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PubMed1998

Risk of severe acute hypersensitivity reactions after rapid paclitaxel infusion of less than 1-h duration.

On the basis of the safety of the 1-h paclitaxel infusion schedule in prior studies we attempted to evaluate the feasibility of a shorter infusion schedule (< 1-h), given the general lack of published data or of attempts at applying this strategy. Before receiving paclitaxel, all patients were premedicated with promethazine, dexamethasone, and ranitidine; they were then given paclitaxel at a dose of 175 mg/m2 diluted in 150 ml normal saline. Four patients were evaluated, two with breast cancer, one with ovarian carcinoma, and one with non-small-cell lung cancer. All had received at least two prior cycles of paclitaxel and had never exhibited any hypersensitivity reaction. In all four patients, adverse signs and symptoms were observed at 5-15 min after the start of paclitaxel administration. These included generalized erythema (three patients), angioedema (all patients), sinus tachycardia (all patients), dyspnea (all patients), and increased sweating (all patients). One patient experienced acute diarrhea. Significant changes in vital signs were recorded in all patients, but there was no dysrhythmia or syncope. Thereafter, drug infusion was interrupted and supportive measures were initiated with dimethidene maleate, ranitidine, and methylprednisolone. In all patients, symptoms resolved over the next 15-30 min, and paclitaxel was reinstituted at the standard 1-h rate with no further sequelae. Paclitaxel administration in < 1 h did not prove to be safe in the current pilot experience and, therefore, cannot be recommended.

Antineoplastic Agents, Phytogenic↗

PubMed2005

Mirtazapine use in resistant hyperemesis gravidarum: report of three cases and review of the literature.

BACKGROUND: Hyperemesis gravidarum is a serious health problem for the fetus and the mother. Effective treatment regimens are obscure in patients with severe symptoms. Our aim was to use mirtazapine in hyperemesis gravidarum patients who failed to respond to conventional anti-emetic drugs. CASES: Three pregnant women who had severe hyperemesis gravidarum. All patients had dehydration, ketonuria, hypokalemia, and weight loss. All failed to respond to conventional anti-emesis treatment regimens, such as metoclopramide and promethazine. Al patients had mirtazapine 30 mg/day within the intravenous fluid support approximately for 1 week. All responded to mirtazapine within 24 h and were able to resume diet within a few days after the initiation of treatment. None of these pregnant women had any disturbing symptoms of emesis throughout the pregnancy and had healthy newborns. CONCLUSION: Mirtazapine seems to be an effective treatment modality in patients with severe hyperemesis gravidarum who do not respond to conventional anti-emesis treatment regimens. Larger-scaled studies should be performed to show the effectiveness of mirtazapine in pregnant women with severe hyperemesis gravidarum who may request pregnancy termination.

Adult↗

PubMed1996

Psychological and clinical effects of renal biopsy performed using sedation.

A sedation regimen using sequential oral trinepazine, intravenous Pethco (pethidine, chlorpromazine and promethazine) and diazemuls was evaluated in children having native kidney (n = 17) and transplant kidney (n = 17) biopsies. Biopsy was successful in all cases, with no serious side effects. A self-reported scale of memory recall and pain perception showed the optimal time for biopsy to be between 30 and 90 min after the intravenous Pethco. The child's level of distress was measured by a self-reported scale, a parent-reported scale and an observational scale for doctors and nurses; 45% of children rated themselves highly distressed prior to the procedure, their parents being the best assessors of this distress. Younger children and those undergoing native kidney biopsy had less understanding of the procedure. Children's worries could be clearly categorised into procedural and outcome issues: those undergoing transplant biopsy were more worried about outcome, whereas those undergoing native kidney biopsy were more worried about the procedure.

Adolescent↗

PubMedDate not supplied

Antihistamines in the treatment of dermatitis.

