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Xantomas eruptivos: A propósito de dos casos familiares Eruptive xanthomas: Two familial clinical cases
M V Guardati,M G Díaz,E Carbó Amoroso,M A Reyes
Revista Argentina de Dermatología , 2008,
Abstract: Se presentan dos pacientes de sexo masculino, familiares de primer grado, tabaquistas y etilistas severos, sin antecedentes patológicos conocidos. Ambos presentan en forma eruptiva la aparición de xantomas y uno de ellos una pancreatitis necrohemorrágica atribuida a su hipertrigliceridemia, complicación muy grave de este trastorno. Si bien los xantomas eruptivos no son muy frecuentes de observar, deben hacernos sospechar en una dislipidemia severa, confirmándola con una examen de laboratorio que pondrá de manifiesto una elevación significativa de los triglicéridos y frecuentemente alteración de los niveles de glucosa en sangre. Además, el estudio histopatológico de las lesiones mostrará macrófagos cargados de lípidos, de aspecto espumoso e infiltrado polimorfonuclear y mononuclear en dermis. We report a case of two male patients, first-grade relatives, who are heavy drinkers and smokers but apparently have no pathological records. Both show eruptive xanthomas and one of them presents acute necrotic and hemorrhagic pancreatitis due to hypertriglyceridemia, a serious complication of this disorder. Despite the fact that eruptive xanthomas are not frequently observed, they should make us suspect an instance of severe dyslipidemia. In order to verify it, a laboratory test will show a dramatic raise of serum triglyceride levels and usual changes in the blood glucose levels. Moreover, a histopathologic study of the lesion will reveal macrophages full of lipids (foam cells) with polymorphonuclear and mononuclear infiltrate.
Xantomas eruptivos: A propósito de dos casos familiares
Guardati,M V; Díaz,M G; Carbó Amoroso,E; Reyes,M A; Weidmann,J; Parry,F; Iribas,J L;
Revista argentina de dermatolog?-a , 2008,
Abstract: we report a case of two male patients, first-grade relatives, who are heavy drinkers and smokers but apparently have no pathological records. both show eruptive xanthomas and one of them presents acute necrotic and hemorrhagic pancreatitis due to hypertriglyceridemia, a serious complication of this disorder. despite the fact that eruptive xanthomas are not frequently observed, they should make us suspect an instance of severe dyslipidemia. in order to verify it, a laboratory test will show a dramatic raise of serum triglyceride levels and usual changes in the blood glucose levels. moreover, a histopathologic study of the lesion will reveal macrophages full of lipids (foam cells) with polymorphonuclear and mononuclear infiltrate.
Moderate Hypertriglyceridemia Revealed by Acute Chest Syndrome, a Milky Appearance Serum and Prior History of Recurrent Acute Pancreatitis in a Type 2 Diabetes Black Patient: A Case Report  [PDF]
Fran?ois Bompeka Lepira, Vita Eulethère Kintoki, Jean-Robert Risassi Makulo, Fabien Mbala Kintoki
World Journal of Cardiovascular Diseases (WJCD) , 2016, DOI: 10.4236/wjcd.2016.611046
Abstract: Although the “triglyceride paradox” states that hypertriglyceridemia is less frequent in Blacks and the risk of pancreatitis increases with severe hypertriglyceridemia, we herein report on a case of moderate hypertriglyceridemia revealed by an acute chest syndrome and a milky appearance serum in a 47-year-old type 2 diabetes black patient with prior history of recurrent acute pancreatitis. In addition to insulin therapy and coronary angioplasty, the combination of a statin and a fibrate resulted two months later in a substantial improvement in triglyceride levels and a normal serum appearance.
