The A-allele of the common FTO gene variant rs9939609 complicates weight maintenance in severe obese patients.

OBJECTIVE: The A-allele of the fat mass and obesity-associated (FTO) gene variant rs9939609 has been associated with increased body weight, whereas no effect on weight loss during weight reduction programs has been observed. We questioned whether the AA-genotype interferes with weight stabilization after weight loss. DESIGN: We conducted a monocentric, longitudinal study involving obese individuals. The FTO gene variant rs9939609 was genotyped in participants attending a weight reduction program that was divided into two phases: a weight reduction period with formula diet (12 weeks) and a weight maintenance phase (40 weeks). Body weight, body mass index (BMI), blood pressure and concentrations of blood glucose, total cholesterol, low-density lipoprotein, high-density lipoprotein and triglycerides were determined in week 0 (T(0)), after 12 weeks (T(1)) and at the end in week 52 (T(2)). SUBJECTS: A total of 193 obese subjects aged between 18 and 72 years (129 female, 64 male; initial body weight: 122.4±22.3 kg, initial BMI: 41.8±6.7 kg m(-2)) were included. RESULTS: Genotyping revealed 32.1% TT-, 39.4% AT- and 28.5% AA-genotype carriers. At T (0), carriers of the AA-genotype had significantly higher body weight (P=0.04) and BMI (P=0.005) than carriers of the TT-genotype. Of the 193 participants, 68 discontinued and 125 completed the program. Dropout rate was not influenced by genotype (P=0.33). Completers with AA-genotype showed significantly lower additional weight loss during the weight maintenance phase than TT-genotype carriers (P=0.02). Furthermore, among participants facing weight regain during weight maintenance (n=52), more subjects were carrying the AA-genotype (P=0.006). No influence of genotype on weight reduction under formula diet was observed (P=0.32). CONCLUSION: In this program, the AA-genotype of rs9939609 was associated with a higher initial body weight and did influence success of weight stabilization. Thus, emphasizing the maintenance phase during a weight reduction program might result in better success for AA-genotype carriers.

Tissue inhibitor of matrix metalloproteinase 1 (TIMP1) controls adipogenesis in obesity in mice and in humans.

AIMS/HYPOTHESIS: Extracellular matrix reorganisation is a crucial step of adipocyte differentiation and is controlled by the matrix metalloproteinase-tissue inhibitor of matrix metalloproteinase (TIMP) enzyme system. We therefore sought to define the role of TIMP1 in adipogenesis and to elucidate whether upregulation of TIMP1 in obesity has direct effects on adipocyte formation. METHODS: TIMP1 protein levels and mRNA were measured in lean and obese mice with a focus on levels in adipose tissue. We also analysed the effect of recombinant murine TIMP1 on adipogenesis, adipocyte size and metabolic control in vitro and in vivo. RESULTS: TIMP1 levels were increased in the serum and adipose tissue of obese mouse models. Recombinant murine TIMP1 inhibited adipocyte differentiation in 3T3-L1 as well as in subcutaneous primary pre-adipocytes. Conversely, neutralising TIMP1 with a specific antibody enhanced adipocyte differentiation. In vivo, injection of recombinant TIMP1 in mice challenged with a high-fat diet led to enlarged adipocytes. TIMP1-treated mice developed an impaired metabolic profile with increased circulating NEFA levels, hepatic triacylglycerol accumulation and accelerated insulin resistance. Altered glucose clearance in TIMP1-injected mice was due to changes in adipose tissue glucose uptake, whereas muscle glucose clearance remained unaffected. CONCLUSIONS/INTERPRETATION: TIMP1 is a negative regulator of adipogenesis. In vivo, TIMP1 leads to enlarged adipocytes in the state of overnutrition. This might contribute to the detrimental metabolic consequences seen in TIMP1-injected mice, such as systemic fatty acid overload, hepatic lipid accumulation and insulin resistance.

Weight loss improves endothelial function independently of ADMA reduction in severe obesity.

