Lichenoid contact dermatitis due to aminoglycoside antibiotics.
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Biomedical subjects
Publications and source records attributed to G Lembo.
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The effects of graded lower body negative pressure (-10 and -40 mm Hg) on vascular resistance and plasma vasopressin, norepinephrine, and renin activity were assessed in seven hypertensive subjects with left ventricular hypertrophy and seven sex-matched and age-matched normotensive subjects. In both groups increasing levels of lower body negative pressure induced a progressive decrease in right atrial pressure and an increase in vascular resistance. In normal subjects plasma vasopressin, norepinephrine, and renin activity were progressively raised, whereas only the higher level of stimulation increased plasma renin activity, norepinephrine, and vasopressin in hypertensive subjects. Propranolol induced a significant increase in plasma vasopressin in normal subjects (from 1.3 +/- 0.1 to 2.0 +/- 0.1 pg/ml; p less than 0.05) but not in hypertensive subjects. In this latter condition -10 mm Hg lower body negative pressure failed to increase plasma vasopressin, norepinephrine, and renin activity in normal subjects. Propranolol abolished the change in plasma renin activity in both groups, reduced the increase in vascular resistance induced by -40 mm Hg lower body negative pressure in normotensive subjects, but did not modify the rise in vasopressin elicited by this stimulus in normal subjects or the humoral and hemodynamic reflex responses evoked in hypertensive subjects. These results suggest that cardiopulmonary receptors are involved in the control of vasopressin release in normal subjects, whereas in hypertensive subjects with left ventricular hypertrophy, this control is altered because of an impaired function of cardiopulmonary receptors.
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Thirteen patients of both sexes, affected by a severe form of a papular rosacea, were treated with 13-cis retinoic acid (1 mg/kg/day) for two months. One patient interrupted the treatment after 15 days because of severe blepharitis. The size and number of papules were progressively reduced from the 2nd week, reaching complete regression at the 6th week. Three patients complained of mild blepharitis, nine developed dry cheilitis.
13 patients of both sexes, affected by a severe form of papular rosacea, were treated with 13-cis retinoic acid (1 mg/kg/day) for 2 months. One patient interrupted the treatment after 15 days because of severe blepharitis. The size and number of papules were progressively reduced from the 2nd week, reaching complete regression at the 6th week. Three patients complained of mild blepharitis, 9 patients developed dry cheilitis.
We studied the influence of atrial natriuretic factor (ANF) infusion on the reflex increase in forearm vascular resistance in normotensive subjects. Reflex vasoconstriction was induced by cardiopulmonary receptor unloading [lower body negative pressure (LBNP), -20 mmHg for 15 min] or by carotid baroreceptor deactivation (+60 mmHg increase in external neck pressure by a pneumatic neck-chamber). Atrial natriuretic factor induced a significant increase in the reflex forearm vasoconstriction to LBNP, but did not modify systemic and regional reflex haemodynamic responses to carotid baroreceptor deactivation. These results suggest that ANF has important interactions with the neural control of peripheral circulation. In addition, the study shows that the peptide causes a selective potentiation of the reflex vasoconstrictor response evoked by cardiopulmonary receptor unloading.
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"Releasability" is the theory whereby biochemical events in basophils influence the capacity to release chemical mediators in response to activating stimuli. We have compared the releasability of basophils from 21 young patients with atopic dermatitis (AD) with that from 17 normal donors of matched ages. Basophils were challenged with several different stimuli: rabbit antihuman Fc epsilon (anti-IgE), N-formyl-methionyl-leucyl-phenylalanine (f-met-peptide), Ca++ ionophore A23187, and D2O. Basophils from patients with AD released significantly more histamine both "spontaneously" and in response to D2O than did controls. The basophils of patients with AD were significantly more responsive to anti-IgE and to A23187. There was no difference between the percent f-met-peptide-induced histamine release in patients with AD vs controls. No significant correlation between percent histamine release with optimal or suboptimal concentrations of the stimuli and serum IgE level was found. There was a significant correlation between the sensitivity of the cells to release with f-met-peptide and the response to A23187 both in control and in AD patients. Since basophils are thought to play some role at the site of inflammation in AD, their increased releasability might contribute to the symptoms of these patients.
