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M Krempf

Publications and source records attributed to M Krempf.

At least 37 records · Page 2Linked to original sources

[Intra-vascular lymphoma presenting with respiratory symptoms].

INTRODUCTION: Intra-vascular large cell lymphoma is a rare disease characterised by the proliferation of malignant cells within small blood vessels. CASE REPORT: We report a case of intra-vascular lymphoma presenting with unexplained dyspnoea, hypoxaemia and associated neurological symptom. The diagnosis was made by liver biopsy but the patient ultimately died. CONCLUSIONS: Earlier diagnosis with transbronchial biopsy might have improved the prognosis by allowing more prompt treatment.

Aged↗

[Plastic surgery and obesity: why, when, how?].

In this review, we describe the main surgical procedures used in the plastic surgery of obesity: lipectomies and removal of excess fat tissues after weight loss, liposuction of localised fat deposits, surgery of breast hypertrophies. The main surgical procedures, their indications, their techniques and their long-term results are described. Such surgery should be part of a coherent and structured therapeutic project, defined together with the patient. The management and follow-up should be maintained on the long term after the initial weight loss and the surgical procedure, in order to reinforce the benefit and to prevent a weight regain.

Abdomen↗

Apolipoprotein E kinetics: influence of insulin resistance and type 2 diabetes.

BACKGROUNDS AND AIMS: Insulin resistance related to obesity and diabetes is characterized by an increase in plasma TG-rich lipoprotein concentrations. Apolipoprotein (apo) E plays a crucial role in the metabolism of these lipoproteins and particularly in the hepatic clearance of their remnants. The aim of this study was to explore apoE kinetics of obese subjects and to determine what parameters could influence its metabolism. METHODS: Using stable-isotope labelling technique ([(2)H(3)]-leucine-primed constant infusion) and monocompartmental model (SAAM II computer software), we have studied the plasma kinetics of very-low-density lipoprotein (VLDL) and high-density lipoprotein (HDL) apoE in 12 obese subjects (body mass index (BMI) 27.4-36.6 kg/m(2)): Seven were type 2 diabetics (age 47-65 y; HbA1c 7.1-10.2%) and five were non-diabetics (age 40-51 y, HbA1c: 4.9-5.3%). Six of the diabetic subjects were insulin resistant as assessed by insulin sensitivity index (HOMA 2.6-10.0), while non-diabetic subjects were all insulin sensitive (HOMA 1.2-2.1). RESULTS: Plasma VLDL and HDL apoE concentrations were significantly higher in diabetic than in non-diabetic subjects (5.74+/-1.60 vs 1.46+/-1.74 mg/l, P<0.01 and 17.81+/-6.67 vs 9.97+/-3.32 mg/l, P<0.05). These increased levels were associated with significantly higher absolute production rate (APR) of VLDL and HDL apoE (0.714+/-0.343 vs 0.130+/-0.200 mg/kg/day, P<0.01, and 0.197+/-0.087 vs 0.080+/-0.060 mg/kg/day, P<0.05, respectively) while no significant difference was found for fractional catabolic rate (FCR) of VLDL and HDL apoE (3.44+/-1.64 vs 1.97+/-0.84/day and 0.30+/-0.12 vs 0.19+/-0.09/day, respectively). In the whole population, BMI was not correlated with any of apoE kinetic data. HOMA was positively correlated with FCR of VLDL apoE (r=0.64, P<0.05) and tended to be correlated with APR of VLDL apoE (r=0.58, P=0.06). HbA1c was positively correlated with APR and FCR of both VLDL apoE (r=0.91 and 0.78, P<0.01, respectively) and HDL apoE (r=0.66 and 0.69, P<0.05, respectively). CONCLUSION: Obese diabetics are characterized by elevated VLDL and HDL apoE levels associated with enhancement of VLDL and HDL apoE production rates. Whereas obesity did not influence apoE kinetic parameters in itself, insulin resistance may lead to an increase in VLDL apoE production and fractional catabolic rates. Diabetes and the glycemic control may also specifically influence the kinetics of both VLDL and HDL apoE. All together, these disorders should explain at least part of the increase in VLDL and HDL apoE observed in diabetes.

Adult↗

A new labeling approach using stable isotopes to study in vivo plasma cholesterol metabolism in humans.

