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Biomedical subjects

R Wolf

Publications and source records attributed to R Wolf.

At least 217 records · Page 12Linked to original sources
PubMed1990

Intraocular pressure changes and postural changes of intraocular pressure in experimentally induced Hansen's disease of rhesus, mangabey, and African green monkeys.

In our long term evaluation of patients with Hansen's disease we have frequently found reduction of their intraocular pressure. Furthermore, we noted changes in their intraocular pressure on change of posture. To determine if these changes have any significance we measured the intraocular pressures of 24 experimentally infected and 39 control monkeys in both sitting and reclining positions. We found significant reduction of intraocular pressure in 66.7% compared with controls in the sitting position, and a significant increase in intraocular pressure in 79% when checked first in the sitting then in the reclining position. We offer a possible pathophysiological explanation as to why the changes occur.

Animals↗
PubMed1990

Psoriasis related to angiotensin-converting enzyme inhibitors.

Two mechanisms have been proposed for the pathogenesis of eruptions induced by angiotensin-converting enzyme (ACE) inhibitors: (1) an allergic, immune-mediated reaction and (2) a pharmacologic, dose-dependent response. Two cases of palmoplantar psoriasis are presented, which can be attributed to the induction (case 1) and exacerbation (case 2) of ACE inhibitors. The first patient developed his eruption 2 months after he had received captopril, probably as a result of an allergic immunologic mechanism. This has been based mainly on circumstantial evidence and is further strengthened by the positive result of the mast cell degranulation test. The second patient developed an atenolol-induced, mild plantar psoriasis. She experienced a dramatic flare-up of her psoriatic lesions shortly after she had received an ACE inhibitor. It is suggested that her reaction occurred as a result of the enalapril-induced augmentation of kinin levels in the skin. These 2 patients represent deductive and unusual examples of the two different mechanisms that are responsible for the cutaneous complications of ACE inhibitors.

Aged↗
PubMed1990

A possible case of drug-induced familial pemphigus.

Two sisters developed pemphigus vulgaris and pemphigus erythematosus within 3 years. The diagnosis was confirmed by clinical, histologic and immunofluorescent antibody studies. One of the sisters experienced a common cold before the pemphigus developed and displayed a positive macrophage migration inhibition (MIF) test to a combination drug compounded of paracetamol, caffeine, chlorpheniramine maleate and phenylephrine HCl, which she had received 2 weeks prior to the appearance of the cutaneous lesions. It is suggested that her pemphigus was triggered by the drug. Although the patient had a strong genetic and familial predisposition to pemphigus, her clinical symptoms did not become evident until they were activated through an exogenous factor, namely, the causative drug. This case offers an example of a possible interaction between endogenous, genetic factors, and exogenous, triggering factors in the development of full-blown disease.

Acetaminophen↗
PubMed1989

Internalized myofiber capillaries: observations on their origin and clinical features.

Internalized capillaries limited to type 1 muscle fibers were noted in seven patients. They occurred in each case in association with a similar admixture of neurogenic and myopathic features that included atrophic and hypertrophic fibers, internal nuclei, fiber splitting, and endomyseal and perimyseal fibrosis. Internalized capillaries in enlarged type 1 fibers arose from fiber splits on step section study of four patients. They occurred in the gastrocnemius, quadriceps, and soleus muscles from patients with a variety of disorders that included Becker dystrophy, diabetes mellitus and strenuous leg activities, Achilles tendon rupture, and myotonic dystrophy. Exercise-induced myalgias were noted in the four patients with the most plentiful intramuscular capillaries, and in three of these muscle hypertrophy was present. The concurrence of internalized myofiber capillaries and exercise-induced myalgias may represent an associated biochemical/pathological defect.

Adolescent↗
PubMed1989

Antinuclear antibodies and anticytoplasmic antibodies in bronchial asthma.

