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Biomedical subjects

T Rosenthal

Publications and source records attributed to T Rosenthal.

At least 199 records · Page 11Linked to original sources
PubMed1981

Labetalol-induced toxic myopathy.

Labetalol has been successful in treating hypertension, and few side effects have been reported, although there have been cases of muscle pain during treatment. A patient with essential hypertension treated with labetalol 600 mg daily complained of muscle pains, particularly in the legs. No neurological abnormality was found, but the activity of muscle enzymes in the blood was high. Findings on electromyography were compatible with myositis and electron microscopical findings suggested toxic myopathy. Labetalol was stopped for 10 days, and the muscle pain disappeared and enzyme activity returned to normal. When labetalol was restarted the pain returned and enzyme activities rose. Myopathy should be considered in patients experiencing muscle pain after treatment with labetalol.

Adult↗
PubMed1981

Use of labetalol in hypertensive patients during discontinuation of clonidine therapy.

Eleven hypertensive patients in whom clonidine therapy had to be discontinued, were treated prophylactically with labetalol, in order to avoid a possible hypertensive crisis. Most of the known side effects, which are consistent with the withdrawal phenomenon were observed, e.g. tremor, insomnia and apprehension, but headaches and flushing did not occur. Blood pressure levels remained unchanged, despite up to a 20-fold increase in plasma catecholamines. The lack of change in serial measurements of plasma cyclic AMP level appears to indicate that adequate adrenergic blockade was induced by labetalol. Since labetalol is a potent anti-hypertensive drug, and is also effective in avoiding a possible hypertensive crisis due to withdrawal of clonidine, we propose to use it as the drug of choice whenever discontinuation of clonidine therapy is indicated.

Adult↗
PubMed1980

The effect of chlorthalidone on serum lipids and lipoproteins.

The effect of chlorthalidone treatment on serum lipids and lipoproteins was investigated in 21 hypertensive patients. Chlorthalidone caused an increase in total serum and low density lipoprotein (LDL) cholesterol, but not in high density lipoprotein (HDL) cholesterol. Serum and lipoprotein triglycerides also increased. Our findings suggest that chlorthalidone increases serum concentrations of "atherogenic" lipoproteins (LDL and VLDL), and possibly decreases the levels of a "beneficial" lipoprotein, namely HDL. Thus, the use of this medication may increase a major atherosclerosis risk factor.

Adult↗
PubMed1980

Minoxidil in the treatment of refractory hypertension.

Minoxidil, a powerful vasodilator, is a very effective antihypertensive drug. It was used to treat 22 patients, most of whom were refractory to conventional antihypertensive medication. There was a swift and definite drop of blood pressure in all cases. In 7 patients with renal disease, renal function did not deteriorate during the administration of Minoxidil, and it improved dramatically in the eighth patient. Side effects of the drug were hirsutism, fluid retention, and in 1 patients a pruritic bullous eruption which disappeared when the drug was discontinued.

Adolescent↗
PubMed1980

Minoxidil in the treatment of refractory hypertension.

Minoxidil, a powerful vasodilator, is a very effective antihypertensive drug. Twenty-two patients, who were mostly refractory to conventional anti-hypertensive medication, were treated with this drug. There was a swift and definite drop of blood pressure in all cases. In 7 patients with renal disease, renal function did not deteriorate during the administration of minoxidil, and it improved dramatically in the eighth patient. Side effects of the drug were hirsutism, fluid retention, and in 1 patient a pruritic bullous erruption which disappeared when the drug was discontinued.

Adolescent↗
PubMed1980

Myocardial infarction in a young woman with systemic lupus erythematosus.

We describe the case of a young woman with systemic lupus erythematosus (SLE) who suffered an acute myocardial infarction (MI). The patient was treated by corticosteroids in addition to the usual management for acute MI. The role of arteritis in producing the infarction is also discussed.

Adult↗
PubMed1980

Atenolol in hypertension: a cardioselective drug.

The efficary of atenolol given one daily was assessed in 41 otherwise healthy hypertensive patients over a period of six months. Twelve patients whose blood pressure was not well-controlled on methyldopa and chlorthalidone and 11 patients who were treated previously with other beta-blockers all benefited from atenolol which appeared to be effective and well-tollerated. Ten patients complained of fatigue not necessarily related to a drop in blood pressure, and two of headache. Respiratory functions were assessed in a double blind trial on 30 patients. No significant changes in any of the expiratory flow rates were recorded after three months of continuous treatment with atenolol in either smokers or nonsmokers.