A method to study reverse cholesterol transport in humans was developed using stable isotopes and kinetic analysis. Three normolipidemic subjects received simultaneous intravenous infusions of deuterated leucine and (13)C-acetate for 14 and 8 hours, respectively. Deuterium enrichment was measured in protein-bound leucine in apolipoproteins (apo) B-100 and A-I (using gas chromatography coupled with mass spectrometry [GCMS]) and (13)C-enrichment in unesterified cholesterol and cholesteryl ester (using gas chromatography coupled to isotope ratio mass spectrometry [GC-C-IRMS]) in very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) during the tracer infusion. Curves were analyzed using multicompartmental analysis. This protocol is suitable to quantify the different processes involved in reverse cholesterol transport (RCT) in humans, including cholesterol esterification, transfer of cholesteryl ester from HDL towards apo B-100-containing lipoproteins, and the contribution of VLDL, LDL, and HDL in the final steps of RCT. In agreement with previous data from kinetic analysis of radiotracer experiments, our results suggest that in fasting normolipidemic subjects the major fraction of cholesteryl ester enters plasma through esterification in HDL (more than 95%). The major fraction of cholesteryl ester disappears through apo B-100-containing lipoproteins (VLDL and LDL) catabolism (mean of 82%) rather than through removal from HDL (mean of 18% with approximately an equal part for apo AI-dependent and independent catabolism, respectively, 7% and 11%). We conclude that this protocol could be applied to study the modulation of these processes by nutrition, diseases, or pharmacologic treatments.

Acetates↗

Effect of dietary omega-3 fatty acids on high-density lipoprotein apolipoprotein AI kinetics in type II diabetes mellitus.

The effect of a dietary fish oil supplementation on metabolism of HDL was studied in type II diabetes mellitus. Endogenous labeling of HDL-apo AI was performed using a 14 h primed infusion of D3-leucine in five diabetic patients before and 2 months after treatment with maxEPA(R). Isotopic enrichment curves were analyzed using a monoexponential function. After treatment, plasma cholesterol level remained unchanged (205.4+/-41.9 vs. 206.8+/-30.7 mg/dl, NS), whereas plasma triglycerides were decreased (155.4+/-67.9 vs. 202.6+/-32.2 mg/dl, P=0.06). Plasma apo AI was similar under maxEPA(R) (116.0+/-25.6 vs. 111.8+/-25.4 mg/dl, NS), and HDL-cholesterol and HDL-triglycerides were also not markedly changed (30.2+/-10.0 vs. 27.1+/-10 mg/dl, and 15.3+/-9.8 vs. 19.2+/-10.4 mg/dl, NS). HDL-apo AI fractional catabolic rate (FCR) and absolute production rate (APR) were significantly decreased after treatment with maxEPA(R) (0.27+/-0.09 vs. 0.37+/-0.08 pool day, P<0.05, and 12.1+/-2.8 vs. 16.1+/-3.3 mg/kg per day, P<0.05). These findings showed an effect of maxEPA(R) on kinetics of apolipoprotein AI in type II diabetes mellitus, probably linked to changes in plasma triglyceride level.

Apolipoprotein A-I↗

Negative and independent influence of apolipoprotein E on C-reactive protein (CRP) concentration in obese adults. Potential anti-inflammatory role of apoE in vivo.

BACKGROUND: Obesity is frequently associated with an increase in the early inflammation marker C-reactive protein (CRP), insulin resistance and changes in lipoprotein metabolism. Increased CRP is known as an independent cardiovascular risk factor. Since the apolipoproteins (apo) E and CIII components of HDL are associated with reduced cardiovascular risk and since apoE has in vitro anti-inflammatory effect, we have investigated the relationships between apoE, apoCIII (in apoB and non apoB containing lipoproteins) and CRP in obese adults. METHODS: The following parameters from 34 healthy obese fasting women (age 22-64 y, body mass index (BMI) 28-68 kg/m2) were measured: (1) ApoE and apoCIII, in total plasma, in apoB- (E LpB, CIII LpB) and non-apoB-containing lipoproteins (E LpnonB, CIII LpnonB); (2) CRP and cytokine secreted by adipose tissue (TNF-alpha and its soluble receptor TNFR2); (3) triglyceride, HDL-cholesterol, systolic blood pressure, diastolic blood pressure, waist and hip circumferences, insulin, glucose. HOMA, a marker of insulin sensitivity, and the ratio E/CIII in LpB and LpnonB were calculated. RESULTS: CRP was positively correlated with BMI (P<0.05), waist circumference (WC, P<0.05), triglyceride (P<0.05) and negatively correlated with apoE (P<0.01) and E LpnonB (P<0.05). Two multiple regression models including parameters related to CRP with a P<0.25 were run stepwise to assess their independent contribution to CRP concentration. In the first model (including BMI, WC, HOMA, insulin, triglyceride, apoE, E LpnonB), apoE was the best predictor of CRP (P=0.01) together with triglyceride (P=0.02) and BMI (P=0.08). The second model took into account E/CIII LpnonB ratio with the parameters included in the first model. In this second model, E/CIII LpnonB was the best predictor of CRP (P=0.007), explaining 39% of CRP variance. CONCLUSION: ApoE is strongly correlated with CRP and could have an anti-inflammatory effect in vivo in obese subjects. This correlation could be limited to LpnonB lipoproteins, depending on their apoE and CIII relative content.

