Valsartan-Induced Angioedema

2003 ◽  
Vol 37 (7-8) ◽  
pp. 1024-1027 ◽  
Author(s):  
Brian K Irons ◽  
Ashwani Kumar

OBJECTIVE: To report a case of dose-dependent angioedema secondary to the use of the angiotensin-receptor blocker (ARB) valsartan. CASE SUMMARY: A 64-year-old Hispanic woman presented with swelling of the lips shortly after an increase in her valsartan dose for uncontrolled hypertension. Other potential causes were not identified. The angioedema subsequently resided after a dosage reduction and observation. Use of the Naranjo probability scale indicated a probable relationship between the angioedema and valsartan therapy in this patient. DISCUSSION: Drug-induced angioedema is often associated with the use of angiotensin-converting enzyme (ACE) inhibitors and is probably secondary to their effects on bradykinin levels. ARBs are thought to produce few, if any, cases of angioedema if excess bradykinin levels are the root cause of angioedema secondary to ACE inhibitor use. Several potential ARB-induced cases of angioedema have been reported. The exact mechanism of angioedema induced by drugs in both of these classes is unknown. Animal data suggest that there may be a relationship between ARB use and increased tissue bradykinin levels secondary to stimulation of angiotensin II AT2 receptors. CONCLUSIONS: This is the third reported case of valsartan-induced angioedema and the first thought to be dose dependent. Practitioners should be aware of this potential adverse effect of valsartan, although the underlying cause is still not known.

2005 ◽  
Vol 39 (6) ◽  
pp. 1128-1130 ◽  
Author(s):  
Anuradha S Gopalachar ◽  
Venita L Bowie ◽  
Parag Bharadwaj

OBJECTIVE: To report a case of sulfhemoglobinemia in a patient receiving phenazopyridine for a urinary tract infection. CASE SUMMARY: A 63-year-old white woman presented to the emergency department with complaints of fatigue and bluish discoloration of her body that had gradually progressed over the previous 6–8 weeks. About 4 months prior to presenting to the emergency department, she had started taking phenazopyridine, an over-the-counter medication for symptoms of dysuria. Because the cyanosis did not improve after the patient received oxygen and methylene blue, sulfhemoglobinemia was suspected and confirmed by spectrophotometer analysis. DISCUSSION: Sulfhemoglobin is a green-pigmented molecule containing a sulfur atom in one or more of the porphyrin rings. It is a rare cause of cyanosis, which is usually drug induced. Sulfhemoglobinemia is suspected when a cyanotic patient has normal to near-normal oxygen tension, laboratory reports of elevated methemoglobin, and does not respond to methylene blue therapy. Sulfhemoglobinemia is relatively rare, despite the widespread use of drugs that have been reported to cause it. Predisposing factors, such as chronic constipation, present in our patient, have been suggested as a source of hydrogen sulfide. CONCLUSIONS: This case of sulfhemoglobinemia, which occurred after the patient took phenazopyridine, is considered a probable adverse event according to the Naranjo probability scale.


2005 ◽  
Vol 39 (5) ◽  
pp. 970-972 ◽  
Author(s):  
Agnès Henry ◽  
Bruno Charpiat ◽  
Thierry Vial ◽  
Serge Franchini ◽  
François J Cuilleret ◽  
...  

OBJECTIVE: To describe the unmasking of pheochromocytoma in a patient treated with amisulpride and tiapride. CASE SUMMARY: A 42-year-old white man developed acute hypertension with severe headache and vomiting 2 hours after the first doses of amisulpride 100 mg and tiapride 100 mg. Both drugs were immediately discontinued, and the patient recovered after subsequent nicardipine and verapamil treatment. Abdominal ultrasound showed an adrenal mass, and postoperative histologic examination confirmed the diagnosis of pheochromocytoma. DISCUSSION: Drug-induced symptoms of pheochromocytoma are often associated with the use of substituted benzamide drugs, but the underlying mechanism is unknown. In our case, use of the Naranjo probability scale indicated a possible relationship between the hypertensive crisis and amisulpride and tiapride therapy. CONCLUSIONS: As of March 24, 2005, this is the first reported case of amisulpride- and tiapride-induced hypertensive crisis in a patient with pheochromocytoma. Physicians and other healthcare professionals should be aware of this potential adverse effect of tiapride and amisulpride.


