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Biomedical subjects

E Pilger

Publications and source records attributed to E Pilger.

At least 19 recordsLinked to original sources
PubMed2004

Midaortic syndrome and celiac disease: a case of local vasculitis.

Midaortic syndrome is a variety of aortic coarctation, located in the distal thoracic aorta, the abdominal aorta or both, involving the intestinal and renal vessels, usually presenting with renovascular arterial hypertension. Underlying conditions are thought to be Takayasu's arteritis, von Recklinghausen's disease, and connate hypoplasia. Celiac disease is an inflammation in the small intestine, triggered by an allergic reaction to gluten. It is known to be associated with a variety of other autoimmune disorders, e.g., dermatitis herpetiformis (Duhring's disease), insulin-dependent diabetes mellitus, and IgA nephropathy. We describe the case of a young woman who presented with claudication of the lower limbs, therapy-refractory arterial hypertension, and untreated celiac disease. We found a midaortic syndrome, characterized by severe stenosis of the infrarenal aorta, of both renal arteries (more pronounced on the right side) and of the inferior mesenteric artery. We assume that-after having excluded other possible pathogeneses-the underlying condition is a local vasculitis in the abdominal aorta and the renal and mesenteric arteries due to the chronic inflammation of untreated celiac disease. We performed a percutaneous transluminal angioplasty together with implantation of two stents into the infrarenal aorta and the right renal artery and started treating the celiac disease by dietary intervention. The patient is now under regular medical control and observation.

Adult↗
PubMed2004

The evaluation of the no-independent vasodilatative effect of iloprost in isolated perfused Guinea pig hind limbs.

AIM: In critical limb ischemia vasodilatators play an important role in the treatment of the disease. Considering that the endothelium is seriously damaged in these patients, we wanted to evaluate if the vasodilatative effect of iloprost does or does not depend on the endothelium by using the model of the isolated perfused guinea pig hind limb. METHODS: A catheter was inserted via the distal aorta and common iliac artery. After stabilization, iloprost was administered at a dosage of 0.1 microM. In a subsequent series of experiments precontraction of the peripheral vascular bed was achieved with 40 mM KCl followed by 0.1 microM iloprost. In a 3rd series of experiments L-NAME (100 microM) was administered after the equilibration period for 30 minutes, followed by 0.1 microM iloprost. In the 4th series of experiments, after the administration of L-NAME (100 microM), KCl (40 mM) was administered to precontract the vascular bed and iloprost 0.1 microM was added. RESULTS: The administration of iloprost alone and after addition of KCL induced a significant decrease in vascular resistance(-49.6+/-14.1% [x+/-SEM, n=7]). The addition of L-NAME did not affect vascular resistance. The consecutive addition of iloprost reduced vascular resistance significantly (-4.2+/-0.7% [x+/-SEM, n=7]). After addition of L-NAME 100 microM and precontraction with KCl 40 mM, iloprost once again significantly reduced peripheral vascular resistance (-51.5+/-14.4% [x+/-SEM, n=6]). Reduction of peripheral vascular resistance by iloprost was comparable to that without L-NAME. CONCLUSION: Our data show that iloprost at a dosage of 0.1 microM achieves a significant reduction in peripheral vascular resistance and that the vasodilatative effect of iloprost is independent of NO. Iloprost therefore seems to be an ideal vasodilatative drug for the treatment of patients with impaired endothelial function.

Animals↗
PubMed2004

Diminished response to activated protein C is not correlated with severity of peripheral arterial occlusive disease.

INTRODUCTION: Poor response to activated Protein C (APC) is a well established risk factor for venous thromboembolism. More recently, the hypercoagulable state which results from diminished response to APC has also been associated with arterial thrombosis. Some studies showed a clear association between low response to APC with advanced arterial disease, others, however, failed to support these data. Thus, there is ongoing dispute about the impact of a hypercoagulable state upon progression of atherosclerosis. MATERIAL AND METHODS: We investigated APC ratios and the existence of Factor V Leiden in 800 patients with documented peripheral arterial occlusive disease (PAD). Clinical symptoms according to Fontaine stages II (intermittent claudication), III (rest pain) and IV (gangrene) and the ankle/brachial index served as parameters for the severity of PAD. RESULTS: There was no association between low response to APC or existence of Factor V Leiden and the clinical stage of PAD or ankle/ brachial index. CONCLUSION: Our data suggest that poor response to APC is not correlated with the severity of peripheral arterial occlusive disease.