Adipose Tissue↗

Influence of remnant accumulation markers on plasma concentrations of two lipoprotein(a) subspecies (containing or free of apoE).

Lipoprotein(a) [Lp(a)], an atherosclerosis marker, has 2 subspecies differing in structure and composition that can easily be distinguished by the presence or absence of apolipoprotein E (apoE). The subspecies containing apo E [Lp(a):B:E] is found mainly in the very-low-density lipoprotein (VLDL) size range, while that free of apoE [Lp(a):B] is found mainly in the LDL size range. As little is known about the physiologic function of these subspecies, this study investigated Lp(a):B and Lp(a):B:E concentrations in a population of normotriglyceridemic and moderately hypertriglyceridemic subjects in fasting state and attempted to determine the parameters influencing their plasma concentrations. The subjects studied (n = 98) had a mean total Lp(a) concentration of 108 mg/dL (28 to 252, minimum to maximum), a mean Lp(a):B concentration of 92.6 mg/dL (5 to 254), and a mean Lp(a):B:E concentration of 15.6 mg/dL (0 to 137). These results indicate that Lp(a):B:E, even in normolipidemic subjects, constitutes a detectable part of total Lp(a), ie, a mean percentage of 16.2% (0% to 96%). Multiple stepwise regression analyses showed that triacylglycerol has no independent effect on the concentration of Lp(a) subspecies, and that remnant accumulation markers, such as the E/LpB:E molar ratio (number of apoE per particle containing both apoB and apoE) and apoE-LpB (mass of apoE bound to particles containing both apoB and apoE), have a strong independent effect on this concentration. A strong positive influence of E/LpB:E on Lp(a):B:E subspecies was noted, as well as a negative influence of apo E-LpB on Lp(a):B subspecies. Taken together, these results suggest that the apoE bound to LpB:E particles plays a dominant role in the concentration of Lp(a) subspecies and that a redistribution of Lp(a) subspecies occurs under the influence of the apoE content of triacylglycerol-rich lipoprotein particles.

Adult↗

Effect of low-density lipoproteins on apolipoprotein AI kinetics in heterozygous familial hypercholesterolemia.

In patients with heterozygous familial hypercholesterolemia (FH), both synthetic and clearance rates of high-density lipoproteins (HDL) are increased compared with control subjects. According to in vitro data on hepatocytes, the expanded pool size of low-density lipoproteins (LDL) in FH could partly explain the enhanced HDL production. Therefore, we have tested the hypothesis that a reduction of LDL pool size, achieved by LDL-apheresis, is associated with a downregulation of HDL synthesis. We studied the kinetics of HDL by infusing [5,5,5-(2)H(3)]-leucine in 7 heterozygous FH patients before and after 3 biweekly LDL-apheresis using dextran sulfate columns. Both plasma and LDL-cholesterol levels were decreased after LDL-apheresis (169 +/- 35 v 422 +/- 27 mg/dL, P <.05, and 85 +/- 19 v 327 +/- 52 mg/dL, P <.05, respectively). Plasma triglyceride level was unaffected (162 +/- 43 v 176 +/- 35 mg/dL, not significant [NS]) and HDL composition remained stable (HDL-cholesterol 29 +/- 6 v 37 +/- 7 mg/dL, NS, and HDL-triglyceride 20 +/- 6 v 19 +/- 8 mg/dL, NS). Plasma apolipoprotein AI (apo AI) was also similar (122 +/- 20 v 115 +/- 18 mg/dL, NS). Mean HDL-apo AI fractional catabolic rate (FCR) was slightly higher (0.41 +/- 0.07 v 0.36 +/- 0.14 pool/d, NS), and absolute production rate (APR) was increased (22.1 +/- 5.7 v 18.0 +/- 5.7 mg/kg/d, P <.05) after LDL-apheresis. These human kinetic data suggest that LDL do not play a major role on HDL production in heterozygous FH patients.