Adult↗
PubMed1979

Defective cardiovascular reflexes and supersensitivity to sympathomimetic drugs in autonomic failure.

In 10 patients with chronic autonomic failure the clinical features and cardiovascular reflexes were correlated with the pressor responses to intravenous noradrenaline and tyramine. In all patients there was an exaggerated response to noradrenaline but a normal or only mildly exaggerated response to tyramine. Patients with lack of sinus arrhythmia and by implication baroreceptor reflex loss had greater responsiveness to pressor drugs than patients with preservation of this reflex. The responses to tyramine infusions imply that there must be sufficient noradrenaline released at defective sympathetic endings for a pressor response to occur. However, the lack of rise of plasma noradrenaline following tyramine, except in the patients with pure autonomic failure, clearly separates these responses from those of normal subjects. These results can be explained by the presence of lesions of both central and peripheral sympathetic pathways in patients with chronic autonomic failure and multiple system atrophy or Parkinsonism. The peripheral lesion, which is incomplete, may consist of replication of the receptors so causing supersensitivity with a duration of response that is little prolonged. The peripheral defect in the two patients with pure autonomic failure was found to be more complex and the prolonged response in one of these patients suggests the possibility of defective re-uptake or metabolism of noradrenaline. Clearly further study of the defects of sympathetic endings is required, including the use of other techniques such as catecholamine fluorescence. The extreme supersensitive responses underline the need for blood pressure monitoring during pressor drug studies prior to treatment, if the hazards of recumbent hypertension are to be avoided.

Adult↗
PubMed1979

Sympathetic reflex responses during treatment of essential hypertension with hydrallazine and oxprenolol.

1. The short term effects of hydrallazine, oxprenolol and oxprenolol plus hydrallazine were studied in five patients with essential hypertension. 2. The increase in pulse rate caused by hydrallazine was prevented by combined treatment with oxprenolol, which also lowered the high plasma noradrenaline levels, associated with the use of hydrallazine. 3. Plasma renin activity was higher in the supine and standing positions with hydrallazine than with oxprenolol alone and with the patients standing this high renin level was prevented by simultaneous treatment with oxprenolol. With the patients supine, combination of oxprenolol with hydrallazine resulted in a mean plasma renin activity which was less than half that with hydrallazine alone, although this difference was not statistically significant. 4. The combination of oxprenolol with hydrallazine did not lower the blood pressure further, but reduced the increased sympathetic activity which occurred with hydrallazine alone.

Blood Pressure↗
PubMed1979

Angiotensin-converting enzyme inhibitor (SQ 20881) in the diagnosis of renovascular hypertension.

SQ 20881, an angiotensin-converting enzyme inhibitor, was given to 12 patients with renovascular hypertension and to 1 patient with unilateral parenchymatous renal disease in order to evaluate the role of renin-angiotensin systems in their hypertension. Plasma renin activity (PRA) and aldosterone were assayed in systemic blood before and after the injection of SQ 20881. In 5 patients PRA was also measured separately in each renal vein. Blood pressure decreased, PRA increased, and aldosterone level decreased in the 12 renin-dependent patients. When PRA was sampled separately from each renal vein, the increase was larger on the side of the affected kidney. Four patients with a positive test underwent corrective surgery, and in all blood pressure became normal. SQ 20881 is a useful agent in evaluating the contribution of renin in patients with hypertension.

Adolescent↗
PubMed1979

Angiotensin II and K challenge following prolonged ACTH administration to normal subjects.

Twelve healthy male volunteers on a normal Na and K intake and ambulatory received ACTH (40 IU, im) twice daily for 5 days followed by 2 days of angiotensin II (5--13 ng/kg body weight/min for 60 min) or oral K citrate (30 mEq./h x 3). A discordance in the aldosterone-stimulating and pressor responses of angiotensin II was unmasked with only the latter response being positive following ACTH-induced refractoriness. K loading was a much more potent natriuretic stimulus than angiotensin II treatment. In contrast to angiotensin II, K could selectively enhance aldosterone secretion by overcoming the inhibition in secretion of the mineralocorticoid induced by prolonged ACTH exposure.

Administration, Oral↗