The presence of antinuclear antibodies and anticytoplasmic antibodies was evaluated in the sera of 50 patients with bronchial asthma and 35 matched control subjects with miscellaneous medical diseases with the use of an indirect immunofluorescent assay with HEp-2 cells as substrate. The results were compared to age, sex, atopic status, dose, and duration of the antiasthmatic medication, immunotherapy, severity of the disease, and presence or absence of myalgia. The patients had mild to moderate asthma. The incidence of fluorescent anticytoplasmic antibodies (FACA) in the sera of patients with asthma was statistically significant (p = 0.02) in comparison to FACA in the sera of the control subjects. The combined incidence of fluorescent antinuclear antibodies (FANA) and FACA was found to be significantly higher among atopic subjects with asthma (p = 0.03) and the subjects with asthma and with myalgia (p less than 0.05). The 20% incidence of FACA in this group of subjects with asthma was significantly greater (p less than 0.0001) than the reported 2.7% incidence of FACA in a group of patients with various rheumatologic diseases. Variables, such as dose and duration of antiasthma medications and immunotherapy did not appear to influence the presence of FANA and FACA in their sera. The significance of positive FANA and FACA in this group of subjects with asthma is not known and needs to be evaluated by long-term studies.

Antibodies↗
PubMed1989

Computerized documentation for lithium outpatients (routine and research data).

To follow up the status and further outcome of patients with recurrent affective and schizoaffective disorders treated in a lithium/prophylactic treatment outpatient (LOP) clinic the authors have developed a documentation system based on a database, which ASCII files. This system should be useful as a basis for optimal treatment and is helpful for special research purposes regarding prophylactic treatment (lithium salts, carbamazepine, antidepressants, etc.). The documentation system consists of two parts, one for routine documentation system consists of two parts, one for routine monitoring including basic data, global course, and routine form with side-effects, and another one for research purposes with documentation of laboratory findings, EEG, and documentation of every cycle which can be added easily. Moreover, with this documentation system it will be possible to compare results from different research centres.

Computers↗
PubMed1989

Paget's disease of the nipple resembling an acantholytic disease on microscopic examination.

Two biopsies of an erosive lesion of the nipple had an appearance of an acantholytic disease without showing malignant cells. Only a third biopsy through the nipple with removal of a larger portion revealed some nests of atypical, large cells with clear cytoplasm, typical of Paget's disease. Immunohistochemical findings with carcinoembryonic antigen confirmed the diagnosis of Paget's disease of the nipple. This is the first case of Paget's disease which shows extensive acantholysis on microscopic examination and which resembles pemphigus vulgaris histologically. Acantholytic diseases are easily distinguished from Paget's disease and have never been mentioned in the differential diagnosis of this disease. A large biopsy through the nipple with the removal of a liberal portion of the nipple is suggested in every case of a suspected unilateral lesion of the nipple in order to avoid the overlooking of small nests of Paget's cells, as in our first biopsies, showing a histological picture of an acantholytic disease.

Acantholysis↗
PubMed1989

Atenolol-induced cutaneous vasculitis.

We present a case of cutaneous vasculitis apparently due to an adverse reaction to atenolol. The causal relationship between the drug and the eruption was based mainly on circumstantial evidence. It has been further strengthened by positive results of the indirect rat mast cell degranulation test. The number of published cases of reaction to atenolol is limited. Cutaneous vasculitis has, to the best of our knowledge, never been reported as an adverse reaction to atenolol, although it is not a rare side effect of other beta blocker drugs including propranolol and practolol. Atenolol should be added to the list of beta blocker medications that may produce cutaneous vasculitis.

Atenolol↗
PubMed1989

[Hemodynamic effect of subchronic therapy with 120 mg isosorbide dinitrate in a slow release form in minimal to moderate post-infarct heart failure].

In 16 patients (12 male, 4 female; age 48-73 years, mean = 62.2 years) with left heart failure NYHA Class II-III after myocardial infarction hemodynamic measurements by Swan-Ganz-Catheterization were performed before and after a 3-week therapy with a single dose of 120 mg ISDN in slow-release form. No patient received vasodilators and surgical revascularization was not indicated. Hemodynamics were measured before, 2 and 10 h after ISDN at rest and during exercise. Both before (rest/exercise: LVFP = 18.9 +/- 8.1 +/- 8.1/31.2 +/- 10.5 mmHg) and after 3 weeks (20.6 +/- 8.9/33.1 +/- 14.4 mmHg) ISDN significantly reduced LVFP 2 h (12.1 +/- 5.9/19.0 +/- 10.1 and 11.7 +/- 5.8/20.5 +/- 10.4 after 3 weeks) and 10 h (12.2 +/- 4.6/23.5 +/- 11.0 and 13.0 +/- 3.8/25.8 +/- 11.7 mmHg after 3 weeks) after application. No significant changes of heart rate were observed. In a subgroup of patients hemodynamic control after a 1-year treatment with 120 mg ISDN revealed a sustained reduction of LVFP at rest and during exercise. There is no significant evidence for the development of nitrate tolerance using this treatment regimen in chronic left heart failure.