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32 ethylenediamine-sensitive patients were studied to determine cross-sensitivity reactions. Reaction to other aliphatic polyamines proved to be very high, whereas no significant result was obtained to antihistamines, either topically or orally.
Hypertrophy in response to increasing blood pressure in primary hypertension leads to important functional consequences for the left ventricle. In fact, the progression of hypertensive heart disease, from an adaptive left ventricular hypertrophy with compensated ventricular function to severe hypertrophy with left ventricular failure, has been long thought to be related to the severity and duration of hypertension. Antihypertensive treatment seems to prevent or minimize the occurrence of left ventricular hypertrophy, but questions arise as to whether this therapy is also able to restore normal hemodynamic conditions, or at least to minimize the hemodynamic abnormalities. This review aims at summarizing current knowledge on the effects of the antihypertensive treatment with beta-blockers, including tertatolol, on hypertension-induced left ventricular hypertrophy. The pathogenetic mechanisms underlying the cardiovascular changes associated with hypertension are discussed. A decrease in left ventricular wall thickness as well as in left ventricular mass has been reported in most of the studies performed with different types of beta-adrenergic blocking agents. The extent of this reduction seems to be related not only to the fall in systemic blood pressure, but also to a decrease in sympathetic stimulation. With regard to the functional consequences of hypertension, the reversal of left ventricular hypertrophy following antihypertensive treatment with beta-blockers is usually associated with an improvement in left ventricular performance. This phenomenon can hardly be ascribed to the direct effects of beta-blocking agents. It is more likely to be related to the concomitant reduction in the afterload and to the improved left ventricular compliance, associated with a decrease in left ventricular wall thickness.
Two sibs with palmo-plantar keratosis and dendritic corneal opacities, previously described as suffering from Richner-Hanhart syndrome by other authors, about 25 years ago, showed increased plasma and urine tyrosine levels. Their neurological and mental features were within normal limits. A comprehensive review of the literature showed a total of 47 cases of fully documented tyrosinemia type II; 8 more patients also had the clinical features of the disease, but aminoacidemia had never been observed. The importance of early diagnosis is stressed, since a low tyrosine-phenylalanine diet dramatically improves the symptoms and may prevent mental retardation.
We studied the response of forearm vascular resistance to lower body negative pressure (LBNP) at -10 and -40 mmHg in seven established hypertensives with left ventricular hypertrophy (LVH) and seven age-matched normotensive controls. To evaluate the specific role of ventricular baroreceptors, we also investigated the effects of propranolol on the reflex response. Under control conditions, graded LBNP induced a progressive decrease in central venous pressure (CVP) and increased forearm vascular resistance. Changes in CVP and forearm vascular resistance were inversely correlated both in controls (r = -0.944) and in hypertensives (r = -0.960), P less than 0.001 for both. No difference was found between the regression slopes obtained for the two groups (normotensives, -30; hypertensives, -40; NS). After propranolol there was a significant reduction in the increase in forearm vascular resistance induced by -40 mmHg LBNP in normotensives but not in hypertensives. Consequently, the slope of the regression delta CVP/delta forearm vascular resistance was reduced in normotensives (-21) but not in hypertensives. In contrast, propranolol did not attenuate the vasoconstrictor response to other stimuli. Left ventricular hypertrophy therefore seems to be associated with changes in the role of the different cardiopulmonary receptor areas during mediation of the haemodynamic response to stimulated orthostatic stress.
The authors report an unusual case of Rubinstein-Taybi Syndrome, in which alterations such as blepharoptosis, unilateral microphthalmia, bilateral and inferior iris, lens, and choroidal colobomas and unilateral optic nerve pit are present in addition to apparently spontaneous multiple keloids. A histopathological study of the skin and a culture of fibroblasts have pointed out a reduction of the cell duplication time.
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