Autoimmune gastrointestinal dysmotility (AGID) is a limited form of autoimmune autonomic neuropathy occurring idiopathically or in a paraneoplastic context. This disorder is considered rare, but is underrecognized as a cause for GI dysmotilities of varying anatomic extent, severity, and duration. We describe the diagnosis and management of an instructive case.
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Concurrent exposure to pyridostigmine bromide (PB), permethrin (PERM) and/or N,N-diethyl-m-toluamide (DEET) may have contributed to the development of a syndrome that appears to have afflicted military personnel who served during the Gulf War. The present experiment sought to evaluate the behavioral effects of these compounds alone, or in various combinations, in male and female rats. Subjects were exposed to a multiple fixed-ratio (FR) 50, fixed-interval (FI) 2-min schedule of reinforcement. PB dose-dependently decreased FR and FI response rates. FR responding was disrupted by lower doses and there were no differences between the sexes. PERM vehicle administration decreased response rates maintained by both schedules of reinforcement; this was offset by an increase in response rate after the administration of the intermediate dose of PERM. The highest dose of PERM decreased both FR and FI response rates. FR rates in male rats were more disrupted than those in female rats. Only the highest dose of DEET decreased FR and FI response rates in male and female rats. FR rates were more disrupted in female rats than in male rats. Synergistic effects were only observed when FI response rates decreased in male rats upon exposure to half the low dose of PB with half the low dose of PERM or half the low dose of PB with half the low dose of DEET. The results of this experiment thus show that small doses of PB, PERM and DEET disrupt well-established, schedule-controlled behavior in male and female rats in a schedule- and gender-dependent manner; schedule-dependent and gender-dependent synergistic effects were also observed. The mechanism by which the compounds exert these behavioral effects remains to be determined.
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Pyridostigmine increased RR intervals (before: 886+/-27 ms vs. after: 1054+/-37 ms) and decreased QTc dispersion (before: 72+/-9 ms vs. after: 45+/-3 ms), without changing other electrocardiographic variables (PR segment, QT interval, QTc, and QT dispersion).
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Thirty-four patients with a diagnosis of myasthenia were identified from either the hospital's or treating physician's database.
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Among the symptoms that may occur with smoking withdrawal, constipation is relatively frequent, but little studied.
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Mean RE values at 15 minutes, when the maximum effect of pyridostigmine was anticipated, showed a statistically significant difference between groups (53.8 ± 10.5 in group P and 48.0 ± 8.8 in group C; P = 0.030). However, mean SE at 15 minutes showed no significant difference between the two groups (P = 0.066). At 15 minutes, there were significant differences in the TOF ratio between the two groups (P < 0.001).
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Clinical and electromyographic effects of either succinylcholine (Suc) or vecuronium bromide (VEC) were compared during induction and maintenance of neuromuscular blockade for pelvic laparoscopy.
The aim of this study was to investigate the mechanisms by which glucocorticoids inhibit GH secretion in man. In 10 normal volunteers subjects we compared the pattern of GHRH-induced GH release to that elicited by similar challenge given 60 min after a pretreatment with drugs affecting adrenergic and muscarinic cholinergic neurotransmission, both in basal situations and after having induced hypercortisolism. In a first study (P), synthetic GHRH [GRF-(1-29); 1 microgram/kg, i.v.] was administered 60 min after giving placebo. In other experiments, the administration of propranolol (PRO; 40 mg, orally), or clonidine (CLO; 0.300 mg, orally), or pyridostigmine (PD; 120 mg, orally) was followed by GHRH administration 60 min later. These experiments were repeated after giving a nocturnal dose of dexamethasone (DEX; 8 mg, orally at 2300 h). The administration of DEX significantly (P < 0.05) blunted the GH response to GHRH (peaks: 10.7 +/- 3.9 vs. 20.3 +/- 5.5 micrograms/L; DEX vs. P study, respectively). Conversely, either beta-adrenergic blockade (PRO), or alpha 2-adrenergic agonism (CLO), or the enhancement of muscarinic cholinergic tone (PD) significantly increased the GH response to GHRH (peaks: 43 +/- 4.6, 55.6 +/- 5.6 and 51.2 +/- 7, micrograms/L; PRO, CLO, and PD, respectively; P < 0.01 vs. P study). After nocturnal DEX administration, both PRO and CLO, but not PD, were able to reverse the inhibitory effect of DEX on GHRH-elicited GH release (peaks: 39 +/- 5.5, 25.9 +/- 3.9 and 12.9 +/- 3.1, micrograms/L; DEX + PRO, DEX + CLO, and DEX + PD, respectively). However, whereas the potentiating effect of PRO on GHRH-elicited GH release was still observed under hypercortisolism, it was lacking for both CLO and PD when these drugs were given in this situation. These data suggest that the inhibitory effect of glucocorticoid excess on GH release is due to increased hypothalamic somatostatin secretion which appears to be dependent on DEX-induced enhanced beta-adrenergic responsiveness. Moreover, the data further support a major role of hypothalamic alpha 2-adrenergic and beta-adrenergic activities in GH neuroregulation in man.