BACKGROUND: Atopic dermatitis (AD) is an inflammatory skin disorder that is exceedingly challenging to treat. A prominent feature of AD is chronic pruritus. Early evidence suggested that pruritus in AD was partially due to mast cell release of histamines. Conversely, recent studies do not validate the role of histamine in the pathogenesis of pruritus. Conventional management continues to include the wide use of antihistamines to treat the persistent itch, however, there is an urgent need for therapy which will reduce the severity of pruritus for these patients. OBJECTIVE: To review the evidence in the literature for the use of antihistamines in the treatment of atopic dermatitis. METHODS: A MEDLINE search (1966-2002) was performed to obtain studies examining the use of antihistamines in the treatment of atopic dermatitis. Search terms included: atopic dermatitis; eczema; antihistamines; azatadine; brompheniramine; cetirizine; chlorpheniramine; clemastine; cyclizine; cyproheptadine; desloratadine; diphenhydramine; fexofenadine; hydroxyzine; loratadine; meclizine; promethazine; trimeprazine. Further references were gathered from these publications. RESULTS: Historically, antihistamines have been used in the treatment of AD. However, this review shows that the evidence for its use is inconclusive. At present, several antihistamines continue to provide relief of pruritus by central sedation, and they can also be used therapeutically for concomitant allergic conditions associated with AD. More clinical trials examining the therapeutic efficacy of antihistamines, especially with the newer nonsedating antihistamines, are necessary to elucidate their role in the treatment of AD. CONCLUSION: Dermatologists require additional evidence regarding the efficacy of antihistamines and their mechanism of action in the treatment of AD to enhance patient care.

Dermatitis, Atopic↗

PubMed2005

Safety and efficacy of ureteroscopic lithotripsy for ureteral calculi under sedoanalgesia--a prospective study.

OBJECTIVE: To establish the safety and efficacy of ureteroscopic lithotripsy (URSL) under sedoanalgesia. PATIENTS AND METHODS: This study was conducted at Department of Urology (Banaras Hindu University, India) among 124 patients with ureteral stones, between July 2000 and August 2003. Majority of the patients (59.68%) presented with lower ureteric calculi, 24.19% presented with upper ureteric calculi and 16.13% had middle ureteric calculi. All patients were given injection diclofenac sodium (75 mg) promethazine hydrochloride (12.5 mg) deep intramuscular 30 minutes the before procedure. Injection midazolam 0.03 mg/kg body weight slowly given intravenously immediately before the procedure for achieving sedation. Injection fentanyl 50 mcg intravenously given slowly just before introducing the ureteroscope into ureter for achieving intravenous analgesia. Patients were observed for few hours after completion of procedure and oral questions were asked as per proforma, which included tolerance, intensity of pain and percentage of pain experienced by the patients. Patients were discharged thereafter. RESULTS: 87.10% of patients opined that the procedure was acceptable. Only 4.84% opined this procedure was painful. According to present pain intensity score (PPI) in this study 79.03 patients experienced only mild pain, 11.29% cases rated procedure as discomforting, 6.45 rated procedure as distressing and only 3.23% rated as horrible procedure. As per visual analogue scale for assessment of pain 80.65 of cases rated only 20% pain score (in a scale of 0-100). 9.68% cases rated 30% and 6.45% rated 50%. Only two patients in middle ureteric group rated 100% pain. Overall success rate in fragmenting stone was 91.94, where as for lower ureteric calculi it was 97.30%; for upper and, middle ureteric calculi it was 86.66% and 80%, respectively. CONCLUSION: Ureteroscopic lithotripsy can be performed on day care basis under sedoanalgesia which is fairly tolerated by the patients with unremarkable complications and difficulty.

Adolescent↗

PubMed1998

Diabetic and Nondiabetic Gastroparesis.

Nutritional support is essential in treating patients with gastroparesis. Initially, dietary changes should be instituted to reduce extra fat and bulk, and patients should be encouraged to eat frequent small meals with liquid supplementation. Enteral feeding should be introduced in the event of weight loss or persistent vomiting. Medical therapy is usually necessary early in treatment. Cisapride is the initial agent of choice and may be combined with an antiemetic agent, such as promethazine or chlorpromazine or, if side effects occur, ondansetron and granesitron. If cisapride is ineffective or contraindicated, metoclopramide is a reasonable option, though limited by side effects. Erythromycin is useful in the acute treatment of postoperative ileus and hospitalized gastroparetic patients, but its role is limited based on concerns about poor long-term effectiveness and antimicrobial resistance. Once domperidone becomes available in the United States, it will be useful for its promotility and antiemetic qualities. Combination therapy should be considered if monotherapy with cisapride or metoclopramide alone is ineffective. While not yet well studied, combination therapy has the potential to offer dramatic benefit for patients with refractory gastroparesis. Metoclopramide may be added to cisapride for patients with breakthrough symptoms or refractory chronic symptoms. Other combinations include metoclopramide with erythromycin, domperidone with cisapride, and domperidone with erythromycin. In the future, gastric pacing may become an effective option for patients not responding to medical therapy. Total gastrectomy should be performed only for end-stage gastroparesis when all other therapy has failed. Both procedures should be reserved for centers that specialize in severe gastric motility disorders.

