascular permeability. These associations are of potential importance in understanding the pathogenesis of xanthoma formation and in the identification of patients at risk from coronary atherosclerosis.
Clin Exp Dermatol 1992 May
PMID:Normolipaemic plane xanthomas: an association with increased vascular permeability and serum lipoprotein(a) concentration. 145 6

The concern about long-term toxicity of oral synthetic retinoids has developed because many patients, especially those with genodermatoses, require lifelong therapy. Several organ systems are at risk, especially the hepatic, skeletal, and cardiovascular systems. Although acute hepatotoxicity is a rare side effect of etretinate and acitretin therapy, prospective studies have not demonstrated chronic liver toxicity. The frequency of bone changes induced by retinoids is difficult to estimate, because this adverse effect is usually asymptomatic and requires x-ray or scintigraphic examination for detection. Atherosclerosis develops in many patients who receive long-term retinoid therapy, but the extent to which the process is aggravated by drug-induced hyperlipidemia is not known. Many patients have now been treated with either etretinate or isotretinoin continuously for as many as 15 years and have not developed any signs of severe chronic toxicity. However, continued intense surveillance is recommended for patients expected to require lifelong therapy.
J Am Acad Dermatol 1992 Dec
PMID:Long-term safety of retinoid therapy. 146 Jan 22

Solar radiation provokes a lifelong series of destructive changes in the supporting elastic tissues of "exposed" skin. Called actinic elastosis/lysis (or actinic "aging"), the sequence begins in early life as simple elastic hyperplasia, converts in middle life to progressive actinic elastotic degeneration, and, in late life, typically ends with a stage of resorption (elastolysis) and atrophy ("aged" skin). Superficial "exposed" arteries such as the temporal artery participate in the same sequence of degenerative elastotic changes, which, as in the skin, may provoke granulomatous responses in a few of the many subjects affected. In the case of the temporal artery, a contingent outcome may be giant cell (temporal) arteritis and its recognized systemic vascular expression, polymyalgia rheumatica. Actinic commotion at the surface of the body is often massive in degree and extent and may be expected to exert a deleterious autoimmune impact on the essential elastic tissues of the arterial system. For this reason, solar radiation should be recognized as a risk factor for other elastic-related vascular diseases, including atherosclerosis and aneurysms. Man-made radiations may be exacerbating the effects of predominant solar radiation. Of the many radiant bands that make up the actinic (electromagnetic) spectrum, little is known for certain about the identity of those that cause these prevalent disorders of elastic tissue. Until this void is filled, more care should be taken with solar and the other "safe" radiations.
J Am Acad Dermatol 1991 May
PMID:A study of elastic tissue and actinic radiation in "aging," temporal arteritis, polymyalgia rheumatica, and atherosclerosis. The actinic storm in the modern world. 186 51

The contribution of a craniocerebral injury (CCI) to the clinical picture of psoriasis in 53 invalids of the Great Patriotic War is discussed. In remote periods after CCI the patients with psoriasis develop disorders of the adaptation and trophic function of the nervous system associated with metabolism impairments and early atherosclerosis. The diversity of clinical symptoms because of a number of concomitant diseases favors the development of grave clinical manifestations of the dermatosis, which fact calls for more thorough examinations of this patient population, for a differentiated approach to the choice of optimal therapy, and for active prophylactic check-ups.
Vestn Dermatol Venerol 1989
PMID:[Characteristics of the course of psoriasis in World War II disabled veterans with a history of craniocerebral trauma]. 253 13

A 33-year-old female has developed Werner's syndrome. The prognosis of the condition is unfavourable because of early symptoms of diabetes and atherosclerosis.
Vestn Dermatol Venerol 1989
PMID:[Werner's syndrome]. 261 73

Much has been learned in the past two decades about the impact of omega-3 fatty acids on human biology. These distinctive fatty acids are derived principally from marine sources such as fish and fish oil. They are rapidly incorporated into cell membranes after their ingestion in the diet and subsequently may alter a myriad of cellular functions. For example, eicosapentaenoic acid and docosahexaenoic acid may inhibit the synthesis of several prostaglandins and leukotrienes, as well as reduce the cellular production of cytokines or growth factors such as interleukin-1 or platelet-derived growth factor. Some of these functional changes found after fish-oil ingestion may have therapeutic implications in the treatment of human disease. Studies are now underway to investigate the effect of fish-oil preparations or more-purified omega-3 fatty acids on arterial injury, thrombosis or atherosclerosis, as well as to study their effects in certain inflammatory or cutaneous disorders, such as psoriasis. This paper will review the current body of research on marine oils and will focus specifically on the effects of omega-3 fatty acids in vascular biology and associated disease states. The potential toxicity of these fatty acids will be discussed, as well as current indications (or lack of them) for their therapeutic use in humans.
J Invest Dermatol 1989 Aug
PMID:The vascular effects of omega-3 fatty acids. 266 16

Many patients with lipoprotein disorders are at increased risk for the development of premature atherosclerosis and, less commonly, other disorders that cause systemic morbidity. In some of these patients, xanthomas also develop and provide cutaneous markers for the lipoprotein disorder. As advances in molecular biology refine our understanding of lipoprotein metabolism, it has become increasingly clear that several types of xanthomas are associated with specific disease states. This article presents a differential diagnosis of xanthomas that incorporates contemporary thinking about lipoprotein disorders and focuses on the relationship between abnormalities in lipoprotein metabolism, content, or structure and the development of specific xanthomas.
J Am Acad Dermatol 1988 Jul
PMID:Dermal, subcutaneous, and tendon xanthomas: diagnostic markers for specific lipoprotein disorders. 304 20

We describe five patients aged 50 years or above who had severe atherosclerosis and necrotizing vasculitis. The vasculitis was seen in the small vessels of four patients and in the medium-sized vessels of one. All five patients had multiple necrotic ulcerative skin lesions, and two underwent amputation. Our cases suggest that the relationship between the two disorders changes and exacerbates the clinical and pathological expression of each disease.
Br J Dermatol 1988 Sep
PMID:Necrotizing vasculitis and atherosclerosis. 196 35

The ability to recognize diverse clinical forms of xanthomas, such as tuberous, planar, eruptive and tendinous, is important in the detection of underlying systemic disease. A variety of primary genetic disorders, as well as numerous secondary conditions such as diabetes, obstructive liver disease, thyroid disease, renal disease, and pancreatitis, can lead to hyperlipoproteinemia that results in the formation not only of xanthomas but also of life-threatening vascular atherosclerosis. An understanding of the pathogenesis of the underlying lipoprotein alterations provides a rational approach to therapy utilizing dietary manipulations and drugs. Such treatment is capable of correcting most disorders of lipid metabolism, and, if appropriate therapy is initiated at the first sign of xanthoma evolution, it may prevent progression of atherosclerosis, provide resolution of xanthomas, and in some instances prevent serious pancreatitis.
J Am Acad Dermatol 1985 Jul
PMID:Xanthomas and hyperlipidemias. 403 Nov 42


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