This prospective study was performed in order to establish whether improvement of endothelial function after weight reduction can be explained by a decrease of elevated asymmetric dimethyl arginine (ADMA), an inhibitor of endogenous NO-synthase (eNOS). Therefore, 21 obese subjects (BMI: 41.1±6.4 kg/m(2)) were studied at baseline and after 12 weeks of weight reduction with a very low calorie diet. Biochemical and clinical parameters of endothelial function were assessed before and after weight loss. Biochemical parameters were determined by measurement of ADMA and soluble intercellular adhesion molecule (sICAM). Clinical parameters were assessed by pulse wave analysis (PWA). Weight intervention resulted in a 21.4±6.8 kg reduction of body weight from 119.7±12.8 kg at study start to 98.3±11.6 kg at study end (p<0.001). Accordingly, biochemical markers improved under weight reduction (ADMA from 0.47±0.07 mmol/l to 0.42±0.08 mmol/l; p=0.002; ICAM from 276±42 ng/ml to 236±29 ng/ml; p<0.001). Further, clinical parameters of functional endothelial function improved with an increase of deltaRI after salbutamol inhalation from -1% before to -9% after weight reduction (p=0.02). Interestingly, improvement of endothelial function correlated with improved HOMA index only (r=-0.60, p=0.04) but not with reduced ADMA levels, improved hypertension or reduced body weight. In conclusion, weight reduction with a very low calorie diet improves endothelial function measured by pulse wave velocity. The missing correlation with ADMA suggests possible further mechanisms underlying this observed effect, for example, improvement of insulin resistance.

The -174G>C IL-6 gene promoter polymorphism and diabetic microvascular complications.

This study examined a possible association of the G>C polymorphism at nucleotide -174 in the promoter region of the interleukin-6 (IL-6) gene (rs1800795) with the prevalence of diabetic complications in 235 patients with type 1 and 498 patients with type 2 diabetes. Genotyping was performed using polymerase chain reaction (PCR) and subsequent cleavage by Nla III restriction endonuclease. Analyzing all diabetic patients together demonstrated that 301 patients (41.1%) carried the GG genotype, 114 (15.6%) the CC genotype, and 318 (43.3%) were heterozygous for the GC genotype. However, there was no correlation of any of the genotypes with the prevalence of diabetic nephropathy or diabetic neuropathy, but subjects with the CC genotype had a significantly higher prevalence of diabetic retinopathy compared to patients with the GC and GG genotype (p=0.016). This association was mainly lost when a logistic regression model was adjusted for diabetes duration (p=0.07). Consistently, a weak but not significant association of the polymorphism with diabetic retinopathy was observed when type 1 and type 2 diabetic patients were analyzed separately (patients with type 1 diabetes: p=0.12; patients with type 2 diabetes: p=0.09). Analogically, no association of the polymorphism was found for diabetic nephropathy or diabetic neuropathy in these groups. In conclusion these data suggest no major influence of the -174G>C variant in the promoter region of the IL-6 gene on the development of microvascular complications in patients with diabetes.

A M55V polymorphism in the SUMO4 gene is associated with a reduced prevalence of diabetic retinopathy in patients with Type 1 diabetes.

AIMS: We studied the association between a functionally relevant M55V polymorphism in the SUMO4 gene with microvascular diabetic complications in patients with type 1 diabetes. METHODS: 223 patients with type 1 diabetes were studied using polymerase chain reaction and subsequent cleavage by restriction endonucleases for the M55V SUMO4 gene variant. RESULTS: No effect of the polymorphism on diabetic neuropathy or diabetic nephropathy was found, but heterozygous or homozygous patients for the M55V polymorphism in the SUMO4 gene had a markedly reduced prevalence of diabetic retinopathy (odds ratio 0.37, 95%-confidence interval (CI) [0.32;0.43]; p=0.004). Furthermore, a multiple logistic regression model showed an age and diabetes duration independent effect of the M55V polymorphisms on the prevalence of diabetic retinopathy (p=0.03), but not of diabetic neuropathy or nephropathy. CONCLUSIONS: Our data indicate that the M55V polymorphism in the SUMO4 gene is associated with a reduced risk of diabetic retinopathy in type 1 diabetes. Thus, the results of our study suggest that posttranslational modification of proteins via SUMO4 could contribute to the development of certain diabetic complications.

