Male sexual function is more than erection.
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Biomedical subjects
Publications and source records attributed to K Lehmann.
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Acute myocardial infarction (AMI) leads to left ventricular dysfunction, the extent of which predicts mortality. We studied the effect of very early enalapril treatment in patients with left ventricular failure (Killip classification II-III) resulting from AMI. In a double-blind randomized trial, patients on conventional treatment were started on placebo (PL, n = 15) or 2.5 mg enalapril (EN, n = 15) twice daily as early as 24 to 30 h after AMI and were followed up over a period of 21 days. One patient died in each treatment group. There were three dropouts in the placebo group (progressive heart failure requiring antiotensin-converting enzyme inhibition) and one dropout in the enalapril group (malignant ventricular arrhythmias). Plasma atrial natriuretic peptide (ANP) and norepinephrine decreased similarly in both groups from elevated baseline concentrations. The patients with the highest baseline ANP levels died in both groups: EN: 579 fmol/ml (mean 65.3 +/- 34.4 fmol/ml), PL: 403 fmol/ml (mean 63.5 +/- 37.6 fmol/ml). Killip classification improved in 9 of 13 patients on enalapril but only in 5 of 11 patients on placebo. On echocardiography an increase in fractional shortening (FS) (3.2 +/- 7.5%, p < 0.05) was found with enalapril only. Patients on placebo required more diuretics, and plasma aldosterone increased threefold. Thus, very early enalapril treatment may help prevent left ventricular failure after AMI. Extremely high initial plasma ANP concentrations may predict an unfavorable outcome.
We have karyotyped a total of twelve ependymomas using GTG-banding including seven for which preliminary results have already been published. One case showing hyperdiploid main line with two marker chromosomes was further analyzed by nonisotopic chromosome in situ suppression hybridization. It was shown that the marker chromosomes consisted of 1q, 14q and 1q, and 22q. The possible role of chromosome 22 in ependymomas and the usefulness of fluorescence in situ hybridization for cytogenetic analysis in tumor investigation are discussed.
Anecdotal observations suggest that renal dysfunction may occur when unadjusted doses of angiotensin-converting enzyme inhibitors are administered to patients on long-term lithium treatment. Although no systematic experimental studies or controlled clinical observations are available, lithium is known to activate the renin angiotensin system through several mechanisms. In addition, direct interactions between lithium and angiotensin II may take place on a cellular level. We propose that (1) renal function should be closely monitored when patients on lithium treatment are given angiotensin-converting enzyme inhibitors and that (2) doses of both drugs should be chosen with caution to avoid serious drug interaction.
A substantial number of young men with erectile dysfunction have neither systemic disease nor a trauma in their history. We are familiar with impotence after major trauma but it is an unanswered question whether subclinical trauma may also induce arterial degeneration with subsequent erectile dysfunction. In a period of 36 months 129 patients underwent penile arteriography. After excluding those with major surgery, trauma or psychogenic impotence 91 angiograms were reevaluated. Special attention was paid to atherosclerotic and to focal occlusive arterial disease (> 50% stenosis) in the hypogastric-cavernous branch. 12 angiograms showed normal arteries, 59 typical atherosclerotic and 20 focal occlusive arterial disease. The mean age of patients with atherosclerosis was 53 +/- 8 years versus 35 +/- 14 years of those with focal lesions (p < 0.0001). 30% with focal arterial lesions were subject to subclinical trauma. 68% with atherosclerotic disease had clinical relevant atherosclerotic risk factors. Latency between onset of erectile dysfunction and presentation at the impotence clinic was 51 months in patients with focal lesions and 39 months in those with atherosclerotic disease (nonsignificant). We conclude that subclinical trauma of the hypogatric-cavernous arteries can induce focal arterial lesions with significant impairment of perfusion. This pathology may contribute to erectile dysfunction. These patients are significantly younger and they suffer from clinically evident impotence approximately 18 years earlier than patients whose impotence is clearly of atherosclerotic origin. Focal arterial lesions due to subclinical trauma are described for the first time as an etiology of erectile dysfunction. Further studies are needed to confirm these results.