Journal Article↗

PubMed2005

Tardive Dystonia.

Tardive dyskinesia is a movement disorder that develops after exposure to dopamine receptor blocking agents. Less well-appreciated are other, more recently described tardive syndromes that are phenomenologically distinct from tardive dyskinesia and respond to different treatments. Patients may simultaneously have more than one tardive syndrome. Major subtypes of tardive syndromes include tardive dyskinesia, characterized by orobuccolingual, truncal, or appendicular, choreiform movements; tardive dystonia, characterized by sustained, stereotyped muscle spasms of a twisting or turning character; and tardive akathisia, characterized by an inner sense of restlessness or unease. The sensation often is unpleasant and may be accompanied by repetitive, purposeless movements (stereotypies), such as pacing. Less common tardive syndromes include tardive myoclonus, tardive tourettism, and tardive tremor. Tardive syndromes often are a source of great distress and disability to patients and may be permanent, despite discontinuing the responsible medication. Prevention, early detection, and prompt management are the major clinical focus. When a patient develops a tardive syndrome appropriate actions include 1) review of the primary diagnosis that prompted starting a dopamine receptor blocking agent; 2) characterization of the movement disorder(s); 3) where possible, discontinuation of dopamine blocking agent or replacement with a less potent alternative agent; 4) gradual withdrawl of the offending drug because some patients have an exacerbation of a tardive syndrome after abrupt withdrawal; and 5) assessment of the severity of symptoms and development of a treatment plan based on the phenomenology, with the goal of maximizing patient comfort and function. Although tardive dyskinesia typically develops after chronic exposure to dopamine receptor blocking agents, it, and other variants (such as tardive dystonia) can develop very rapidly after treatment. There seems to be no minimal safe duration of exposure for the development of a tardive syndrome. It is important to recognize that anti-emetics, which are dopamine receptor blockers, such as prochlorperazine, promethazine and metoclopramide, can cause tardive syndromes. Clinicians should become familiar with antipsychotic agents that have a lower risk of causing tardive syndromes, such as clozapine, quetiapine, and olanzapine. We review treatment options for tardive dystonia.

Journal Article↗

PubMed1987

Delayed, ferrous iron-dependent peroxidation of rat liver microsomes.

Measurement of both chemiluminescence (CL) and the formation of 2-thiobarbituric acid-reacting substances (TBAR) has been used to study the delayed, nonenzymatic lipid peroxidation (LP) initiated in rat liver microsomes by ferrous chloride. Following Fe2+ addition, the CL technique revealed a burst of light emission (peak, Phase II) which was preceded by a period of little or no detectable photon production (delay, Phase I) and succeeded by an increased emission (Phase III). Analysis of TBAR indicated a low rate of LP during the delay which increased more than fivefold during a 1-min period and which corresponded to the CL peak. The delay length depended on both the Fe2+ concentration and the microsome concentration; increased Fe2+ yielded longer delays while increased microsome concentration decreased the delay. As reported by others [J. R. Bucher, M. Tien, and S. D. Aust (1983) Biochem. Biophys. Res. Commun. 111, 777-784; J. M. Braughler, L. A. Duncan, and R. L. Chase (1986) J. Biol. Chem. 261, 10282-10289], Fe3+ also decreased the delay. The ferric-nitrilotriacetate (Fe3+-NTA) complex was found to be more efficient than "free" Fe3+ [Fe(NO3)3]; a 100 microM concentration of the 1:1 Fe3+-NTA complex eliminated the delay due to 100 microM Fe2+, whereas 400 microM Fe(NO3)3 reduced the delay from 17.5 to 2.5 min. Incubation under reduced O2 tension demonstrated a requirement for O2 during the delay. The use of antioxidants [butylated hydroxytoluene, (+)-catechin, promethazine, and uric acid] and inhibitors of the Haber-Weiss reaction (mannitol, Tris buffer, dimethyl sulfoxide, catalase, and superoxide dismutase) indicated that the initiating species has characteristics of a weak oxidizing radical capable of either hydrogen or electron abstraction from suitable target molecules. We hypothesize that the delay that is sensitive to the Fe2+:microsome ratio is due to reductive elimination of the initiating species by "free" Fe2+. The nature of the initiating species has yet to be determined; however, the argument is presented that the perferryl ion (Fe3+-O2-.) may possess the characteristics required for the initiator.