The DG10S478 variant in the TCF7L2 gene is not associated with microvascular complications in type 2 diabetes.

OBJECTIVE: The DG10S478 variant in the transcription factor 7-like 2 (TCF7L2) gene is a tetranucleotide repeat with six alleles. Alleles 0, 8 and 12 were found to account for 98% of chromosomes in population based controls. The composite allele X (non zero) has been associated with type 2 diabetes while allele 0 (no insertion) was described as protective. However, no data exist about the influence of DG10S478 variants on manifestation of diabetes and development of diabetic complications. METHODS: 250 patients with type 2 diabetes were tested for the DG10S478 allele X and its association with diabetic complications, age at diagnosis of diabetes and BMI. RESULTS: Allele 0 was found in 42.4% of the examined patients, 45.2% of the participants were found to be heterozygous and 12.4% homozygous for the composite allele X. The correlation of allele X with the age at diagnosis of diabetes was not significant. There was also no association of allele X with retinopathy, nephropathy or neuropathy. Only the correlation with BMI was statistically significant. CONCLUSIONS: The DG10S478 variant seems to have no influence on manifestation of diabetes and the development of microvascular complications.

Postprandial mononuclear NF-kappaB activation is independent of the AGE-content of a single meal.

OBJECTIVE: Dietary uptake of Advanced Glycation Endproducts (AGE) is supposed to potentially contribute to inflammatory reactions linked to vascular dysfunction and late diabetic complications. One mechanism by which dietary AGE might exert these effects is by activation of the proinflammatory transcription factor NF-kappa-B. The aim of this study was to analyze the postprandial effects of a casein meal with low or high AGE content on postprandial NF-kappaB activation in peripheral blood mononuclear cells (pBMC) of healthy volunteers. RESEARCH DESIGN AND METHODS: Casein was heated for 40 h at 50 degrees C in the presence of sorbitol or glucose, resulting in either minimal (Sorbitol [S]-casein) or large (glucose [G]-casein) amounts of AGE-modified casein. Nine healthy volunteers ate 250 g of both types of casein, whereas both meals were separated at least by 2 weeks. Plasma and pBMC were taken before and 2 h after each meal. Thereafter, the defined AGE carboxymethyllysine (CML) was determined by ELISA and Western blot. NF-kappaB activation in pBMC was assayed using Electrophoretic Mobility Shift Assays (EMSA) and Western blot analysis. RESULTS: S-casein contained only minor amounts of CML and no pentosidine, while G-casein contained large amounts of both. 2 h after ingestion, the S-casein or the G-casein-meal, both, resulted in a non-significant increase in plasma CML and in the intracellular CML-content of pBMC. This was paralleled by a highly significant increase in postprandial mononuclear NF-kappaB-binding activity. Remarkably, neither the extent of NF-kappaB induction (178% for S-casein, 188% for G-casein), nor composition of the NF-kappaB heterodimer (mainly consisting of NF-kappaB p50/p65) were significantly different after intake of S-casein or G-casein. Consistently, Western blots confirmed an increased NF-kappaBp65 nuclear translocation and a decrease of NF-kappaBp65 in the cytoplasm, while no difference in postprandial NF-kappaB nuclear translocation was observed following intake of S-casein or G-casein. CONCLUSION: Postprandial mononuclear NF-kappaB activation after a single meal is independent of the AGE-content of the ingested protein.

Spontaneous dissection of the popliteal artery in a young man. A rare cause of the blue toe syndrome.

Spontaneous arterial dissection in peripheral arteries of the extremities is an extremely rare event. We report a case of a spontaneous dissection of a nonaneurysmal popliteal artery in an otherwise healthy 36-year-old man that came to clinical attention as an acute blue toe syndrome. The diagnosis was primarily made by high-resolution duplex ultrasound that revealed a dissection flap (length: 15.5 mm; thickness: 0.4 mm) together with the partially thrombosed false lumen at the dorsal wall of the left popliteal artery (degree of local diameter reduction: 56%). Further work-up by means of contrast-enhanced MR-A and conventional DSA confirmed a moderate stenosis of the popliteal artery compatible with focal dissection and excluded other causes such as popliteal artery entrapment syndrome. Under full-dose intravenous anticoagulation with unfractionated heparin that was switched to oral anticoagulation with vitamin K antagonists (target INR: 2-3) and conservative management of the blue toe the patient made a gradual, but eventually complete clinical recovery over 8 weeks.