The assessment of an erectile dysfunction (ED) includes the history, a clinical examination and blood tests. There is some confusion about which basic hormonal tests are needed at the beginning of clinical evaluation. We feel that with the results from our patients we could help to answer this question. From 1 January 1990 until the December 31 1993 we evaluated 1134 patients for ED. Those who favoured a surgical correction of their ED were fully evaluated by nocturnal penile tumescence testing, penile arteriography, intracavernosal injection of vasoactive agents and dynamic pharmaco-cavernosometry. The results from these tests were correlated with luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone and prolactin. 183 (16.1%) of our patients with a mean age of 45 +/- 14 were fully evaluated. From these patients 76 were excluded because their ED was posttraumatic, undoubtedly psychogenic or could not be proven by the tests mentioned above. From the 107 patients finally included in this study, 90 had normal endocrine parameters. 17 patients had low testosterone. 14 of these patients had otherwise completely normal hormonal tests without evidence of secondary hypogonadism. Three patients had their low testosterone levels confirmed by repeated measurements. In addition, prolactin was significantly increased, and FSH and LH were near or below the lower reference value. When evaluating patients for the first time because of an erectile dysfunction, the measurement of testosterone as a single endocrine test is adequate. If testosterone is low, repeated measurements, combined with LH, FSH and prolactin, will identify patients with an ED due to an endocrine disease.
We reviewed the literature regarding acute therapy of manic patients and compared these recommendations with actual practice by reviewing 399 therapies in 100 patients each from two psychiatric care centres between 1975 und 1991. Higher age, more serious disease and a higher percentage of compulsory commitments are typical of patients treated in institutions with a mandatory admission policy as compared to university clinics, which are not compelled to admit patients. The treatment methods practised in both centres deviated greatly from recommendations in the literature. In spite of widespread therapeutic recommendations, lithium and carbamazepin are seldom employed for acute treatment; neuroleptic agents were preferred for all grades of severity. Combinations of more potent antipsychotics with more sedative neuroleptics were preferred. In contrast, the chosen substances, the preferred combinations and the application form varied considerably. The state mental hospital preferred haloperidol and levomepromazin; in the university clinic clozapin and perphenazineoenanthate were important adjuncts. Both clinics remained in the low therapeutic range of dose recommendations. There were no statistically meaningful differences with regard to either the total amount of chlorpromazine equivalents applied or the duration of inpatient care. In the first one-tenth of the total treatment period, 85% of the maximal dose reached in the second tenth is already given. A continual reduction begins thereafter, until app. 40% of the peak dose in reached. Active treatment of side effects as well as more common use of depot neuroleptics in order to minimize custodial treatment, may explain the lower number of compulsory admissions in the university hospital. Extreme interindividual differences in both dosage and length of stay help in elucidating the apparently contradictory results of comparative investigations with small patient groups. Previous treatments have little or no predictive value due to large intraindividual variations.
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The usefulness of routine clinical application of the urokinase plasminogen activator in prostate cancer was evaluated. The urokinase values of prostate cancer confined to the organ, with extraprostatic spread and with metastatic disease did not differ and showed no significant difference in comparison with benign prostatic hyperplasia. Urokinase is not a useful parameter in clinical routine.