Adult↗

Effect of low-density lipoprotein apheresis on kinetics of apolipoprotein B in heterozygous familial hypercholesterolemia.

The acute reduction of low-density lipoprotein (LDL) cholesterol obtained by LDL-apheresis allows the role of the high level of circulating LDL on lipoprotein metabolism in heterozygous familial hypercholesterolemia (heterozygous FH) to be addressed. We studied apolipoprotein B (apoB) kinetics in five heterozygous FH patients before and the day after an apheresis treatment using endogenous labeling with [(2)H(3)]leucine. Compared with younger control subjects, heterozygous FH patients before apheresis showed a significant decrease in the fractional catabolic rate of LDL (0.24 +/- 0.08 vs. 0.65 +/- 0.22 day(-1); P < 0.01), and LDL production was increased in heterozygous FH patients (18.9 +/- 7.0 vs. 9.9 +/- 4.2 mg/kg.day; P < 0.05). The modeling of postapheresis apoB kinetics was performed using a nonsteady state condition, taking into account the changing pool size of very low density lipoprotein (VLDL), intermediate density lipoprotein, and LDL apoB. The postapheresis kinetic parameters did not show statistical differences compared with preapheresis parameters in heterozygous FH patients; however, a trend for increases in fractional catabolic rate of LDL (0.24 +/- 0.08 vs. 0.35 +/- 0.09 day(-1); P = 0.067) and the production of VLDL (13.7 +/- 8.3 vs. 21.9 +/- 1.6 mg/kg.day; P = 0.076) was observed. These results suggested that the marked decrease in plasma LDL obtained a short time after LDL-apheresis is able to stimulate LDL receptor activity and VLDL production in heterozygous FH.

Adult↗

In vivo evidence for the role of lipoprotein lipase activity in the regulation of apolipoprotein AI metabolism: a kinetic study in control subjects and patients with type II diabetes mellitus.

The aim of this study was to delineate the role of lipoprotein lipase (LPL) activity in the kinetic alterations of high density lipoprotein (HDL) metabolism in patients with type II diabetes mellitus compared with controls. The kinetics of HDL were studied by endogenous labeling of HDL apolipoprotein AI (HDL-apo AI) using a primed infusion of D(3)-leucine. The HDL-apo AI fractional catabolic rate (FCR) was significantly increased (0.32 +/- 0.07 vs. 0.23 +/- 0.05 pool/day; P < 0.01), and HDL composition was changed [HDL cholesterol, 0.77 +/- 0.16 vs. 1.19 +/- 0.37 mmol/L (P < 0.05); HDL triglycerides, 0.19 +/- 0.12 vs. 0.10 +/- 0.03 mmol/L (P < 0.05)] in diabetic patients compared with healthy subjects. HDL-apo AI FCR was correlated to plasma and HDL triglyceride concentrations (r = 0.82; P < 0.05 and r = 0.80; P < 0.05, respectively) and to homeostasis model assessment (r = 0.78; P < 0.05). Postheparin plasma LPL activity was decreased in type II diabetes (6.8 +/- 2.8 vs. 18.1 +/- 5.2 micromol/mL postheparin plasma.h; P < 0.005) compared with that in healthy subjects and was correlated to the FCR of HDL-apo AI (r = -0.63; P < 0.05). LPL activity was also correlated with HDL cholesterol (r = 0.78; P < 0.05), plasma and HDL triglycerides (r = -0.87; P < 0.005 and r = -0.83; P < 0.05, respectively), and homeostasis model assessment (r = -0.79; P < 0.05). In addition, the LPL to hepatic lipase ratio was correlated with the catabolic rate of HDL (r = -0.76; P < 0.06). These results suggest that a decrease in the LPL to hepatic lipase ratio in type II diabetes mellitus, mainly related to lowered LPL activity, could induce an increase in HDL catabolism. These alterations in HDL kinetics in type II diabetes proceed to some extent from changes in their composition, probably linked to an increase in triglyceride transfer from very low density lipoprotein particles, in close relationship with LPL activity and resistance to insulin.

