Hypertriglyceridemie se řadí mezi stavy, které mohou vyvolat jednu z nejzávažnějších forem akutní pankreatitidy (AP). S velmi vysokou pravděpodobností hrozí riziko vzniku perzistentního multiorgánového selhání a abdominální katastrofy [1]. Incidence akutních pankreatitid zapříčiněných vlivem hypertriglyceridemie celosvětově stoupá. Vzhledem k nevhodným stravovacím návykům především západní populace, pandemii obezity a nedostatku pohybu lze předpokládat, že se tento trend bude prohlubovat [2]. Výše uvedená příčina tvoří v současnosti v některých populacích až jednu třetinu případů AP. Akutní pankreatitida vzniká typicky při hypertriglyceridemii > 1 000 mg/dl (> 11,3 mmol/l). Přestože není specifická léčba akutní pankreatitidy stále známá, existuje možnost užití intervence v podobě terapeutické plazmaferézy, s jejímž využitím máme na našem pracovišti dlouhodobé zkušenosti.

Hypertriglyceridemia is one of the conditions that can cause one of the most severe forms of acute pancreatitis (AP). There is a very high risk of developing persistent multi-organ failure and abdominal catastrophe [1]. The incidence of acute pancreatitis due to hypertriglyceridemia is increasing worldwide. Given the inappropriate dietary habits of mainly Western populations, the obesity pandemic and lack of exercise, this trend can be expected to intensify [2]. The aforementioned causes currently account for up to one-third of AP cases in some populations. Acute pancreatitis typically develops when hypertriglyceridemia is > 1,000 mg/dl (> 11.3 mmol/l). Although the specific treatment of acute pancreatitis is still unknown, there is a possibility of using an intervention in the form of therapeutic plasmapheresis, with which we have long experience at our department.

• MeSH
• Hypertriglyceridemia * complications   therapy   MeSH
• Humans MeSH
• Pancreatitis * etiology   physiopathology   therapy   MeSH
• Plasmapheresis methods   MeSH
• Risk Factors MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

Následující článek referuje kazuistiku dvaceti devítileté ženy, která byla hospitalizována pro těžké bolesti břicha vzniklé při akutní pankreatitidě (AP). Během prvních diagnostických kroků byla zjištěna extrémně vysoká hladina triacylglycerolů (TAG), nicméně po stabilizaci stavu byla pozorována také narůstající kalcemie vlivem adenomu příštítného tělíska. Oba stavy jsou už samy o sobě vyvolávajícími faktory. Ale který z nich byl zlomový?

The following article presents the case report of a 29-year-old woman who was hospitalized for severe abdominal pain caused by acute pancreatitis (AP). During the first diagnostic steps, an extremely high level of triacylglycerols (TAG) was detected. However, after stabilisation of the condition, increasing calcaemia due to parathyroid adenoma was also observed. Both conditions are precipitating factors in themselves. But which one was the breaking point?

• MeSH
• Pancreatitis, Acute Necrotizing * etiology   therapy   MeSH
• Adult MeSH
• Drainage methods   MeSH
• Endoscopy, Digestive System methods   MeSH
• Hypercalcemia complications   MeSH
• Hypertriglyceridemia complications   MeSH
• Humans MeSH
• Risk Factors MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Female MeSH
• Publication type
• Case Reports MeSH

• MeSH
• Diabetes Mellitus MeSH
• Hypertriglyceridemia * diagnosis   complications   MeSH
• Middle Aged MeSH
• Humans MeSH
• Pancreatitis * diagnosis   etiology   physiopathology   therapy   MeSH
• Aged MeSH
• Treatment Outcome MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Publication type
• Case Reports MeSH

BACKGROUND: Hypertriglyceridemia is the third most common cause of acute pancreatitis (AP). It has been shown that hypertriglyceridemia aggravates the severity and related complications of AP; however, detailed analyses of large cohorts are contradictory. Our aim was to investigate the dose-dependent effect of hypertriglyceridemia on AP. METHODS: AP patients over 18 years old who underwent triglyceride measurement within the initial three days were included into our cohort analysis from a prospective international, multicenter AP registry operated by the Hungarian Pancreatic Study Group. Data on 716 AP cases were analyzed. Six groups were created based on the highest triglyceride level (<1.7 mmol/l, 1.7-2.19 mmol/l, 2.2-5.59 mmol/l, 5.6-11.29 mmol/l, 11.3-22.59 mmol/l, ≥22.6 mmol/l). RESULTS: Hypertriglyceridemia (≥1.7 mmol/l) presented in 30.6% of the patients and was significantly and dose-dependently associated with younger age and male gender. In 7.7% of AP cases, hypertriglyceridemia was considered as a causative etiological factor (≥11.3 mmol/l); however, 43.6% of these cases were associated with other etiologies (alcohol and biliary). Hypertriglyceridemia was significantly and dose-dependently related to obesity and diabetes. The rates of local complications and organ failure and maximum CRP level were significantly and dose-dependently raised by hypertriglyceridemia. Triglyceride above 11.3 mmol/l was linked to a significantly higher incidence of moderately severe AP and longer hospital stay, whereas triglyceride over 22.6 mmol/l was significantly associated with severe AP as well. CONCLUSION: Hypertriglyceridemia dose-dependently aggravates the severity and related complications of AP. Diagnostic workup for hypertriglyceridemia requires better awareness regardless of the etiology of AP.