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Aminostigmin, a novel reversible inhibitor of cholinesterase developed in Russia, has been tried in management of poisoning with cholinolytyics, antihistamine drugs, tricycle antidepressants and derivatives of 1,4-benzodiazepine. The treatment of 144 patients with aminostigmin and 20 patients with galantamin showed close to similar efficacy of these drugs. The scheme of aminostigmin administration is proposed warranting fast relief of cholinolytic syndrome in subjects poisoned with cholinolytics, antihistamine drugs and antidepressants. Benzodiazepines poisoning was unresponsive to aminostigmin. Rare side effects were caused by overdose. Aminostigmin is an effective antidote in cholinolytic poisoning.
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Many factors have been considered as possible causes of the unexplained illness reported by veterans of the Gulf War (GW). In this study, we report an analysis of risk factors and unexplained illness in a population-based sample of GW veterans who underwent clinical evaluation. Multiple risk factors were compared in 241 veterans who met criteria for unexplained illness and 113 healthy controls. Results suggest that GW unexplained illness is most highly associated with combat conditions, heat stress, and having sought medical attention during the GW. When controlling for multiple simultaneous exposures during the GW, interactions around pyridostigmine bromide, insecticides and repellents, and stress were not significant. These results indicate that most unexplained illness in GW veterans cannot be explained by neurotoxic effects of exposures to chemicals that inhibit cholinesterase activity.
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Pyridostigmine is an acetylcholinesterase inhibitor commonly used in the treatment of myasthenia gravis. We describe a patient who developed a rash after recently being started on pyridostigmine and give a general review of leukocytoclastic vasculitis.
The protection afforded by TCP (thienylcylohexylpiperidine), a non-competitive blocker of N-methyl-D-aspartate (NMDA) receptors, against the seizures and lethality produced by 2 x LD50 of soman (62 micrograms/kg, sc), an irreversible inhibitor of cholinesterase, was studied in guinea-pigs. In the presence of additional anticholinergic medication (pyridostigmine: 0.2 mg/kg, sc, 30min prior to soman; atropine sulphate: 5mg/kg, im, 1 min post-soman), TCP pretreatment (2.5mg/kg, im, 30 or 15 min prior to soman) did not generally prevent the appearance of soman-induced status epilepticus but did arrest it after 30-40 min in 80% (TCP-30min) or 100% (TCP-15min) of the convulsing subjects. Moreover, in all subjects treated curatively, TCP was able to interrupt ongoing status epilepticus in approximately 20, 10 or 8 min when it was administered 5, 30 or 60min respectively after the onset of epileptiform tracings on EEG. All of these curatively administered animals survived and recovered remarkably well. On every criteria examined (latency-to-seizure arrest, 24hr-survival rate, clinical recovery), injection of 2.5mg/kg TCP after 90min of seizures appeared slightly less efficient compared to earlier curative administration. Therefore, our study (a) establishes that the previously reported capacity of MK-801 (dibenzocyclohepneimine) to counteract soman toxicity is not unique and could be extended to other non-competitive inhibitors of NMDA receptors; (b) shows that TCP could easily prevent and, above all, interrupt soman-induced seizures; furthermore, TCP appears the first compound ever tested on soman poisoning that still displays satisfactory anticonvulsant activity after such a long duration of initial status epilepticus (90min); therefore, TCP might be of special value for the delayed therapy for soman poisoning; (c) confirms that NMDA receptors are involved in the maintenance of seizures and play an important role in other processes implicated in the overall toxicity (including the lethal respiratory effects) of soman poisoning.