Adult↗

[Dietary recommendations for dyslipidemic individuals].

Diet prescription is a fundamental first-line element in the management of patients with dyslipidemia. Weight loss should be a primary goal for all overweight patients. A 5 to 10% weight loss is often sufficient to obtain a significant improvement in lipid levels. Dietary fat should not provide more than 30% of total calorie intake. Saturated fatty acids should not exceed 7% and polyunsaturated fatty acids should also be limited to 7 to 10%. For monounsaturated fatty acids the dietary allowance can be a bit wider, up to 15% of total calorie intake. Carbohydrates, particularly complex carbohydrates, should replace the fat calories. Dietary fiber (more than 20g/d) as well as soy protein or phyto-sterols can be helpful in reducing LDL-cholesterol by about 10%. Consumption of fruits and vegetables should also be encouraged because they provide antioxidants that have effects on other cardiovascular risk factors. Long-term education is needed to encourage the patient to comply with this type of diet. Psycho-behavioral strategies can be useful here.

Antioxidants↗

[Obesity and cardiovascular risk].

Overweight and obesity are recognised as responsible for an increase in vascular risk and in excess mortality due to cardio-vascular diseases. This is especially true in presence of increased visceral (central) fat distribution, a key factor for insulin-resistance, the main component of the metabolic syndrome X. Cardio-vascular risk in overweight and obese subjects appears strongly correlated with the common risk factors, more frequently present in these patients: type 2 diabetes, hypertension, lipid abnormalities. Weight reduction improves all risk factors and decreases the patient's global vascular risk. The improvement in the various risk factors is significant with a moderate weight loss (10% of the initial weight). Weight reduction should been obtained always with nutritional-hygienic means (physical activity, weight-reducing diet...) maintained for several months. Only when these approaches appear to be insufficient, the need for an associated pharmacological treatment has to be considered. Amongst the weight-reducing drugs currently available or close to be, orlistat has demonstrated its interest in the glycemic control of type 2 diabetic patients, and its favourable effect in hypertensive patients. Available clinical studies have clearly shown the more marked effect of orlistat in comparison to placebo in reducing the various risk factors. So far, few studies have been conducted to assess the effects of the specific drug therapy on the control of metabolic abnormalities and risk factors in overweight or obese patients, except in type 2 diabetic patients for whom, most of the oral anti-diabetic agents have been tested in overweight or obese diabetic population.

Cardiovascular Diseases↗

[Acquired right-to-left shunt with normal right heart pressure].

Intracardiac right-to-left shunting through a patent ovale foramen (POF) despite normal right-sided pressures is an uncommon cause of dyspnea with posture worsening in adults. We report herein 6 cases which sum up etiological circumstances, diagnostic workup and management of this syndrome. The main reported etiopathologic mechanism is consistent with a change in the internal configuration of the right atria leading to preferential blood flow from inferior vena cava through patent foramen ovale. The treatment lies on surgical closure of the septal defect, which can now be performed using a noninvasive percutaneous procedure.

Aged↗

[Skin and osteoarticular bacterial infections of the diabetic foot. Ulcers of the diabetic foot: epidemiology and physiopathology].

EPIDEMIOLOGY: There are more than 2 million diabetics in France. Fifteen percent have suffered at one time or another from a foot ulcer. This condition accounts for 20% of all admissions of diabetic patients and for 50% of corresponding hospitalization stays. Fifteen to 25% of diabetic foot ulcers lead to an amputation, the patients being in the 45-65 year age range. Fifty percent of the amputated patients will have a contralateral amputation within the next 5 years. PATHOPHYSIOLOGY: Diabetic foot ulcers result from damage caused by diabetic neuropathy and micro- or macroangiopathy. Ulceration is favored by usually minimal trauma and secondary infection. The neuropathy causes deformations and sensorial disorders. Repair is hindered by the often precarious vascular supply. Reduced antibacterial defense related to high serum glucose levels and impaired diapedesis favor superinfection. MANAGEMENT: Careful physical examination and appropriate explorations are required for proper care giving the patient the best chances for cure.

Aged↗