An Acute Edematous Pancreatitis Case caused by Probably Hypertriglyceridemia: Case Report
Ertugrul Kayacetin,Ruhusen Kutlu,Ayse Demir
TAF Preventive Medicine Bulletin , 2010,
Abstract: Hypertriglyceridemia is one of the non-biliary, eluding important causes of acute pancreatitis. Currently, there is no standardized protocol to treat these patients. We presented a case with acute edematous pancreatitis caused by hypertriglyceridemia in this case report. The patient, then, complicated with a pseudocyst in the pancreas and bilateral pleural effusion. We aimed to present this case with acute pancreatitis due to the probable hypertriglyceridemia and to show how one can handle these complications. [TAF Prev Med Bull 2010; 9(3): 263-268]
Incidence of pancreatitis, secondary causes, and treatment of patients referred to a specialty lipid clinic with severe hypertriglyceridemia: a retrospective cohort study
Supna Sandhu, Ahmad Al-Sarraf, Catalin Taraboanta, Jiri Frohlich, Gordon A Francis
Lipids in Health and Disease , 2011, DOI: 10.1186/1476-511x-10-157
Abstract: A retrospective cohort study was conducted on patients presenting non-acutely to the Healthy Heart Program Lipid Clinic at St. Paul's Hospital with a TG level > 20 mM (1772 mg/dl) between 1986 and 2007. Ninety-five patients with TG > 20 mM at the time of referral were identified, in who follow up data was available for 84. Fifteen patients (15.8%), with a mean outpatient TG level of 38.1 mM, had a history of acute pancreatitis. Among 91 additional patients with less severe HTG, none had a history of pancreatitis when TG were between 10 and 20 mM. Among patients with TG > 20 mM on presentation, 8 (8.5%), with a mean TG level of 67.8 mM, exhibited eruptive xanthomata. A diet high in carbohydrates and fats (79%) and obesity (47.6%) were the two most frequent secondary causes of HTG at initial visit. By 2009, among patients with follow up data 53% exhibited either pre-diabetes or overt Type 2 diabetes mellitus. Upon referral only 23 patients (24%) were receiving a fibrate as either monotherapy or part of combination lipid-lowering therapy. Following initial assessment by a lipid specialist this rose to 84%, and remained at 67% at the last follow up visit.These results suggest hypertriglyceridemia is unlikely to be the primary cause of acute pancreatitis unless TG levels are > 20 mM, that dysglycemia, a diet high in carbohydrates and fats, and obesity are the main secondary causes of HTG, and that fibrates are frequently overlooked as the drug of first choice for severe HTG.Hypertriglyceridemia (HTG), classically defined as fasting plasma triacylglycerols (triglycerides, TG) > 2.3 mM or 200 mg/dl, or 1.7 mM (150 mg/dl) in the definition of metabolic syndrome [1], is a common laboratory finding. Severe hypertriglyceridemia, e.g., TG > 20 mM (1772 mg/dl), is much rarer and almost always caused by a combination of inherited and secondary factors [2,3]. Genetic disorders leading to hypertriglyceridemia include familial combined hyperlipidemia, familial hypertriglyceridemia,
Necrotizing Pancreatitis with Hypertriglyceridemia Development Results: A Case Report  [PDF]
?brahim Yetim,Orhan ?zkan,Güven? Diner,Ayd?n Kaplan
Journal of Clinical and Analytical Medicine , 2011, DOI: 10.4328
Abstract: Acute pancreatitis due to hypertriglyceridemia is a relatively rare clinical entity. Acute pancreatic necrosis is a life threatening form of acute pancreatitis in which early recognition and treatment is important. Necrotising pancreatitis should be treated immediately. We presented a case of pancreatic necrosis due to hypert riglyceridemia which required surgical intervention. We performed necrosectomy. After surgery the patient recovered. We presented the case in order to mention necrotising pancreatitis arising from hypertriglyceridemia and requiring surgical exploration.