1993 ◽  
Vol 27 (7-8) ◽  
pp. 950-955 ◽  
Author(s):  
José A. Sacristán ◽  
Javier A. Soto ◽  
María A. de Cos

OBJECTIVE: To report 11 cases of possible erythromycin-induced hearing loss and to review all cases reported in the literature. CASE SUMMARY: In the 11 cases reported, the following are reviewed: Age, gender, time to onset of and recovery from hypoacusis in relation to erythromycin administration, presence or absence of renal or hepatic disease, underlying disorders, and concurrent administration of other drugs. Hypoacusis appeared with dosages equal to or higher than 4 g/d in patients with a mean age of 52.5 ± 19 years, a high percentage of whom (45 percent) presented with renal impairment. The hearing loss was reversible in all cases, and subsided a few days (median=3) after dosage reduction or drug discontinuation. DISCUSSION: Our patients' characteristics are similar to those of patients reported in the literature. Most data indicate that erythromycin-induced hypoacusis is a dose-dependent effect; however, its occurrence in patients otherwise free from disposing factors suggests that it is idiosyncratic. CONCLUSIONS: Erythromycin administered for appropriate indications and dosage adjustments in patients with impaired renal and/or liver function may prevent or reduce the incidence of erythromycin-induced hypoacusis.


1982 ◽  
Vol 243 (6) ◽  
pp. E499-E504
Author(s):  
N. S. Krieger ◽  
P. H. Stern

The cardiotonic agent amrinone has been postulated to directly affect Na-Ca exchange. Because stimulated bone resorption has been proposed to require Na-Ca exchange, we examined the effects of amrinone on bone. Amrinone inhibited release of Ca from neonatal mouse calvaria in organ culture stimulated by parathyroid hormone (PTH), 1,25-dihydroxyvitamin d3, or prostaglandin E2. Inhibition was dose dependent and maximal at 2 X 10(-4) M. The effect of amrinone differed from the inhibitory effects of calcitonin, ouabain, or nigericin in that 1) 6-h exposure to amrinone alone prevented the effect of subsequently added PTH; 2) amrinone was only partially effective if added after resorption was initiated by 24-h treatment with PTH; 3) coincubation with amrinone and PTH during the first 48 h of culture allowed for a response to PTH after amrinone was removed; no such protection by a stimulator occurred with ouabain or nigericin. Also submaximal concentrations of amrinone plus calcitonin, ouabain, or nigericin gave greater than additive inhibition of Ca release. Amrinone had no effect on basal bone cAMP or on the acute stimulation of cAMP by PTH. The results suggest that amrinone could have a more direct interaction with the pathway involved in stimulated bone resorption than the other inhibitors.


1990 ◽  
Vol 17 (3) ◽  
pp. 224-227
Author(s):  
Henning F. Bjerregaard

The aim of the present study was to investigate the site and mode of trifluoperazine (TFP) action on cell membrane transport by the use of isolated frog skin. This cellular system gives access to the apical (outer) and basolateral (inner) membranes of the polarised epithelial cells. Both apical and basolateral TFP addition induced a dose-dependent stimulation of Na transport, and depolarised the cellular potential. The data indicate that TFP acts by increasing the Na permeability of the apical membrane. However, the mechanisms localised in the apical and basolateral membranes are quite different. Basolateral TFP addition increased Na transport due to a stimulation of PGE2 synthesis, whereas apical TFP addition abolished Na inhibition of the apical Na channels, and thereby enhanced the Na transport. An acute toxic effect on the electrophysiological parameters was noted after addition of high apical TFP concentrations (50–100μM). This toxic effect was dependent on the presence of Na in the apical solution.


Author(s):  
K. Z. Young ◽  
N. M. P. Cartee ◽  
S. J. Lee ◽  
S. G. Keep ◽  
M. I. Ivanova ◽  
...  

1990 ◽  
Vol 124 (2) ◽  
pp. 225-232 ◽  
Author(s):  
J. J. Hirst ◽  
G. E. Rice ◽  
G. Jenkin ◽  
G. D. Thorburn

ABSTRACT The effect of protein kinase C activation and dibutyryl cyclic AMP on oxytocin secretion by ovine luteal tissue slices was investigated. Several putative regulators of luteal oxytocin secretion were also examined. Oxytocin was secreted by luteal tissue slices at a basal rate of 234·4 ± 32·8 pmol/g per h (n = 24) during 60-min incubations.Activators of protein kinase C: phorbol 12,13-dibutyrate (n = 8), phorbol 12-myristate,13-acetate (n = 4) and 1,2-didecanoylglycerol (n = 5), caused a dose-dependent stimulation of oxytocin secretion in the presence of a calcium ionophore (A23187; 0·2 μmol/l). Phospholipase C (PLC; 50–250 units/l) also caused a dose-dependent stimulation of oxytocin secretion by luteal slices. Phospholipase C-stimulated oxytocin secretion was potentiated by the addition of an inhibitor of diacylglycerol kinase (R59 022; n = 4). These data suggest that the activation of protein kinase C has a role in the stimulation of luteal oxytocin secretion. The results are also consistent with the involvement of protein kinase C in PLC-stimulated oxytocin secretion. The cyclic AMP second messenger system does not appear to be involved in the control of oxytocin secretion by the corpus luteum. Journal of Endocrinology (1990) 124, 225–232