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1. Pyridostigmine bromide was administered subcutaneously (0.4 mumoles/kg) in mice twice a day for 3 weeks. The activities of the predominant (G1, G4 and A12) molecular forms of acetylcholinesterase were determined in diaphragm, extensor digitorum longus (EDL) and soleus muscles. 2. After the treatment the G4 and A12 forms were reduced in diaphragm, but increased in EDL and soleus. One week later all forms were elevated in all three muscles. At 2 weeks the activity had returned to normal in diaphragm but not in EDL and soleus. 3. A single dose of pyridostigmine was administered in mice which had been pretreated for 3 weeks and left untreated for 2 weeks, and in control mice. 4. In the controls there was no significant effect on the enzyme activities in diaphragm up to 5 days, but there were decreases in EDL, and increases in soleus. In the pretreated group all three forms were increased in diaphragm, especially the A12 form. In soleus and EDL there was a prolonged decrease in all forms, although in the soleus the A12 activity remained above normal. 5. Repeated treatment with pyridostigmine caused delayed changes in functional acetylcholinesterase. Furthermore the treatment had altered the sensitivity of the muscles to the drug.
Retrospective noncomparative case series.
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This experiment was designed to assess the effects of acute and repeated administration of pyridostigmine bromide (a carbamate with prophylactic and therapeutic uses) on response acquisition. Experimentally naïve, male Sprague-Dawley rats were exposed to a situation in which lever presses were either immediately followed by food-pellet presentation or after a 16-s resetting delay. Different groups of rats received either one acute administration of pyridostigmine bromide (10 mg/kg, by gavage) or repeated pyridostigmine administration for 7 days (1.5 mg/kg/day, by gavage). Other groups were treated with distilled water for the same period of time. Both acute and repeated pyridostigmine bromide administration decreased serum cholinesterase levels by approximately 50%, but neither treatment affected brain cholinesterase levels in our assay. Acute and repeated drug administration produced the same behavioral effects. Subjects exposed to the 0-s delay conditions obtained many more food pellets than those exposed to the 16-s delay conditions. Administration of pyridostigmine bromide delayed the onset of responding in some, but not all, of the subjects in the treated groups, independent of the delay condition to which they were exposed. Many more responses were observed on an inoperative lever during the 16-s delay conditions than during the 0-s delay conditions, especially during the 16-s delay condition in which subjects had received acute vehicle administration. Whether or not these effects of small doses of pyridostigmine bromide on response acquisition are of central or peripheral origin will need to be determined in future studies, as response acquisition in the present experiment may have been affected by pyridostigmine's effects on gastrointestinal functioning and/or motor activity.
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Following their return from deployment, Gulf War (GW) veterans reported widespread joint and muscle pain at rates that far exceeded those of soldiers returning from other conflicts. It is widely believed that exposure to insecticides, repellants and nerve gas prophylactics contributed to the symptoms of Gulf War Illness (GWI), but an animal model of GW pain has been elusive. In our previous work, we observed that 4-8 weeks exposure to pyridostigmine bromide (PB), permethrin and chlorpyrifos could produce persistent alterations in the physiology of Nav1.9 and Kv7 expressed in deep tissue nociceptors of the dorsal root ganglion. However, behavioral assessments from these same rats were not consistent with a delayed pain syndrome similar to that of GWI pain. In the present studies, we intensified the exposure to anticholinesterases PB and chlorpyrifos while retaining the same dosages. Animals receiving the intensified protocol for 30 days exhibited significant increases in resting for about 8 weeks after exposure. Thereafter, all measures were comparable to controls. Animals treated with intensified anticholinesterases for 60 days exhibited increased resting and reduced movement 12 weeks post-exposure. In whole cell patch studies, muscle and vascular nociceptor KDR and Kv7 ion channels exhibited increased amplitude relative to controls (e.g., normalized current and/or peak conductance) at 8 weeks post-exposures; however, at 12 weeks post-exposure, the amplitude of these currents was significantly decreased in muscle nociceptors. In current clamp studies, muscle nociceptors also manifested increased action potential duration, afterhyperpolarization and increased discharge to muscarinic agonists 12 weeks post-exposure. The decline in activity of muscle nociceptor KDR and Kv7 channel proteins was consistent with increased nociceptor excitability and a delayed myalgia in rats exposed to GW chemicals.