Continuous passive motion in the prevention of deep-vein thrombosis: a randomised comparison in trauma patients.

There is a high risk of venous thromboembolism when patients are immobilised following trauma. The combination of low-molecular-weight heparin (LMWH) with graduated compression stockings is frequently used in orthopaedic surgery to try and prevent this, but a relatively high incidence of thromboembolic events remains. Mechanical devices which perform continuous passive motion imitate contractions and increase the volume and velocity of venous flow. In this study 227 trauma patients were randomised to receive either treatment with the Arthroflow device and LMWH or only with the latter. The Arthroflow device passively extends and plantarflexes the feet. Patients were assessed initially by venous-occlusion plethysmography, compression ultrasonography and continuous wave Doppler, which were repeated weekly without knowledge of the category of randomisation. Those who showed evidence of deep-vein thrombosis underwent venography for confirmation. The incidence of deep-vein thrombosis was 25% in the LMWH group compared with 3.6% in those who had additional treatment with the Arthroflow device (p < 0.001). There were no substantial complications or problems of non-compliance with the Arthroflow device. Logistic regression analysis of the risk factors of deep-vein thrombosis showed high odds ratios for operation (4.1), immobilisation (4.3), older than 40 years of age (2.8) and obesity (2.2).

Plasma myostatin is only a weak predictor for weight maintenance in obese adults.

BACKGROUND: Predicting an individual's success in a non-surgical weight loss approach is a demanding need since obesity is becoming an epidemic burden. A possible predictive marker is myostatin, a member of the transforming growth factor b superfamily, which has been shown to be an important regulator of muscle homeostasis. METHODS: In the present study, we analyzed myostatin as a marker to predict weight loss of patients that participated in a 2 phased weight reduction program, comprising a weight loss period of 12 weeks and a weight stabilization period of 40 weeks. Therefore, 62 obese individuals with a mean BMI of 40.6 kg/m(2) were included. Plasma myostatin was measured with ELISA at the beginning (T0), after weight loss (T1) and at the end of the program (T2). RESULTS: Although significant weight loss of -23.9±14.9 kg was achieved, myostatin did not change significantly during the program (T0>T1: p=0.46; T1>T2: p=0.70; T0>T2: p=0.57). Myostatin at baseline did neither negatively correlate with the achieved weight loss in the weight reduction phase (T0>T1: r=0.27, p=0.16) nor with weight loss during the whole program (T0>T2: r=0.20, p=0.29). Only a minor correlation with myostatin levels after weight loss with weight regain during maintenance period was detected. (T1>T2: r=-0.37, p=0.05). CONCLUSION: Plasma myostatin might be suitable in predicting weight regain after marked weight loss, but no association with weight loss was observed in patients undergoing a non-surgical weight loss program. Therefore, myostatin does not seem to be a predictor for success in non-surgical weight loss approaches.

Microcirculation and tolerability following i.v. infusion of PGE1 and iloprost: a randomized cross-over study in patients with critical limb ischemia.

In a randomized cross-over study, the effect of PGE(1) and iloprost on microcirculation as well as the tolerability was investigated in 36 patients with peripheral arterial occlusive disease stage III and IV according to Fontaine. Patients received PGE(1) and iloprost by single 3-h i.v. infusions on two different days at doses recommended by the manufacturers or in previous studies (PGE(1): first hour 20 microg, next 2h 30 microg each. Iloprost: first hour 0.5 ng/kg/min, next 2h 1.0 ng/kg/min). Transcutaneous oxygen pressure (tcPO(2)) values increased much more with PGE(1). Median tcPO(2) increase over baseline 30 min after the end of infusion was 9 and 2 mmHg for PGE(1) and iloprost, respectively, corresponding to median AUC differences from baseline of 1050 and 210 min mmHg. Because of its exploratory character, the study was not powered to test for significance. Adverse effects occurred in 19.4% (PGE(1)) and 30.6% (iloprost) of patients. Dose reduction was required in 3 patients receiving iloprost (hypotension, nausea, irritation of the infused vein), and in none receiving PGE(1).