Animals↗

PubMed1995

The effect of protoporphyrin on the susceptibility of human erythrocytes to oxidative stress: exposure to hydrogen peroxide.

Binding of protoporphyrin caused a perturbation of the erythrocyte membrane, as reflected by a change in cell shape from discoid to echinocyte, and a concomitant increase in mean cellular volume and K(+)-loss. Protoporphyrin-induced changes could be prevented by the presence of BaCl2, whereas binding of protoporphyrin was not affected. Exposure of erythrocytes to hydrogen peroxide leads to K(+)-leakage and lipid peroxidation. In de presence of protoporphyrin, H2O2-induced K(+)-leakage was enhanced, whereas lipid peroxidation was inhibited. The increase in H2O2-induced K(+)-leakage by protoporphyrin was not affected by diamide or various K+ channel blockers, but could be prevented by the addition of BaCl2. The inhibition of lipid peroxidation, on the other hand, was not affected by BaCl2. These results indicate that the enhancement of H2O2-induced K(+)-leakage was most likely caused by the change in cell shape. Addition of chlorpromazine and promethazine, positively charged molecules that induce stomatocytosis, did not cause an enhancement of H2O2-induced K(+)-leakage.

Cell Size↗

PubMed1983

Inhibition of synexin activity and exocytosis from chromaffin cells by phenothiazine drugs.

Synexin activity was found to be inhibited by low concentrations of the phenothiazine drugs, trifluoperazine and promethazine. Both drugs were also similarly effective at blocking nicotine and veratridine-induced catecholamine secretion from cultured chromaffin cells. These data thus indicate that synexin may be a target of phenothiazine drugs when they block secretion from chromaffin cells.

Adrenal Medulla↗

PubMed1986

[3H]mepyramine binding to histamine H1 receptors in bovine retina.

The promethazine-sensitive [3H]mepyramine binding was used to determine the presence of histamine H1 receptors in membranes from bovine retina. Specific mepyramine binding to retinal membranes was reversible, saturable and of high affinity. The apparent dissociation constant (KD = 2.2 +/- 0.4 nM) and the density of binding sites (Bmax = 60.9 +/- 5.1 fmol/mg protein), obtained in equilibrium studies, were similar to those found in bovine brain cortex. Binding was stereospecific and the inhibitory potencies of H1 and H2 antagonists indicated that [3H] mepyramine binding sites in the retina have characteristics of H1 receptors.

Aminopyridines↗

PubMed1982

Dissociation of cell death from covalent binding of paracetamol by flavones in a hepatocyte system.

Paracetamol metabolism and toxicity were studied in isolated rat hepatocytes. Cell damage, due to paracetamol, was shown to be dose dependent and was worse in cells from animals pre-treated with phenobarbitone. Exposure to 10 mM paracetamol for 1 hr caused a loss of intracellular reduced glutathione (GSH) and a later progressive leakage of isocitrate dehydrogenase (ICD). Treatment with (+)catechin, 3-O-methyl(+)catechin and promethazine reduced or prevented the paracetamol-induced ICD leakage. Similarly, studies on covalent binding of paracetamol showed that 3-O-methyl(+)catechin, which "protected" the cells, did so without affecting the amount of material bound covalently to cellular protein. Incubation in tissue culture for 24 hr, after prior treatment with paracetamol +/- the protective agent, showed that the protected cells remained viable and attached to tissue culture plates much better than did the "unprotected" cells. These results suggest that the protective effect is much more than just a temporarily delayed cell death. GSH loss and covalent binding of paracetamol metabolites to cell protein are not sufficient causes of cell death, although they may act as starting points in the chain of events leading to cell death.