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Pretreatment with 0.015 mg/kg VEC compared to 2 mg alcuronium led to a more pronounced decline in T1% and TOF-ratio (P less than 0.001). The time interval between injection of the intubation dose and complete relaxation (T1% less than or equal to 5%) was shorter in group Suc- than in VEC-pat. (P less than 0.001). Suc provides better intubation conditions than VEC (P less than 0.05). Recovery from muscle relaxation was faster in Suc- than in VEC-pat. (P less than 0.001). During Suc infusion in 8 patients a phase-II block (TOF ratio less than or equal to 30%) was observed.
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There was only a modest non-significant increase in supine blood pressure and PRI. In contrast, acetylcholinesterase inhibition significantly increased orthostatic blood pressure and PRI and reduced the fall in blood pressure during head up tilt. Orthostatic heart rate was reduced after the treatment. The improvement in orthostatic blood pressure was associated with a significant improvement in orthostatic symptoms.
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To compare the pharmacokinetic parameters of pyridostigmine bromide dispersible tablets and common tablets in rabbits.
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PB does not appear to have detrimental physiological or performance consequences at the recommended 30-mg dose, or at twice that dose, when evaluated under non-stressful laboratory conditions.
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Increased age does not alter the outcomes of thymectomy for myasthenia gravis. Older patients can expect to have similar responses and require a similar number of postoperative medications as younger patients, but with a higher short-term morbidity.
We used the comet assay, as a well-established genotoxicity test, to investigate whether malathion, diazinon, pyridostigmine bromide, piperonyl butoxide, silafluofen, and fipronil had genotoxic effects on tonsil specimens taken from 85 patients.
1. The duration of neostigmine or pyridostigmine antagonism of a (+)-tubocurarine (Tc) neuromuscular blockade was determined in the cat anterior tibialis-peroneal nerve preparation with and without ligated renal pedicles. 2. The infusion rate of Tc required to maintain a 90% depression of twitch tension was reduced from 8.8 +/- 1.4 (s.e.) to 3.4 +/- 0.6 mugkg-1 min-1 by renal pedicle ligation. 3. Renal pedicle ligation resulted in an increased duration of antagonism of Tc by both neostigmine and pyridostigmine.
Pyridostigmine bromide (PB) is a reversible cholinesterase inhibitor used for treatment of myasthenia gravis and for prophylactic protection against organophosphate nerve agent. We previously showed PB can induce apoptotic death in rat brain following systemic treatment. To study mechanisms by which PB induces brain cell death, cultured rat cerebellar granule cells were used. Cytotoxicity was determined after exposure to PB (10-1000 microM) for 24 h; a high concentration of PB (>500 microM) significantly increased lactate dehydrogenase release, which was reduced by pretreatment with the antioxidant, N-t-butyl-alpha-phenyl-nitrone (PBN). Apoptosis, as determined by TUNEL staining, was concentration dependent (10-250 microM) after a 24-h exposure and cytotoxicity was confirmed by gel electrophoresis of DNA, release of cytochrome c from mitochondria, elevation of caspase activity, and electron microscopy. The oxidant-sensitive fluorescent dye 2',7'-dichlorofluorescin diacetate was used to detect reactive oxidative species (ROS) generation. Pretreatment with PBN, superoxide dismutase, catalase, or the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) blocked PB-induced ROS generation and apoptotic cell death. Pretreatment with atropine or MK-801 blocked ROS generation and the subsequent neurotoxicity, showing that both muscarinic and NMDA receptors mediate the response. DNA extracted from PB-treated cells revealed oligonucleosomal fragmentation on gel electrophoresis and antioxidants attenuated the DNA fragmentation, providing further evidence for a link of ROS generation and apoptosis. These results indicate that muscarinic receptor-mediated ROS generation is an initiating factor in PB-induced apoptotic cell death and activation of the NMDA glutamate receptor is directly linked to the response.