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Biomedical subjects

M Böhm

Publications and source records attributed to M Böhm.

At least 91 records · Page 5Linked to original sources
PubMed2002

[Therapy of verapamil poisoning with noradrenaline and the phosphodiesterase inhibitor enoximone].

HISTORY: A 40 year old patient was transferred to the intensive care unit five hours after the ingestion of 2.4 g of verapamil. ADMISSION FINDINGS: Clinical investigation and invasive monitoring showed signs of cardiogenic shock. THERAPY: Despite primary detoxification and administration of calcium and norepinephrine no adequate cardiovascular stabilization could be achieved. Only when the phosphodiesterase inhibitor enoximone was added, an increase in myocardial inotropy and a stable cardiovascular state was achieved which was also due to the vasoconstrictory effect of norepinephrine overcoming vasodilatation induced by enoximone. CONCLUSION: Detoxification, calcium supplementation and catecholamines are established therapeutic measures. An additional therapy with phosphodiesterase inhibitors is a promising step in conquering predominant heart failure and hypotension.

Adult↗
PubMed2002

Evaluation and clinical application of a new method for measuring activity of von Willebrand factor-cleaving metalloprotease (ADAMTS13).

Thrombotic thrombocytopenic purpura (TTP) is associated with acquired or congenital deficiency of a plasma von Willebrand factor-cleaving protease (VWFcp). Based on partial amino acid sequence and genome-wide linkage analysis of pedigrees with congenital TTP, VWFcp was recently identified as a new member of the ADAMTS family and designated ADAMTS13. We developed a new, rapid, and simple method for measuring VWFcp activity based on the positive correlation between VWF multimeric size and Ristocetin cofactor activity (VWF:RCo). After dilution of plasma with low ionic Tris buffer and activation of the protease with barium chloride, a VWF concentrate is digested in the presence of urea. Subsequently, the residual VWF:RCo of the samples is assessed and used to calculate the VWFcp activity of the samples. The accuracy of the new technique is verified by estimating VWFcp activity for 282 plasma samples with the RCo-based assay and the original immunoblotting assay. The method is reproducible as shown by low intra- and interassay coefficients of variation (2.8% and 7.5% for normal samples, respectively, and 8.7% and 12.9% for abnormal samples, respectively). Furthermore, the clinical application of the new method is illustrated by measuring VWFcp of 14 patients with 22 episodes of acute TTP as well as other thrombotic, thrombocytopenic, or hemolytic disorders. Severe VWFcp deficiency was restricted to patients with acute, classic TTP. The majority of patients with low titer inhibitor respond to plasma exchange treatment with increase of VWFcp activity, whereas VWFcp deficiency persists in some patients with high titer inhibitor despite clinical remission.

Biomarkers↗
PubMed2002

[Coronary-subclavian steal syndrome].

HISTORY AND CLINICAL FINDINGS: A-46-year-old woman with generalized atherosclerosis and coronary triple vessel disease was admitted with recurrent angina pectoris 17 months after primarily successful triple coronary artery bypass grafting (CABG). The symptoms were induced by exercise of the arms, e. g. carrying shopping bags in the left hand. INVESTIGATIONS: Stress technetium scans showed pronounced left ventricular ischemia of the anterior wall and apex during left upper limb exercise in comparison to bicycle exercise. The coronary angiography showed reverse flow in the internal mammary artery (IMA) graft to the left anterior descending artery (LAD), and aortography disclosed blockage of the proximal left subclavian artery. TREATMENT AND COURSE: : The patient declined percutaneous transluminal interventions or surgical procedures of the left subclavian artery. Because of mild angina and the lack of neurological symptoms, she was discharged on optimal drug treatment. CONCLUSION: : Patients with recurrence of cardiac symptoms after CABG surgery and IMA graft may have a coronary-subclavian steal syndrome. Clinically, these patients present with arterial blood pressure differences between left and right arm of typically more than 20 mmHg. The therapy of choice are percutaneous transluminal revascularization procedures of the subclavian artery.

Coronary Artery Bypass↗
PubMed2002

Pretreatment with interleukin-2 modulates peri-operative immuno-dysfunction in patients with renal cell carcinoma.