A 63bp deletion in the promoter of rage correlates with a decreased risk for nephropathy in patients with type 2 diabetes.

Several polymorphisms have been identified in the RAGE-promoter region that might modulate the outcome of disease. Here we analyse the association of a 63bp deletion (delta63) spanning from bp - 407 to bp - 345 with diabetic nephropathy. The deletion was determined using the polymerase chain reaction (PCR) in a cross-sectional study with 1087 patients with type 1 diabetes (n = 559) and type 2 diabetes (n = 528). 475 patients with osteoporosis served as disease independent control. The prevalence of the heterozygous genotype did not significantly differ between the three groups (type 1: 2.15 %, type 2: 2.27 %, controls: 1.47 %), indicating that heterozygous delta63 is not related to the manifestation of diabetes. Homozygous carriers were not identified in this study. The heterozygous delta63 genotype, was associated with a reduced prevalence of diabetic nephropathy in patients with type 2 diabetes (OR = 0.06; 95 % CI: [0.05, 0.07]), but not in patients with type 1 (OR = 1.49; 95 % CI: [1.14, 1.94]). We conclude, that patients with type 2 diabetes and the 63bp deletion in the promoter of RAGE seem to be protected from diabetic nephropathy. The observed difference between type 1 and type 2 diabetes might point to diverse pathomechanisms of nephropathy in both types of diabetes.

SieScape: a new sonographic dimension with fictive images.

SieScape is a new data processor that produces continuous sonographic images of large structures. It works without mechanical control of position and can be used with any transducer. Its accuracy and reproducibility is relevant for measurements and has to be investigated. With the ultrasound equipment of Siemens, type Elegra (5- and 7-MHz linear array transducer), we did repetitive measurements of linear superficial distances, curved circumferences and diameters of human legs. Finally, we tried to do continuous investigations of vascular structures to produce SieScape images. The linear superficial distances of 150 mm were underestimated (147.4+/-3.3 mm). Diameter measurements of the calf, with an adjusted depth of 40 mm, tended to give more accurate values than measurements with a depth of 70 mm, which were all overestimated. The circumferences of the calf measured between superficial markers were calculated as too small. SieScape really provides new sonographic documentation. The SieScape images are fictive, because they do not exactly reproduce anatomic dimensions.

On the metabolism of prostaglandin E1 administered intravenously to human volunteers.

We have demonstrated recently the formation of a biologically active metabolite of prostaglandin (PG) E1, 13,14-dihydro-PGE1, during intravenous infusions of PGE1 in patients with peripheral arterial occlusive disease. We have now investigated the levels of the immediate precursor of 13,14-dihydro-PGE1, the biologically inactive 15-keto-13,14-dihydro-PGE1, during intravenous administration of 20 micrograms, 40 micrograms or 80 micrograms PGE1 over a period of 60 min to human volunteers. It was found that levels of 15-keto-13,14-dihydro-PGE1, but not those of PGE1 itself, increased in a dose-dependent manner. Thus, increased formation of 13,14-dihydro-PGE1 from 15-keto-13,14-dihydro-PGE1 with increasing doses of PGE1 can be expected to occur. It remains to be investigated, to which extent formation of small amounts of 13,14-dihydro-PGE1 during intravenous infusion of PGE1 could contribute to the therapeutic effects of PGE1 in patients with peripheral arterial occlusive disease.

[Osteitis diagnosis in a group of angiology patients: a comparison of X-ray and nuclear medicine studies]. / Osteitisdiagnostik in einem angiologischen Patientengut: Vergleich von röntgen- und nuklearmedizinischen Untersuchungen.