• MeSH
• Adult MeSH
• Hypertriglyceridemia complications   MeSH
• Internationality MeSH
• Cohort Studies MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Pancreatitis etiology   MeSH
• Prospective Studies MeSH
• Risk Factors MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Multicenter Study MeSH

Introduction: The development of metabolic syndrome-associated renal dysfunction is exacerbated by a number of factors including dyslipidemia, ectopic deposition of lipids and their toxic metabolites, impairment of lipid metabolism, and insulin resistance. Renal dysfunction is also affected by the production of proinflammatory and profibrotic factors secreted from adipose tissue, which can in turn directly impair kidney cells and potentiate insulin resistance. In this study, we investigated the manifestation of renal lipid accumulation and its effect on renal dysfunction in a model of metabolic syndrome-the hereditary hypertriglyceridemic rat (HHTg)-by assessing microalbuminuria and targeted urinary proteomics. Male Wistar control rats and HHTg rats were fed a standard diet and observed over the course of ageing at 3, 12, and 20 months of age. Results: Chronically elevated levels of triglycerides in HHTg rats were associated with increased levels of NEFA during OGTT and over a period of 24 hours (+80%, P < 0.01). HHTg animals exhibited qualitative changes in NEFA fatty acid composition, represented by an increased proportion of saturated fatty acids (P < 0.05) and a decreased proportion of n-3 PUFA (P < 0.01). Ectopic lipid deposition in the kidneys of HHTg rats-triglycerides (+30%) and cholesterol (+10%)-was associated with markedly elevated microalbuminuria as ageing increased, despite the absence of microalbuminuria at the young age of 3 months in these animals. According to targeted proteomic analysis, 3-month-old HHTg rats (in comparison to age-matched controls) exhibited increased urinary secretion of proinflammatory parameters (MCP-1, IL-6, IL-8, P < 0.01) and decreased urinary secretion of epidermal growth factor (EGF, P < 0.01) before manifestation of microalbuminuria. Elevation in the urinary secretion of inflammatory cytokines can be affected by increased relative expression of MCP-1 in the renal cortex (P < 0.05). Conclusions: Our results confirm dyslipidemia and ectopic lipid accumulation to be key contributors in the development of metabolic syndrome-associated renal dysfunction. Assessing urinary secretion of proinflammatory cytokines and epidermal growth factor can help in detecting early development of metabolic syndrome-associated renal dysfunction.

• MeSH
• Albuminuria etiology   urine   MeSH
• Urinalysis MeSH
• Biomarkers blood   urine   MeSH
• Early Diagnosis MeSH
• Time Factors MeSH
• Cytokines urine   MeSH
• Epidermal Growth Factor urine   MeSH
• Hypertriglyceridemia blood   complications   genetics   urine   MeSH
• Lipids blood   MeSH
• Inflammation Mediators urine   MeSH
• Metabolic Syndrome blood   complications   genetics   urine   MeSH
• Disease Models, Animal MeSH
• Kidney Diseases blood   etiology   urine   MeSH
• Rats, Transgenic MeSH
• Rats, Wistar MeSH
• Predictive Value of Tests MeSH
• Proteomics * MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

The risk of development of metabolic syndrome can be increased by hypertriglyceridemia. A search for effective therapy is a subject of considerable attention. Therefore, our hypothesis is that the fish oil (containing polyunsaturated fatty acids; n-3 PUFA) in a combination with silymarin can more effectively protect against hypertriglyceridemia-induced metabolic disturbances. The study was conducted using a unique non-obese strain of rats with hereditary hypertriglyceridemia an accepted model of metabolic syndrome. Adult male rats were treated with n-3 PUFA (300 mg/kg/day) without or with 1 % micronized silymarin in a diet for 4 weeks. The treatment with the diet containing n-3 PUFA and silymarin significantly reduced concentrations of serum triglycerides (-45 %), total cholesterol (-18 %), non-esterified fatty acids (-33 %), and ectopic lipid accumulation in skeletal muscle (-35 %) compared to controls. In addition, an increase in Abcg5 and Abcg8 mRNA expression (as genes affecting lipid homeostasis) as well as in protein content of ABCG5 (+78 %) and ABCG8 (+232 %) transporters have been determined in the liver of treated rats. Our findings suggest that this combined diet could be used in the prevention of hypertriglyceridemia-induced metabolic disorders.