1997 ◽  
Vol 31 (5) ◽  
pp. 582-585 ◽  
Author(s):  
Anna M Whitling ◽  
Pablo E Pérgola ◽  
John Lee Sang ◽  
Robert L Talbert

OBJECTIVE: TO report a case of agranulocytosis secondary to spironolactone in a patient with cryptogenic liver disease. CASE SUMMARY: A 58-year-old Hispanic woman with cryptogenic cirrhosis was admitted to University Hospital on October 31, 1995. Laboratory data revealed a leukocyte count of 1.0 × 103/mm3 and an absolute neutrophil count (ANC) of 10 cells/mm3. Prior to treatment with spironolactone, the leukocyte count was 10.2 × 103/mm3 and ANC 8400 cells/mm3. Agranulocytosis resolved 5 days following the discontinuation of spironolactone. Results from the bone marrow biopsies before and after treatment with spironolactone suggested that agranulocytosis was caused by the drug's toxic effect on the bone marrow. DISCUSSION: Drug-induced agranulocytosis is a serious adverse effect, occurring at a rate of approximately 6.2 cases per million persons each year. In addition to the case reported here, three other reports of agranulocytosis secondary to spironolactone have been published in the literature. Several factors have been identified that may increase a patient's risk for developing agranulocytosis, including increased age, hepatic or renal impairment, drag dosage and duration, and concurrent medications. CONCLUSIONS: Agranulocytosis secondary to spironolactone is a serious potential adverse effect. Patients with risk factors for developing this adverse effect should be closely monitored since early detection and discontinuation of spironolactone can improve prognosis.


1988 ◽  
Vol 167 (6) ◽  
pp. 1963-1968 ◽  
Author(s):  
L S Gray ◽  
J Gnarra ◽  
E L Hewlett ◽  
V H Engelhard

Cholera toxin (CT), but not pertussis toxin (PT), treatment of cloned murine CTL inhibited target cell lysis in a dose-dependent fashion. The effects of CT were mimicked by forskolin and cyclic adenosine monophosphate (cAMP) analogues. Inhibition of cytotoxicity by CT and cAMP analogs was mediated in part by attenuation of conjugate formation. Additionally, both CT and cAMP analogs blocked the increase in intracellular Ca2+ induced by stimulation of the TCR complex by mAbs. These findings indicate that cAMP inhibits the activity of CTL by two distinct mechanisms and suggests a role for this second messenger in CTL-mediated cytolysis.


2000 ◽  
Vol 203 (8) ◽  
pp. 1373-1381 ◽  
Author(s):  
H. Onken ◽  
A. Schobel ◽  
J. Kraft ◽  
M. Putzenlechner

Split lamellae of the posterior gills of freshwater-adapted Chinese crabs (Eriocheir sinensis) were mounted in a modified Ussing-type chamber, and active and electrogenic absorption of Na(+) and Cl(−) were measured as positive (I(Na)) or negative (I(Cl)) short-circuit currents. Haemolymph-side addition of eyestalk extract stimulated I(Cl) by increasing both the transcellular Cl(−) conductance and the electromotive force for Cl(−) absorption. The effect was dose-dependent. Boiling the eyestalk extract did not change its effectiveness. The stimulating factor passed through dialysis tubing, indicating that it has a molecular mass of less than 2 kDa. R(p)cAMPS, a blocker of protein kinase A, reduced the stimulated I(Cl). Eyestalk extract stimulated I(Na) by increasing the transcellular Na(+) conductance at constant electromotive force. Amiloride-induced current-noise analysis revealed that stimulation of I(Na) was accompanied by an increase in the apparent number of open apical Na(+) channels at a slightly reduced single-channel current. In addition to the electrophysiological experiments, whole gills were perfused in the presence and in the absence of putative transport stimulators, and the specific activities of the V-ATPase and the Na(+)/K(+)-ATPase were measured. Eyestalk extract, theophylline or dibutyryl-cyclic AMP stimulated the activity of the V-ATPase, whereas the activity of the Na(+)/K(+)-ATPase was unaffected. The simultaneous presence of R(p)cAMPS prevented the stimulation of V-ATPase by eyestalk extract or theophylline.


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