Acetaminophen↗

PubMed1982

Striatal synaptosomal tyrosine hydroxylase activity. A model system for study of presynaptic dopamine receptors.

Tyrosine hydroxylase activity determined in striatal synaptosomes by the formation of [3H]H2O from [3,5-3H]tyrosine was used as a system for determining receptor affinities of neuroleptic drugs for the dopamine autoreceptor. Four agonists were tested for their abilities to inhibit tyrosine hydroxylation, and the order of potencies was apomorphine greater than dopamine greater than norepinephrine and buspirone was inactive. The abilities of different neuroleptic drugs to shift the IC50 of apomorphine (500 nM without additional drugs) were used to calculate KB values for each drug. The butyrophenones and (+)butaclamol were the most potent of the drugs tested, while (-)sulpiride and thioridazine were very weak inhibitors of apomorphine. Clozapine, promethazine, (-)butaclamol and (+)sulpiride were all inactive. The order of potencies of antipsychotic drugs at the dopamine nerve-ending autoreceptor correlated closely with clinical dose, but it did not correlate with previous reports of displacement of radiolabeled dopamine or apomorphine striatal membrane binding. This observation combined with the fact that the IC50 of apomorphine at this functional receptor was 100 times the concentration needed to saturate its binding site(s) in radioligand receptor assays suggests that the dopamine autoreceptor is not labeled by nanomolar concentrations of apomorphine or dopamine.

Animals↗

PubMed1985

Inhibitory effect of phenothiazine derivatives on bone in vivo and osteoblastic cells in vitro.

We tested the inhibitory effects of phenothiazine derivatives on bone in vivo and osteoblastic cells in vitro. Chlorpromazine (CPZ) and trifluoperazine (TFPZ) dose-dependently decreased alkaline phosphatase activity in calvariae of rats: half-maximal inhibitory effects of CPZ and TFPZ were at 2.0 and 4.0 mg/kg, respectively. These effects were more specific for calvaria and ileum than for liver and duodenum. CPZ inhibited the proliferation of osteoblastic clone MC3T3-E1 cells to a greater extent than that of liver epithelial clone RLC-18(4) cells in vitro. CPZ, TFPZ and perphenazine (PNZ) also affected rather specifically alkaline phosphatase activity and collagen synthesis and were not cytotoxic. These in vivo and in vitro findings suggest inhibitory effects on osteoblastic cell function(s). However, promethazine (PMZ) had little effect in vivo and in vitro. In addition, increases in serum calcium and phosphate induced by CPZ indicate its possible involvement in bone resorption.

Alkaline Phosphatase↗

PubMed1986

Role of redox cycling and lipid peroxidation in bipyridyl herbicide cytotoxicity. Studies with a compromised isolated hepatocyte model system.

The role of active oxygen species and lipid peroxidation in the toxic effects of diquat, paraquat and other bipyridyl herbicides remains controversial. In vitro studies have shown that these compounds are potent generators of active oxygen species by redox cycling and that they stimulate lipid peroxidation. In vivo studies have failed, however, to show clear evidence of lipid peroxidation resulting from toxic exposures to these compounds. We have directly compared the abilities of three bipyridyl herbicides, diquat (DQ), paraquat (PQ) and benzyl viologen (BV), to generate superoxide anion radical (O2-.) in rat liver microsomes and H2O2 in hepatocytes and correlated this with their relative toxicities to a compromised isolated hepatocyte system. DQ was the most potent generator of O2-. and H2O2, being slightly more potent than BV and much better than PQ. This ability of the bipyridyls to generate active oxygen was positively correlated with the ability to induce toxicity in hepatocytes pretreated with 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) to inhibit their glutathione reductase activity, i.e. DQ greater than BV greater than PQ. DQ caused a rapid depletion of cellular GSH and a concomitant increase in GSSG in this system. Toxicity, measured as loss of plasma membrane integrity, was pronounced after only 30-60 min of incubation and was accompanied by a significant increase in lipid peroxidation. The onset of lipid peroxidation could not be separated temporally from the expression of toxicity. However, the total inhibition of lipid peroxidation by the antioxidants Trolox C, promethazine and N,N'-diphenyl-p-phenylenediamine only delayed toxicity, indicating that, even though lipid peroxidation may play some role in enhancing bipyridyl herbicide toxicity, it is not essential for the toxicity to manifest itself.