• MeSH
• Antioxidants metabolism   MeSH
• Diet * MeSH
• Dyslipidemias therapy   MeSH
• Gene Expression drug effects   MeSH
• Hypertriglyceridemia complications   drug therapy   genetics   MeSH
• Rats MeSH
• Lipids blood   MeSH
• Metabolic Syndrome etiology   prevention & control   MeSH
• Lipid Metabolism drug effects   genetics   MeSH
• Disease Models, Animal MeSH
• Fatty Acids, Omega-3 administration & dosage   MeSH
• Oxidative Stress drug effects   MeSH
• Lipid Peroxidation drug effects   MeSH
• Rats, Wistar MeSH
• Fish Oils MeSH
• Silymarin administration & dosage   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

• MeSH
• Hypertriglyceridemia complications   blood   MeSH
• Hypothyroidism epidemiology   etiology   blood   MeSH
• Middle Aged MeSH
• Humans MeSH
• Prevalence MeSH
• Risk Factors MeSH
• Aged MeSH
• Case-Control Studies MeSH
• Severity of Illness Index MeSH
• Triglycerides blood   MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Overall MeSH

OBJECTIVE: The metabolic health effects of conjugated linoleic acid (CLA), which is one of the principal polyunsaturated fatty acids, are controversial and still not fully accepted. The aim of this study was to examine the effects of CLA on adiposity, ectopic lipid accumulation, and insulin-resistant states in a metabolic syndrome model of non-obese hereditary rats with hypertriacylglycerolmia (HHTg). METHODS: Groups of adult male HHTg rats were fed a high-carbohydrate diet (70% sucrose) with a 2% mixture of CLA isomers, or with the same amount of sunflower oil (control group) for 2 mo. RESULTS: CLA supplementation decreased body weight gain (P < 0.05) and visceral adipose tissue weight (P < 0.01), and distinctively reduced serum triacylglycerols (P < 0.01) and triacylglycerol accumulation in the liver, heart, muscle, and aorta. CLA-treated rats exhibited increased insulin sensitivity in the adipose (P < 0.01), a higher release of fatty acids (P < 0.001), and increased adiponectin secretion (P < 0.01).In the skeletal muscle, CLA supplementation was associated with increased glucose oxidation (P < 0.01) and an elevated anti-inflammatory index (P < 0.05), according to phospholipid fatty acid composition. In the liver, CLA reduced the oxidized form of glutathione and elevated the activity of glutathione-dependent antioxidant enzymes. CONCLUSION: Results suggest that CLA supplementation may protect against HHTg-induced dyslipidemia, ectopic lipid deposition, and insulin resistance. Increased glucose oxidation in the skeletal muscle as well as adiponectin secretion may play a role in the mechanism of the CLA action. Results suggest that CLA could reduce the negative consequences of HHTg and metabolic syndrome.

• MeSH
• Dietary Carbohydrates administration & dosage   adverse effects   MeSH
• Glucose metabolism   MeSH
• Hypertriglyceridemia complications   diet therapy   etiology   MeSH
• Insulin blood   MeSH
• Insulin Resistance * MeSH
• Liver drug effects   metabolism   MeSH
• Linoleic Acids, Conjugated administration & dosage   pharmacology   MeSH
• Muscle, Skeletal drug effects   metabolism   MeSH
• Rats MeSH
• Lipid Metabolism drug effects   MeSH
• Disease Models, Animal MeSH
• Oxidation-Reduction drug effects   MeSH
• Dietary Supplements * MeSH
• Body Weight drug effects   MeSH
• Adipose Tissue drug effects   metabolism   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

• Keywords
• Atorvastatinum,
• MeSH
• Dyslipidemias * diagnosis   drug therapy   complications   metabolism   MeSH
• Drug Therapy methods   MeSH
• Risk Assessment MeSH
• Hypercholesterolemia drug therapy   complications   MeSH
• Hypertriglyceridemia drug therapy   complications   metabolism   MeSH
• Cardiovascular Diseases etiology   metabolism   prevention & control   MeSH
• Clinical Laboratory Techniques methods   MeSH
• Humans MeSH
• Lipids analysis   diagnostic use   MeSH
• Lipoproteins analysis   diagnostic use   metabolism   MeSH
• Aged MeSH
• Practice Guidelines as Topic * MeSH
• Fats analysis   diagnostic use   MeSH
• Life Style MeSH
• Risk Adjustment MeSH
• Check Tag
• Humans MeSH
• Aged MeSH
• Female MeSH

• Keywords
• Sortis,
• MeSH
• Fibric Acids administration & dosage   pharmacology   adverse effects   therapeutic use   MeSH
• Adult MeSH
• Dyslipidemias * diagnosis   drug therapy   therapy   MeSH
• Drug Therapy * methods   statistics & numerical data   utilization   MeSH
• Risk Assessment MeSH
• Hypercholesterolemia drug therapy   complications   MeSH
• Hypertriglyceridemia drug therapy   complications   MeSH
• Cardiovascular Diseases * etiology   complications   prevention & control   MeSH
• Nicotinic Acids administration & dosage   pharmacology   adverse effects   therapeutic use   MeSH
• Middle Aged MeSH
• Humans MeSH
• Fatty Acids, Omega-3 therapeutic use   MeSH
• Risk Factors MeSH
• Practice Guidelines as Topic MeSH
• Hydroxymethylglutaryl-CoA Reductase Inhibitors administration & dosage   pharmacology   adverse effects   therapeutic use   MeSH
• Life Style MeSH
• Bile Acids and Salts administration & dosage   pharmacology   adverse effects   therapeutic use   MeSH
• Risk Adjustment MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Female MeSH