Aged↗
PubMed1989

[Effect of 75 mg retard gallopamil on stress-induced myocardial ischemia].

In a randomized, double-blind, placebocontrolled study 40 patients with exercise-induced ischemic ST depression were given 75 mg gallopamil in slow release form twice daily. The study had 2 periods. After a 3 day run-in-period and a 14 day open therapy period exercise stress-tests were performed on a bicycle ergometer. 5 patients were dropped from this study. 25 of the remaining 35 patients were "responder" defined as a greater than 30% reduction of the ischemic St depression by gallopamil. These patients were randomly assigned to gallopamil or placebo. At the end of the first open period gallopamil significantly reduced the mean ischemic ST depression by 47% from 0.15 to 0.8 mV (p less than 0.0005). Compared with placebo control, the decrease of the ST depression remained unchanged during gallopamil (0.7 mV). In contrast a statistically significant increase of the ischemic St reaction was observed during placebo. Gallopamil significantly improved exercise tolerance. No side effects or adverse reactions were observed. This study demonstrates that gallopamil slow release is a potent calcium-antagonist in reducing exerciseinduced myocardial ischemia and improving stress tolerance.

Administration, Oral↗
PubMed1988

Suppression of preoptic GABA release caused by push-pull-perfusion with sodium valproate.

The in vivo-effects of various concentrations of the anticonvulsant drug sodium valproate--within and above the therapeutic range for humans (40-100 micrograms/ml)--on the release of gamma-aminobutyric acid (GABA) were studied perfusing the preoptic area of unanaesthetized, freely moving ovarectomized rats through push-pull-cannulae at a flow rate of 20 microliters/min with a fraction period of 5 and 15 min, respectively. Local treatment with 40, 80, 100, and 200 micrograms valproate/ml perfusion medium induced a highly significant decrease in preoptic GABA release. After return to valproate-free medium this effect was reversible. A rapid onset and termination of the valproate effect within 5 min could be observed. Going higher with valproate concentrations the suppressive effect became less and at supratherapeutic valproate levels of 1600 micrograms/ml CSF an increase in GABA release could be observed in 4 out of 8 animals. This does response relationship points to a biphasic effect of valproate on the available amount of GABA in the synaptic cleft, which may be produced by at least two different dose-dependent mechanisms of action. The present results indicate that the action of therapeutic concentrations of valproate involves an alteration of GABAergic transmission different from increasing synaptic GABA release. Nevertheless, the data suggest that valproate action, at least at the level of the preoptic area, involves an enhancement of GABAergic transmission causing--via a negative feedback mechanism--the observed suppression of GABA release into the synaptic cleft.

Animals↗
PubMed1988

Variations in aquagenic pruritus and treatment alternatives.

We report our experience in the treatment of two patients with aquagenic pruritus of the elderly and two patients with aquagenic pruritus. Our findings confirm previous reports by others indicating that aquagenic pruritus is not one homogenous entity but rather is composed of two similar but distinct entities, each of which responds to a different treatment. Patients with aquagenic pruritus were helped by adding sodium bicarbonate to the bath water while patients with aquagenic pruritus of the elderly responded to emollients. It is suggested that aquagenic pruritus and aquagenic pruritus of the elderly are two similar but distinct entities. Separating these two entities provides the key to successful treatment, because each of them responds to a different treatment without crossover. This report is only the second report indicating the effectiveness of sodium bicarbonate baths in patients with aquagenic pruritus. It is clear that further examples are needed to confirm these findings.

Adult↗