Activated Protein C Resistance↗
PubMed2003

The role of 2-18F-fluoro-2-deoxy-D-glucose positron emission tomography in the diagnosis of giant cell arteritis of the temporal arteries.

OBJECTIVE: As one of the diagnostic criteria for giant cell arteritis affecting the temporal arteries (temporal arteritis) is still biopsy-proven vasculitis of the affected artery, the aim of our study was to evaluate the value of a non-invasive procedure, 2-(18)F-fluoro-2-deoxy-d-glucose (FDG) positron emission tomography (F-18-FDG-PET), in the diagnosis of Horton's disease. METHODS: During a period of 10 months, 22 consecutive patients with the clinical diagnosis of giant cell arteritis and a positive hypoechogenic halo in duplex sonography were re-examined with F-18-FDG-PET. Six patients had giant cell arteritis involving both the large arteries and the temporal arteries; five patients showed giant cell arteritis only in the large arteries without concomitant involvement of the temporal arteries, and the remaining 11 patients showed only involvement of the temporal arteries. All patients were examined by sonography and F-18-FDG-PET, which was performed before treatment with corticosteroids. RESULTS: All patients with positive signs of giant cell arteritis in duplex sonography, i.e. a hypoechogenic halo in the large arteries (thoracic, subclavian, axillary, iliac, aorta), also showed elevated FDG uptake in the same vessels, with complete agreement in the anatomical distribution of changes. When positive sonography was limited to the temporal arteries, FDG-PET was completely negative in the temporal arteries and all other arterial locations. CONCLUSION: PET is not yet suitable for the diagnosis of temporal arteritis and therefore cannot replace invasive biopsy. F-18-FDG-PET is well suited to the demonstration of giant cell arteritis in arteries exceeding 4 mm in diameter.

Aged↗
PubMed2002

G-455A polymorphism of the fibrinogen beta gene and deep vein thrombosis.

BACKGROUND: Elevated fibrinogen levels have been linked to increased risk for deep venous thrombosis, although it is not clear whether fibrinogen is causal or rather a marker for the presence of other risk factors. A common G/A polymorphism in the gene for the fibrinogen beta-chain (FGB G-455A) is associated with elevated fibrinogen levels. The present study was designed to analyze the role of this genetic marker for deep venous thrombosis. MATERIALS AND METHODS: We performed a case-control study including 307 patients with documented deep venous thrombosis and 316 control subjects. beta-fibrinogen genotypes were determined by allele-specific polymerase chain reaction. RESULTS: GG, GA and AA genotype frequencies were similar among the patients (53.1%, 41.0, 5.9) and controls (51.6%, 42.1, 6.3; P = 0.92). Fibrinogen levels of the patients (median 3.72 g l-1; range 1.93-11.6) did not differ significantly from those of the controls (3.76; 2.17-9.99). Carriers of the homozygous AA genotype had significantly higher fibrinogen levels than noncarriers (patients: 5.32 vs. 3.59; P = 0.024; controls: 6.29 vs. 3.72; P = 0.048). CONCLUSION: Our data suggest that the fibrinogen-elevating FGB G-455A gene polymorphism is not linked to an increased risk for deep venous thrombosis.

Alleles↗
PubMed2002

Effect of aspirin treatment in patients with peripheral arterial disease monitored with the platelet function analyzer PFA-100.