OBJECTIVE: Complex peri-operative immuno-dysfunction occurs in patients with renal cell carcinoma undergoing nephrectomy. Here, the effect of pretreatment with interleukin-2 (IL-2) is addressed. METHODS: Of 63 patients who underwent tumor nephrectomy, 26 patients received 4 doses of 10 Mio IE/m(2) IL-2 b.d. s.c. (i.e. a total of 40 Mio IE/m(2)) a week before operation, 37 did not. Parameters of cellular and humoral immunity (differential blood count, T-cell markers CD2, CD3, CD4, and CD8, B-cell markers CD19 and CD20, monocyte markers CD13 and CD14, NK (natural killer)-cell marker CD16, activation markers CD25, CD26, CD69, and HLA-DR, and cytokines IL-1-receptor antagonist (IL-1RA), IL-2, soluble IL-2-receptor (sIL-2R), IL-6, IL-10, and TGFbeta) were measured in venous blood. Blood was drawn before IL-2, 1 day before and immediately after the operation, and on the 1st, 3rd, 5th, and 10th postoperative day. RESULTS: All patients showed postoperatively elevated leukocyte and granulocyte counts, and elevated serum levels of cytokines IL-6 and IL-10. T-cell and activation markers were decreased. However, all these alterations were less accentuated in patients who had been pretreated with IL-2. Monocyte counts and IL-2 and TGFbeta levels were decreased, but IL-1RA and sIL-2R levels were elevated in pretreated patients. IL-2 related toxicity was WHO grades I-II in all patients, grade III in one patient. The anesthetic regimen had no measurable effect. IL-6 concentrations were higher in renal venous than in venous pool blood, indicating IL-6 production in the tumor in vivo. CONCLUSIONS: Pretreatment with IL-2 modulates peri-operative immuno-dysfunction in patients undergoing tumor nephrectomy. This affects in particular T-cell-mediated immunity and levels of cytokines IL-10 and IL-6. The IL-2 administration scheme used here was followed by distinct counter-regulation including monocytes, IL-2, sIL-2R, IL-1RA and TGFbeta.

Adult↗
PubMed2002

Myocardial fibrosis in transforming growth factor-beta(1) (TGF-beta(1)) transgenic mice is associated with inhibition of interstitial collagenase.

BACKGROUND: TGF-beta(1) mediates effects on fibroblast proliferation and collagen synthesis in the myocardium. The extracellular matrix remodeling depends on the fibrillar collagen degrading matrix metalloproteinases (MMPs) and their inhibitors (TIMPs). The in vivo effects of TGF-beta(1) on the MMP/TIMP system in TGF-beta(1) overexpressing transgenic mice were studied. METHODS: Male Alb/TGF-beta(1)(cys(223,225)ser) transgenic mice (TG) and nontransgenic controls (C; 8 weeks) were examined. Protein expression of collagen type I, -III, interstitial collagenase (Int Coll), MMP-2, -9, TIMP-1, -2, -4 and TGF-beta(1) as well as enzyme activity (MMP-2, -9) were measured (Western blots, zymographic assays). mRNA expression of the interstitial collagenase and MMP-9 was studied with the Light-Cycler based real-time PCR. RESULTS: Overexpression of TGF-beta(1) resulted in a 10-fold increase in plasma and a seven-fold increase in myocardial TGF-beta(1) concentrations. Relative heart weights increased (mg g(-1): 7.8 +/- 0.4 vs. 4.8 +/- 0.6, n = 6; P < 0.01) in TG compared to C. Collagen type I and III increased in TG (1.9-fold and 1.7-fold) compared to controls. Interstitial collagenase protein activity (- 91%) and mRNA expression (-75%) in TG were reduced (P < 0.05-P < 0.001). Gelatinase (MMP-2, MMP-9) expression and activity were not significantly alterated. MMP-inhibitors were increased 2.5-fold (TIMP-1, -4) and 6-fold (TIMP-2) in TG. CONCLUSIONS: TGF-beta(1) produces myocardial fibrosis in vivo. This effect is not only produced by a stimulation of matrix protein formation: a complex regulation of MMP and TIMP interaction, namely decrease of expression and activity of interstitial collagenase and an enhanced inhibition by increased levels of TIMPs, are involved. These mechanisms are optional targets for therapeutic interventions in myocardial diseases.

Animals↗
PubMed2002

Defining the optimum upper heart rate limit during exercise: a study in pacemaker patients with heart failure.