Correct forecasting of prostatic carcinoma by means of serum PSA is limited. Prostatic carcinoma is said to increase PSA 10 times as much as prostatic adenoma. Therefore we evaluated whether PSA in the prostatic fluid is more specific for prostatic carcinoma than the level in the serum. In 31 consecutive patients with prostatic disease blood was taken for serum PSA first and then prostatic fluid (10 microliters) was expressed. The PSA was determined by the Pros-Check test in both the serum and in the prostatic fluid. The collection of the prostatic fluid failed in 7 (22.6%) patients. Of the remaining 24 patients, 5 had documented bacterial prostatitis, 4 had prostatic carcinoma and 15 had benign prostatic hyperplasia (BPH). The serum PSA was 5.6 +/- 5.0 micrograms/l in prostatitis, 148 +/- 208 micrograms/l in prostatic carcinoma and 6.9 +/- 6.8 micrograms/l in BPH. The serum PSA was significantly higher in prostatic cancer (P < or = 0.01) than in prostatitis and BPH. The PSA levels in the prostatic fluid were 14.0 +/- 25.7 x 10(6) micrograms/l in prostatitis, 7.6 +/- 9.7 x 10(6) micrograms/l in carcinoma and 14.0 +/- 14.6 x 10(6) micrograms/l in BPH. There were no statistically significant differences. In the expressed prostatic fluid no significantly different PSA was found in carcinoma, bacterial prostatitis or BPH. In contrast to this, the serum PSA was significantly higher in cancer patients than in prostatitis or BPH. Therefore PSA in the expressed prostatic fluid is no more specific than that in the serum.(ABSTRACT TRUNCATED AT 250 WORDS)
Patient's statements or fears that they may "go crazy" and harm themselves or persons around them are rare, but extremely difficult for all participants to deal with. On the basis of the existing, unsatisfactory literature as well as an analysis of 196 incidents of homicidal-suicidal violence designated by German media as "running amok" and fulfilling defined criteria, we examined whether or not there are predictors for the degree of potential danger inherent in such threats. Impulsive, homicidal-suicidal acts of violence among patients with psychiatric disorders often occur in environments characterised by chronic psychosocial estrangement and isolation. Extremely distressing situations may trigger the course of violence, but the actual act is often planned during a seemingly peaceful interval. Personalities with a high affinity to weapons and a tendency toward acting out seem to increase the potential risks. Such events should be treated analogous to suicidal crises, with a strategy that takes the individual disorder into consideration. The parameters investigated in this paper are not sufficient, even in different combinations, to offer a satisfactory explanation or predict the occurrence of this extremely rare behaviour; further research is necessary.
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OBJECTIVE: To develop prediction rules from clinical and exercise test data identifying patients at high and low risk for cardiovascular events among a group of male veterans. DESIGN: Prognostic study with prospective gathering of data and routine follow-up of consecutive patients referred for exercise testing. Patients only underwent noninvasive evaluation for coronary artery disease. No validation cohort is yet available. SETTING: A 1200-bed Veterans Affairs Medical Center. PATIENTS: Of 3609 men referred for exercise testing between 1984 and 1990, 2546 patients remained evaluable after exclusion of those who underwent subsequent cardiac catheterization, those with significant valvular heart disease, and those who had previous coronary artery bypass surgery. MEASUREMENTS: Evaluation included recording of clinical data on a standardized form and a standard treadmill test followed by assessment of cardiovascular events. RESULTS: During a mean follow-up period (+/- SD) of 2.75 (+/- 18) years, 119 cardiovascular deaths and 44 nonfatal myocardial infarctions occurred in 2546 patients. The Cox proportional hazards model showed the following characteristics to be statistically independent predictors of time until cardiovascular death: history of congestive heart failure or digoxin use, exercise-induced ST depression, change in systolic blood pressure during exercise, and exercise capacity. Using a simple score based on one item of clinical information (history of congestive heart failure or digoxin use) and three exercise test responses (ST depression, exercise capacity, and change in systolic blood pressure), 77% of patients were categorized as low risk (annual cardiac mortality rate, less than 2%), 18% as moderate risk (annual cardiac mortality rate, 7%), and 6% as high risk (annual cardiac mortality rate, 15%; hazard ratio, 10; 95% confidence interval, 6 to 17). This model has not yet been validated. CONCLUSIONS: Variables available from the usual non-invasive work-up of patients with known or suspected coronary artery disease can be used to predict future risk for cardiovascular death.
The cardiovascular effects and pharmacokinetics of once-daily enalapril were studied after single-dose and subchronic treatment in eight patients with hypertension by use of ambulatory blood pressure monitoring. Enalapril, 10 mg, was given at either 7 AM or 7 PM in a randomized crossover design. In addition, inhibition of serum converting enzyme was studied. Subchronic treatment at 7 AM significantly reduced blood pressure during the day but was less effective at night. Subchronic dosing at 7 PM significantly further decreased nighttime blood pressure followed by a slow increase during the day, with no effect on elevated afternoon values. Peak concentrations of enalaprilat were found 3.5 hours (morning) and 5.6 hours (evening) after drug intake (p < 0.05), whereas peak effects occurred 7.4 hours (morning) and 12 hours (evening) after drug administration. In conclusion, 24-hour blood pressure profiles in patients with hypertension were significantly influenced by the time of enalapril dosing. Differences in effect profiles could not be attributed to similar changes in pharmacokinetics or to different time courses of angiotensin converting enzyme inhibition.