Lipoprotein lipase activity and mass, apolipoprotein C-II mass and polymorphisms of apolipoproteins E and A5 in subjects with prior acute hypertriglyceridaemic pancreatitis
Inmaculada Coca-Prieto, Pedro Valdivielso, Gunilla Olivecrona, María Ariza, José Rioja, Pilar Font-Ugalde, Carlota García-Arias, Pedro González-Santos
BMC Gastroenterology , 2009, DOI: 10.1186/1471-230x-9-46
Abstract: Twenty-four survivors of acute hypertriglyceridaemic pancreatitis (cases) and 31 patients with severe hypertriglyceridaemia (controls) were included. Clinical and anthropometrical data, chylomicronaemia, lipoprotein profile, postheparin lipoprotein lipase mass and activity, hepatic lipase activity, apolipoprotein C II and CIII mass, apo E and A5 polymorphisms were assessed.Only five cases were found to have LPL mass and activity deficiency, all of them thin and having the first episode in childhood. No cases had apolipoprotein CII deficiency. No significant differences were found between the non-deficient LPL cases and the controls in terms of obesity, diabetes, alcohol consumption, drug therapy, gender distribution, evidence of fasting chylomicronaemia, lipid levels, LPL activity and mass, hepatic lipase activity, CII and CIII mass or apo E polymorphisms. However, the SNP S19W of apo A5 tended to be more prevalent in cases than controls (40% vs. 23%, NS).Primary defects in LPL and C-II are rare in survivors of acute hypertriglyceridaemic pancreatitis; lipase activity measurements should be restricted to those having their first episode during chilhood.Among patients with acute pancreatitis, 1.3 to 3.5% are due to hypertriglyceridaemia, also known as hypertriglyceridaemic pancreatitis [1,2], some times relapsing and being even more severe than lithiasic acute pancreatitis [3]. Acute hypertriglyceridaemic pancreatitis forms part of the Chylomicronaemia Syndrome, defined as the presence of one or more of the typical signs (eruptive xanthomas, lipidaemia retinalis, recurrent abdominal pain or acute pancreatitis) in a patient with plasma triglyceride concentrations >22.58 mmol/L[4].Genetic causes of the syndrome are rare and include deficiency of lipoprotein lipase (LPL), apolipoprotein C-II, and familial inhibitor of LPL. Other genes are also involved in the catabolism of chylomicrons, such as those for apolipoprotein E, apolipoprotein A-V [5] and glycosylphosphatidyli
Plasmapheresis in hypertriglyceridemia-related pancreatitis: a case report  [cached]
Andrea Tampieri,Patrizia Cenni,Claudia Morselli,Tiziano Lenzi
Emergency Care Journal , 2012, DOI: 10.4081/ecj.2012.2.9
Abstract: Hypertriglyceridemia (HTG) is the third most common cause of acute pancreatitis (AP), accounting for up to 7% of cases. The clinical manifestations are similar to those of AP from other causes, but it may be difficult to recognize because of confounding laboratory investigations induced by HTG, such as a falsely normal serum amylase. Prompt recognition is important to provide adequate treatment. The maintenance of blood triglyceride (TG) levels below 500 mg/dl has been shown to accelerate the clinical improvement in patients with hypertriglyceridemic pancreatitis (HTGP). In many cases series apheresis was effective in reducing HTG and an early initiation is likely to be beneficial in order to prevent recurrence of AP and the development of necrotizing pancreatitis. Definitive guidelines for the treatment of HTGP and randomized trials that compare the effectiveness of apheresis with the medical therapy alone are still lacking.