AIMS: There is no non-invasive method to determine the individual optimum of maximum exercise heart rate. Knowledge of this value is of particular interest in patients with structural heart disease who are prone to tachycardia intolerance. The purpose of this study was to define the optimal maximum heart rate using cardiopulmonary exercise testing and exercise Doppler echocardiography and to compare the results of both approaches. METHODS AND RESULTS: In 49 pacemaker patients with chronotropic incompetence, the optimum upper heart rate limit was determined using cardiopulmonary exercise testing and exercise Doppler echocardiography. The optimum upper rate limit was given by the highest pacing rate which still produced an increase in oxygen consumption, or by that pacing rate which was linked to the lowest value for the Doppler-derived myocardial performance index. In patients with normal left ventricular ejection fraction (>or=55%) the optimum upper rate limit was 86% of age-predicted maximum heart rate, in patients with left ventriuclar dysfunction (ejection fraction <or=45%) it was 75% of the age-predicted maximum rate (P=0.004). The optimum upper rate limit, as defined by cardiopulmonary exercise testing and exercise Doppler echocardiography, were closely correlated (P<0.0001) with a mean deviation of 6+/-6 beats x min(-1). CONCLUSION: Cardiopulmonary exercise testing and exercise Doppler echocardiography are valuable tools which help to determine the optimum upper rate limit in order to avoid excess heart rates in heart failure patients. The application of these methods is not limited to pacemaker patients but may be helpful in therapeutic interventions with chronotropic drugs.

Adult↗
PubMed2001

[Daily activities and circadian variation of ventricular tachyarrhythmias in patients with implanted defibrillator].

BACKGROUND AND STUDY AIM: Acute cardiovascular events may be triggered by physical and mental stress. Does also the typical circadian variation of arrhythmia recurrence (morning peak of events) in patients with implanted cardioverter-defibrillator correlate with the individual circadian variation of physical and mental daily activities? PATIENTS AND METHODS: In 29 consecutive patients with a minimum of three documented ventricular tachyarrhythmias after defibrillator implantation the circadian variation of habitual daily activities was determined in a standardized interview and compared to the individual circadian variation of arrhythmic events saved in the defibrillator event memory during long-term follow-up. RESULTS: The habitually highest physical and mental activity was determined during the time period with most arrhythmic events in 55 % and 23 % of patients, respectively. A comparison of the level of activity during the time period with the highest event frequency to the mean activity level during the rest of the day (without sleeping time) revealed significantly higher physical activity during the time of day with the highest arrhythmia recurrence. There was a positive correlation between circadian variation of arrhythmic events and the sum of all activities (r = 0.34, p < 0.05) and physical activities alone (r = 0.25, p = 0.056) while a relationship to mental activities alone could not be shown (r = 0.02, p = 0.84) CONCLUSION: The circadian variation of acute cardiovascular events may be discussed as an essential factor influencing the circadian variation of habitual daily activities in patients with cardiac disease.

Activities of Daily Living↗
PubMed2001

[Hypersensitivity syndrome during therapy with allopurinol in asymptomatic hyperuricemia with a fatal outcome].

HISTORY AND ADMISSION FINDINGS: A 86-year-old woman with chronic renal failure was treated with allopurinol for asymptomatic hyperuricemia. After one week she developed quickly progressive exanthema, bullous eruptions, epidermolysis, fever of 39.1; C and dyspnoea at rest. DIAGNOSIS, TREATMENT AND COURSE: The diagnosis of an allopurinol-induced hypersensitivity syndrome with toxic epidermal necrolysis was made from the history, the typical clinical picture and a skin biopsy. Initial therapy starts with steroids. Because of a lack of clinical improvement therapy was changed to immunoglobulins. In addition, systemic analgesia and cardiocirculatory supportive therapy were given. Because of increasing somnolence and severe pain intubation and controlled artificial ventilation were initiated. Despite intensive therapy progressive multi- organ failure developed and the patient died 3 weeks after start of symptoms. CONCLUSIONS: The life threatening hypersensitivity syndrome with fever, eosinophilia, hepatitis, renal failure and skin eruptions as severe as epidermal necrolysis is the most dangerous complication of therapy with allopurinol. The trigger seems to be oxipurinol, the main metabolite of allopurinol, which particularly accumulates in patients with renal failure and concomitant therapy with thiazides. There is no specific treatment of the disease. The use of allopurinol in patients with asymptomatic hyperuricaemia is not indicated in most cases. Dose adjustment according to the clearance of creatinine is mandatory.

Aged↗