We performed a content analysis study based on 196 reports in the German press published during the last decade on acts of violence designated as "going berserk" or "running amok (amuck)" and meeting defined criteria. With less than one person per one million men per year running berserk or amok, this is a very rare act of violence, albeit a very dangerous one involving 1.3 deaths and 1.7 injuries per case. Offenders differ from the normal population in regards to the small percentage of women (5%) and high unemployment (40%), and from other violent offenders in that they are normally occupationally well-qualified. Severe psychiatric disorders are overrepresented. A total of 108 cases were classified according to specific syndromes either by specialists or experts on the spot, or on the basis of a description of the signs and symptoms. Of the syndrome-related acts, the most dangerous offences were committed by 10 delusionally ill and 2 psychopathic individuals. 30 less dangerous offenders suffered from paranoid-hallucinatory syndromes. 28 crimes committed in a state of intoxication and 11 "crimes of passion" were the least dangerous. Another 25 persons with an extensive incidence of suicide in the family, without any apparent pre-existing psychiatric disorder, may have gone berserk in the course of a depressive syndrome. Although psychotically ill individuals tend to overreact more often following a minimal slight, under delusions or with no apparent reason at all, on the whole the causes for both the psychotic and other offenders are of a serious nature. Object loss and private disputes on the one hand and social conflicts on the other were of approximately equal significance. The relationship between the offender and his victim is more essential for the course of the occurrence than motives or the type of the psychopathological syndrome. If only family members are attacked, the offenders have usually been inconspicuous, elderly individuals, two thirds of whom can not be allocated to a given syndrome and may be depressive. They kill deliberately and on-target, do not merely injure their victims--hardly ever, in fact--and then commit suicide practically without exception. If strangers are the target of violence, the crimes are generally committed by younger, passive-aggressive, psychopathic, paranoid or intoxicated offenders. They kill only about half of their victims, but injure many, also causing a great deal of damage. They rarely commit suicide.(ABSTRACT TRUNCATED AT 400 WORDS)
Induction of glutathione S-transferase placental form (GST-P) positive hepatic foci has been examined by immunohistochemical analysis in young male Fischer rats 3 weeks after a single i.p. injection of aflatoxin B1 (AFB1). Pretreatment of rats with L-buthionine sulfoximine (BSO), a GSH depleter, at a dose of 4 mmol/kg body wt 4 and 2 h before 1.0 mg AFB1 treatment enhanced both the number of AFB1-induced hepatic foci and the area occupied by these foci by approximately 400 and 575% above their respective controls without affecting the mean diameter of these foci. Pretreatment of rats with 0.1% phenobarbital (PB) in their drinking water for 1 week before AFB1 (1 mg) treatment, inhibited AFB1-induced foci almost completely. However, the number of AFB1-induced foci in PB-pretreated rats was not significantly increased by BSO pretreatment.
Cilazapril, a novel long-acting inhibitor of angiotensin-converting enzyme, markedly suppressed the proliferative response and neointima formation after balloon catheter-induced injury of the carotid artery in a rat model of angioplasty. The reduction in neointima was dose-dependent, required sustained high levels of enzyme inhibition, and was significantly greater in animals treated starting 6 days prior to the procedure than in animals starting treatment the day of catheterization. In experiments with vascular smooth-muscle cells (SMC) in culture, the addition of angiotensin II reduces increased mRNA levels for several growth factors and extracellular matrix proteins. Here we report that Ang II selectively induces mRNA for thrombospondin I, but not for thrombospondin II. Under selected conditions SMC can be induced to proliferate after exposure to Ang II, in vitro and in vivo. Using neutralizing anti transforming growth factor beta (TGF-beta) antibodies we found that Ang II stimulation of proliferation was threefold greater when the anti-TGF-beta was added to the cultures. We suggest (a) that an important effect of Ang II during the proliferative response is the induction of thrombospondin I, which is required for matrix interactions during the formation of neointima, and (b) that, among the complex array of growth factors potentially active in vivo, TGF-beta may be an important negative regulatory factor that limits the proliferative response and prevents restenosis in most cases of angioplasty.