We have used the platelet analyzer PFA-100TM to assess the effect of aspirin (ASA) in patients with documented peripheral arterial disease (PAD). Thirty-one previously untreated patients were recruited. Laboratory investigations, including the collagen and adenosine diphosphate closure time (CADP-CT) and the collagen and epinephrine closure time (CEPI-CT) were performed before and 7 days after treatment with 100 mg ASA per day. Five patients were excluded from the final analysis: one patient did not appear for second examination, in one patient type I von Willebrand disease was diagnosed, and three patients with prolonged CEPI-CT admitted the intake of non-steroidal anti-inflammatory drugs. Prior to ASA treatment, CADP-CT was 90 +/- 15 s (range, 67-124 s) and CEPI-CT was 116 +/- 27 s (range, 78-164 s). There was a significant negative correlation between CADP-CT and von Willebrand factor antigen (r = -0.57, P = 0.001). After treatment with 100 mg ASA per day, CADP-CT was not significantly different (96 +/- 22 s; range, 65-158 s). CEPI-CT, however, was prolonged in all patients, compared with pre-ASA values (226 +/- 82 s; range, 89 to > 300 s). In 12 of 26 patients, CEPI-CT was > 300 s and in another four of 26 patients CEPI-CT was prolonged to more than the upper normal range ('responders'). In the remaining 10 patients, CEPI-CT values did not exceed the upper limit of the normal range ('non-responders'). Five non-responders were re-investigated after intake of 300 mg ASA per day for 3 weeks; in none of these was a CEPI-CT > 165 s recorded. We conclude that 40% of PAD patients have an inadequate response to ASA, as determined by the PFA-100TM CEPI-CT. Whether these patients have a reduced benefit from this treatment remains to be investigated.

Adenosine Triphosphate↗
PubMed2002

The V34L polymorphism of factor XIII and peripheral arterial disease.

BACKGROUND: Factor XIII catalyzes crosslinking of fibrin in the last steps of the coagulation process. A common polymorphism in the gene for factor XIII A subunit (F13A1 V34L) has been associated with a decreased risk for coronary artery disease, cerebrovascular disease, and deep venous thrombosis. METHODS: To analyze the role of this polymorphism in peripheral arterial disease (PAD) we performed a case-control study including 873 patients with documented PAD and a total of 523 controls without vascular disease. The F13A1 genotype was determined by an allele-specific polymerase chain reaction. RESULTS: Genotype distribution and allele frequencies were not significantly different between patients (VV: 51.9%; VL: 40.7%; LL: 7.4%) and controls (VV: 54.7%; VL: 39.2%; LL: 6.1%). Mean age at onset of the disease was significantly higher in LL homozygous subjects than in VV homozygous subjects (67.3 versus 64.1 years, p=0.017). Heterozygous subjects had an intermediate age at onset (65.1 years), suggesting a gene-dose effect. The association of the L34 variant with onset of PAD remained significant after adjustment for other risk factors. The effect was stronger in men than in women. CONCLUSIONS: We conclude that the F13A1 V34L polymorphism was not associated with the presence of PAD in our study, but may be linked to a later onset of the disease.

Aged↗
PubMed2002

Genetic evaluation of the common variant of the endothelial nitric oxide synthase (Glu(298)-><Asp) in patients with thromboangiitis obliterans.

BACKGROUND: Nitric oxide is synthesized by endothelial nitric oxide synthase and plays a key role in adequate endothelial function. An important effect is the reduction of free radicals caused by cigarette smoking, which is the only established risk factor for thromboangiitis obliterans (TAO). In patients with TAO a genetic defect of endothelial nitric oxide synthase may therefore result in deteriorated endothelial function. The aim of our study was to evaluate whether a genetic defect of the common variant of endothelial nitric oxide synthase (Glu(298)-->Asp) can be found in a higher degree in patients with TAO compared to healthy controls. METHODS: We enrolled 42 patients with TAO and 149 healthy subjects. RESULTS: Nineteen patients (45.2%) showed homozygosity for Glu(298) versus 76 (51%) in the control group. The heterozygous status for Glu(298)-->Asp was found among 18 patients (42.9%) compared to 61 (40.9%) members of the control group, which was a nearly equal distribution. Homozygosity for the mutant Asp(298) was slightly elevated in the patient group with 11.9 versus 8.1% in the control group. Allele frequency for Asp(298) was 0.333. CONCLUSIONS: Our data do not show elevated homozygosity for the common variant Glu(298)-->Asp in patients with TAO compared to healthy controls. The limitation of our evaluation is the small number of patients, which is a general problem when evaluating patients with TAO, as this is not a common disease.