PURPOSE: Of the study was to examine the ranking of radiographs and bone scans in the diagnosis of osteitis. PATIENTS AND METHODS: 115 patients with arterial occlusive disease in stage Fontaine i.v. were referred for examination of the peripheral skeletal parts of the lower extremity. 126 radiographs and bone scans were taken. The time between the two examinations was 10 days maximum to enable direct comparison. Leukocyte scintigraphy was employed as gold standard. RESULTS: The sensitivity of radiographs was 47% with a specificity of 91%. Sensitivity and specificity of bone scans was 78% for both values. The positive predictive values for radiographs and bone scans were 88% and 85%, the negative predictive values were between 80% and 97%. CONCLUSION: In the majority of cases osteitis can be diagnosed with relatively inexpensive methods such as conventional x-rays and bone scans. Only in unclear cases further examinations such as leukocyte scintigraphy or magnetic resonance imaging should supplement the diagnosis.

Isovolemic hemodilution: a therapeutical intervention for improving microcirculation.

A controlled reduction of hematocrit levels can be of value in the conservative treatment of inoperable arterial occlusive disease in advanced clinical stages. Long term success can be achieved in up to nearly 50%. The more and the longer the occlusions, the poorer the results.

Duplex sonography of vascularization of venous thrombosis.

BACKGROUND: Changes in the echogenicity of an ageing intravenous thrombus have already been described in B-mode sonography. We tried to investigate the phenomena of vascularisation of the intravenous thrombotic material during the organisation using colour Doppler sonography. METHODS: We carried out a prospective investigation of 8 jugular vein, 6 femoral vein and 1 inferior caval vein thrombosis. The thromboses were investigated with a colour Doppler sonographic device from Siemens, type Elegra, every second or third day for 4 weeks after making the diagnosis. We looked for intrathrombotic colour Doppler signals with an arterial pulsatile blood flow in the pulsed Doppler mode. RESULTS: We found arterial signals in the intravenous thrombus in 8 of the 15 patients. Such arterial Doppler signals were supposed to be arterial vessels which develop during the organisation of the thrombotic material. The arterial vessels appeared only in a short range of time from the 11th to the 25th day and were present in circumscribed areas of the thrombus. Arterial blood vessels in the surrounding tissue of the veins which may supply blood to the intrathrombotic vessels could not be demonstrated. CONCLUSIONS: Thus the intravenous documentation of arterial vessels in an organising intravenous thrombus is possible. This may give information about the mechanism of thrombogenesis and about the degree of organisation and may also help in determining the age of the thrombosis.

The role of comorbidity burden for patients with symptomatic peripheral arterial disease (PAD). A quantitative approach.

AIM: Comorbidity will play an increasingly important role in PAD management. Therefore, we aimed 1) to address the comorbidity load of PAD patients quantitatively and comprehensively, 2) to delineate the effects of composite comorbidity measures on general and disease-specific aspects of quality of life and on crude markers of resource allocation. METHODS: One hundred and one consecutive symptomatic PAD patients (80 males, 21 females; mean age: 66.4 +/- 9.1 years) were assessed by means of a cumulative illness rating scale (CIRS: 14 items; individual item rating from 1 for no through 5 for life-threatening impairment). Outcome measures were the illness severity score (CIRS-IS, mean of all single item scores) and the comorbidity index (CIRS-CI, number of single items with a score of 3, 4 or 5). These comorbidity indices of the PAD patients were compared with those of both 89 elderly community-dwelling volunteers (44 males, 45 females, mean age 77.4 +/- 5.3 years) we had investigated previously and 439 geriatric residents (121 males, 318 females; mean age 84.1 +/- 5.7 years) reported by Parmelee et al. in 1995. Furthermore, the PAD patients estimated their quality of life (LQ), subjective health status (HS), leg pains during either rest or walking on rating scales (ranging from 0 for the best to 10 for the worst result). RESULTS: PAD patients showed very high comorbidity indices and illness severity scores (CIRS-CI: 3.98 +/- 1.60; CIRS-IS: 1.86 +/- 0.29). These proved to be greater than those of both fit community-dwelling elderly subjects (CIRS-CI: 1.82 +/- 1.46; CIRS-IS: 1.62 +/- 0.22) and older institution residents (CIRS-CI: 2.17 +/- 1.85; CIRS-IS: 1.64 +/- 0.34). Furthermore, both CIRS-CI and CIRS-IS were significantly greater in patients with more advanced PAD stage. These indices of comorbidity load were also associated with quality-of-life impairments (r=0.253, p=0.0186), degree of ischemic rest pain (r=0.251, p=0.0196), extent of medication usage (r=0.511, p<0.0001) as well as duration of in-hospital stay (r=0.271, p=0.0084). CONCLUSION: PAD patients have a markedly increased comorbidity burden. This was greater in the more advanced PAD stages and significantly associated with quality-of-life reductions and the extent of resource allocation. A quantitative approach to the comorbidity load in PAD patients appears to be possible by means of such a scale and useful for both clinical and socioeconomic purposes.