Animals↗

PubMed1987

Characterization of histamine type 1 receptors on natural suppressor lymphoid cells.

Using the radioligand H1 antagonist [3H]pyrilamine, we have characterized the histamine type 1 receptor on cloned murine natural suppressor cells (NS). A single, specific binding site for [3H]pyrilamine exists on these cells. The binding was saturable and reversible by various specific H1 receptor antagonists. The rank order of potency for displacement of [3H]pyrilamine binding from the H1 receptor by H1 receptor antagonists was promethazine = pyrobutamine greater than pyrilamine greater than diphenhydramine greater than chlorpheniramine. The histamine type-2 agonists, impromidine and dimaprit, and antagonists, cimetidine and ranitidine, as well as selected non-histamine agonists, did not displace [3H]pyrilamine from its binding sites on the natural suppressor cells. The data indicate that the theoretical KD was 1.1 +/- 0.3 X 10(-7) M while the measured KD of binding for [3H]pyrilamine was 6.0 +/- 0.8 X 10(-8) M; the maximum binding was 4.13 nM and the number of binding sites/cell was 2.14 +/- 0.29 X 10(6) (N = 3).

Animals↗

PubMed1990

Menadione and cumene hydroperoxide induced cytotoxicity in biliary epithelial cells isolated from rat liver.

Biliary epithelial cells (BEC) and parenchymal cells isolated from normal rat liver were exposed in vitro to a number of toxic compounds. BEC were found to be highly sensitive to concentrations of menadione (100 microM) and cumene hydroperoxide (10 microM) that are usually not effective as toxic agents in hepatocytes under normoxic conditions. On the other hand, BEC were not affected by concentrations of carbon tetrachloride or 7-ethoxycoumarin that are known to exert toxic effects on hepatocytes. The development of both menadione- and cumene hydroperoxide-induced toxic injury in BEC followed a common and time-correlated pattern, and included a strong depletion of GSH, depletion of protein thiols and an increase in the extent of cell death. The damage induced by cumene hydroperoxide was found to be independent of lipid peroxidative processes and was prevented by a pre-incubation with desferrioxamine. The cytotoxicity of menadione was further exacerbated by dicoumarol but was not prevented by desferrioxamine or promethazine. The mechanisms underlying BEC injury and death induced by the quinone and by the organic hydroperoxide are discussed in relation to the known biochemical characteristics of BEC.

Animals↗

PubMed1995

Characterization of the potential antioxidant and pro-oxidant actions of some neuroleptic drugs.

It has been suggested in the literature that neuroleptic drugs may be able to exert antioxidant and/or pro-oxidant actions in vivo. The feasibility of this was tested by measuring the ability of chlorpromazine, prochlorperazine, metoclopramide, methotrimeprazine and haloperidol to scavenge biologically relevant oxygen-derived species in vitro. None of the drugs reacted with superoxide radical at a significant rate. Chlorpromazine, prochlorperazine, metoclopramide and methotrimeprazine were very powerful scavengers of hydroxyl radicals, reacting at almost a diffusion-controlled rate. Chlorpromazine showed some ability to inhibit iron ion-dependent hydroxyl radical formation. Chlorpromazine, methotrimeprazine, promethazine and prochlorperazine were powerful inhibitors of iron ion-dependent liposomal lipid peroxidation, scavengers of organic peroxyl radicals and inhibitors of haem protein/hydrogen peroxide-dependent peroxidation of arachidonic acid. Chlorpromazine, prochlorperazine, metoclopramide, methotrimeprazine and haloperidol were powerful scavengers of hypochlorous acid. Haloperidol showed no ability to inhibit lipid peroxidation or to scavenge peroxyl radicals, and reproducibly increased lipid peroxidation catalysed by haem proteins, in both the presence and absence of hydrogen peroxide. The relevance of these in vitro observations to events in vivo is discussed.

Antioxidants↗