Aspartic Acid↗
PubMed2001

Hypothenar hammer syndrome caused by posttraumatic aneurysm of the ulnar artery.

The so-called hypothenar hammer syndrome is a rare entity caused by lesions of the ulnar artery secondary to repetitive trauma to the hypothenar eminence, typically found in persons working with vibrating tools. Its clinical symptoms are pain, stiffness and whitening of the smitten fingers, sometimes in combination with Raynaud's syndrome. Angiographic evaluation of the smitten forearm and hand reveals occlusions, kinking, vasospasm and stenoses of the arteries in the hand and fingers. An aneurysm of the ulnar artery causing the hypothenar hammer syndrome is an even more rare morphological finding. The difficult aspect of treating a hypothenar hammer syndrome is to reopen the occluded vessels. Eventually, circulation deteriorates and skin lesions of the fingers may occur. The advantage of an isolated aneurysm of the ulnar artery is that normal circulation can be restored by vascular surgery, for example, with a vessel interponate. Surgical removal of the isolated aneurysm helps to prevent microembolism to the distal arteries and consequent deterioration of peripheral circulation. We report a young patient who presented with clinical symptoms of the hypothenar hammer syndrome and an aneurysm of the distal ulnar artery, diagnosed by magnetic resonance angiography. The only likely cause of the aneurysm was a bicycle accident some months prior to the occurrence of the aneurysm. The patient underwent vascular surgery and has been free of symptoms during six months of follow-up. A control magnetic resonance angiography performed one month after surgery revealed a normal vascular morphology.

Adolescent↗
PubMed2001

Cystic adventitial degeneration of the popliteal artery-the diagnostic value of duplex sonography.

Cystical adventitial degeneration of the popliteal artery is a disorder which is difficult to diagnose, due to the similarity of the symptoms of people presenting with peripheral arterial occlusive disease (PAOD) or popliteal entrapment syndrome. The only thing that differs from patients suffering from PAOD is the lack of typical risk factors for arteriosclerosis. Typical diagnostic procedures like conventional angiography or magnetic resonance Imaging angiography can be negative, too and therefore misleading. The only which is crucial in the diagnosis of cystic adventitial degeneration of the popliteal artery is to know the morphological background of this disorder, namely that it is a cyst of the adventitia of the artery which leads to a dynamic exercise-dependent flow inhibition. We present a 57-year old white male who had a week's history of intermittent claudication in his left calf. He was lacking of typical risk factors for arteriosclerosis and on first examination all pulses in both lower extremities were palpable and Doppler index on both legs was >1. Only duplexsonography revealed a cystic formation impressing the left popliteal artery in the hight of the rift in the popliteal joint.

Arterial Occlusive Diseases↗
PubMed2001

Blood polymorphonuclear leukocyte activation in atherosclerosis: effects of aspirin.

The aim of the study was to demonstrate an activation of polymorpho-nuclear leukocytes (PMNs) in chronic progressive atherosclerosis (ATH). A group of patients with ATH, and a group of ATH patients under aspirin (ASA) therapy were compared with control persons without atherosclerotic alterations (healthy controls). Each group comprised 15 male age-matched subjects. The following inflammatory parameters related to PMN activities were measured: the polymorphonuclear leukocyte (PMN) blood count; blood PMN migration and reactive oxygen species release in vitro; the blood levels of PMN elastase, malondialdehyde, antibodies to oxidized LDL and soluble ICAM-1. In ATH patients, the PMN blood counts and the share of blood PMNs migrating upon platelet activating factor and leukotriene B4 stimulation were significnatly above the values of the healthy controls, while the other parameters were not significantly altered. ASA treatment attenuated the inflammatory response and reduced the differences between ATH and the healthy controls. It can be concluded that, in patients with chronic progressive atherosclerosis, PMNs are involved in the inflammatory process underlying the disease.

Anti-Inflammatory Agents, Non-Steroidal↗