Color Doppler sonography of arteries associated with perforating veins.

BACKGROUND: It has been known for some time that perforating veins had associated perforating arteries. There has been no way to investigate these arteries preoperatively. The newer high resolution ultrasonic devices enable us to investigate these arteries. We are able to localize, determine the frequency, and measure the size of the arteries associated with perforating veins of the lower extremities. METHODS: All patients were studied in our clinical vascular laboratory. PATIENTS: 55 patients with different degrees of varicosities were studied. MEASURES: Each patient had their perforating veins and arteries investigated with a 7.5 MHz linear array transducer (Siemens, Type Elegra). RESULTS: 73% of the 233 perforating veins identified had an associated perforating artery. No preferred localization of the perforating veins was noted. The number of location did not correlate with the presence or absence of incompetence of the veins. The perforating arteries were located in close proximity to the perforating veins but did not go far into the subcutaneous fat. The maximum systolic velocity was 12+/-8 cm/sec. CONCLUSIONS: The preoperative detection of perforating arteries associated with perforating veins is possible using a color Doppler scanner. Their pathophysiological function and its relation to bleeding complications, wound healing and ulcer healing can be studied using this tool.

Risk factors in young patients with peripheral atherosclerosis.

BACKGROUND: Risk factors and especially the combination of multiple risk factors are associated with the development of atherosclerosis. Therefore, patients with an early manifestation of atherosclerotic disease are likely to show an extraordinary risk profile. We analysed the frequencies and severity of risk factors in young patients with manifest peripheral arterial occlusive disease as compared to old patients. METHODS: We analysed the risk profiles in 303 patients who were sent for interventional treatment of a symptomatic peripheral arterial occlusive disease. The risk profiles were described for different age groups (54 patients under 50 years of age, 194 patients from 51 to 74 years, 55 patients over 75 years). Multiple linear regression analysis and analysis of variance were performed to look for age-dependent effects. RESULTS: Elevated total cholesterol, and triglyceride levels and nicotine abuse were more frequent in patients younger than 50 years. Diabetes mellitus and hypertension were more frequent in patients older than 75 years. The different frequencies for smoking, diabetes mellitus and hypertension were age-related (p<0.05). Concerning laboratory parameters such as HDL- and LDL-cholesterol, fibrinogen, lipoprotein(a) and homocysteine there were no relevant age-related differences in frequency nor in absolute values with the exception of the hematocrit and uric acid. The coincidence with clinically manifest myocardial infarction was 11.15% in the patients under 50 years compared to 20.6% in those aged 51-74 years and 16.4% in those over 75 years, for cerebral stroke it was 5.6%, 17.5% and 14.5%, respectively. Patients under 50 years with peripheral arterial occlusive disease and a history of myocardial infarction were characterised by high levels of total cholesterol, triglyceride and lipoprotein(a). Excluding patients with prior myocardial infarction patients did not show any difference in risk profile between the three age groups. CONCLUSIONS: In a population suffering from manifest peripheral arterial occlusive disease the risk profile in patients under 50 years is not different from that in older patients. In contrast an additional myocardial infarction in such a population is associated with pathological lipid profiles.