Severe/Extreme Hypertriglyceridemia and LDL Apheretic Treatment: Review of the Literature, Original Findings  [PDF]
Olga Diakoumakou,Georgios Hatzigeorgiou,Nikos Gontoras,Maria Boutsikou,Vana Kolovou,Sophie Mavrogeni,Vassiliki Giannakopoulou,Genovefa D. Kolovou
Cholesterol , 2014, DOI: 10.1155/2014/109263
Abstract: Hypertriglyceridemia (HTG) is a feature of numerous metabolic disorders including dyslipidemias, metabolic syndrome, and diabetes mellitus type 2 and can increase the risk of premature coronary artery disease. HTG may also be due to genetic factors (called primary HTG) and particularly the severe/extreme HTG (SEHTG), which is a usually rare genetic disorder. Even rarer are secondary cases of SEHTG caused by autoimmune disease. This review considers the causes of SEHTG, and their management including treatment with low density lipoprotein apheresis and analyzes the original findings. 1. Introduction A positive correlation between high triglycerides (TGs) concentration and coronary heart disease (CHD) has been established in numerous studies [1–11]. Hypertriglyceridemia (HTG) is prevalent in 18.6% of men and 4.2% of women between 16 and 65 years of age. The Adult Treatment Panel (ATP) III guidelines, published 13 years ago [12], described normal TGs concentration <150?mg/dL (<1.6?mmol/L), borderline-high TGs as 150 to 199?mg/dL (1.6–2.2?mmol/L), high TGs as 200 to 499?mg/dL (2.2–5.6?mmol/L), and very high TGs as >500?mg/dL (>5.6?mmol/L). However, severe/extreme hypertriglyceridemia (SEHTG) should be considered when values are greater than 1,000?mg/dL (11.2?mmol/L) because this places individuals at significant increased risk of pancreatitis. With TG values less than 1,000?mg/dL (5.6?mmol/L) one should be focused on the risk of premature CHD [13]. HTG is a feature of numerous metabolic disorders including dyslipidemias, metabolic syndrome, and diabetes mellitus type 2 (DMT2) and can increase the risk of premature CHD [14, 15]. These metabolic disorders may be caused by interactions between genetic and nongenetic factors since those subjects present usually similar clinical features (android type of obesity, ectopic fat deposition, thin arms and legs, increased waist circumference, upper body obesity, and in case of SEHTG eruptive xanthomas) [16, 17]. Visceral fat is considered to behave as ectopic fat deposition. It accumulates TGs in cases when body fat storage exceeds the capacity of fat stores. Furthermore, subjects with HTG usually present insulin resistance, hepatic steatosis, and DMT2. Thus, all the above can be called “hypertriglyceridemic phenotype.” Additionally, several studies (including ours) showed that postprandial HTG is manifested in subjects with hypertriglyceridemic phenotype [18]. HTG may also be due to genetic factors (called primary HTG) and particularly the SEHTG, which is a usually rare genetic disorder. Even rarer are secondary
Hypertriglyceridemia: An indicator of poor prognosis in acute pancreatitis – A hospital based study  [PDF]
Mosin Mushtaq, Abid H Wani, Faud Sadiq, Mudasir Mushtaq, Sameena Tabassum, Taiba Mudasir
Asian Journal of Medical Sciences , 2014, DOI: 10.3126/ajms.v5i4.9971
Abstract: Background and study aims: Hypertriglyceridemia can be a primary cause for acute pancreatitis or secondary to other factors prior to the increase of lipid levels, or both. The aim of our study was to assess the severity of acute pancreatitis with elevation in serum triglyceride levels and report the outcomes of our series. Patients and methods: One hundred twenty?six patients of acute pancreatitis were admitted within 72 hours of onset of symptoms, out of whom 26 patients were excluded during the course of study due to preexisting comorbidities. 100 patients in the study population were divided into group A having serum triglyceride levels ≥500 mg/dl (n = 30) and group B having <500 mg/dl (n = 70) at the time of admission. Results: The mean age of group A was similar to group B (50.2 ± 17.1 vs 49.26 ± 17.2 years; p = 0.860). Most common etiological factor of acute pancreatitis was found to be gall stones (56%) in both groups. Ranson's score at admission in group A was 2.93 ± 0.22 and in group B it was 1.34 ± 0.99. Mortality below two weeks was noted in (12/30, 40%) of group A and (6/70, 8%) of group B patients, which was statistically significant, (p = 0.015). Conclusions: The final conclusion of this study was that patients of acute pancreatitis with elevated triglyceride levels form a morbid group and these should be monitored aggressively for the development of any complications. DOI: http://dx.doi.org/10.3126/ajms.v5i4.9971 Asian Journal of Medical Sciences 2014 Vol.5(4); 21-24
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