We report on a 50-year-old female who developed pulmonary metastasis 12 years following the resection of a thymoma with microscopic capsular invasion. The patient was found to have a mediastinal mass at the age of 18 years; however, she refused to undergo surgery. At the age of 38 years, the patient underwent surgery for resection of the tumor; it was diagnosed as a macroscopically encapsulated thymoma with microscopic capsular invasion. Multiple pulmonary metastases occurred 12 years following the resection of the tumor; all the metastatic masses were resected. Although the patient suffered from myasthenia gravis 4 months following the resection of pulmonary metastases, she remains free of myasthenia gravis with no recurrence of tumor at 2 years post-surgery. Long-term follow-up is essential for the detection of recurrence after resection of a thymoma with microscopic capsular invasion, and surgery could be the best treatment for distant metastasis in case of resectable lesions.
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The use of neuromuscular blocking agents is still controversial in myasthenic patients but rocuronium could be useful after the introduction of sugammadex as a selective antagonist. The aim of the study was to evaluate the use of rocuronium-sugammadex in myasthenic patients undergoing thoracoscopic thymectomy.
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Our results show that beta 2-adrenergic activation by salbutamol is able to inhibit not only the GH rise induced by GHRH, arginine and pyridostigmine, but even the potentiating effect of both arginine and pyridostigmine on the GH response to GHRH. They indicate that catecholamines, acetylcholine and arginine play a major role in GH secretion having opposite influences aimed to balance the function of the hypothalamus-GH-IGF-I axis in man.
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Myographic evaluation of a dose of vecuronium in patients with myasthenia gravis on pyridostigmine therapy.
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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.
Neostigmine (Neo), pyridostigmine (Pyr), and physostigmine (Phy) at low concentrations inhibited acetylcholine (ACh) esterase, thereby indirectly potentiating ACh enhancement of [3H]perhydrohistrionicotoxin (H12-HTX) binding to the channel sites of the nicotinic ACh receptor of Torpedo membranes. However, at higher concentrations, they inhibited ACh action due to their direct binding to the ACh receptor. They displaced binding of [3H]ACh and 125I-alpha-bungarotoxin (alpha-BGT) to the receptor sites with the following order of decreasing potency: Neo greater than Phy greater than Pyr. Furthermore, Neo and Pyr potentiated [3H] H12-HTX binding to the receptor's channel sites. Preincubation of ACh receptors with any of the three carbamates reduced the rate of binding of 125I-alpha-BGT and increased the potency of carbamylcholine in inhibiting 125I-alpha-BGT binding, suggesting that the three carbamates act as partial agonists and potentiate receptor desensitization. Although none of the three carbamates inhibited [3H]H12-HTX binding to the receptor's closed channel conformation, only Phy was a potent inhibitor of [3H]H12-HTX binding to the carbamylcholine-activated conformation. The potency of Phy was not due to the absence of positive charge since Phy methiodide acted similarly. The data suggest that the major action of the three carbamates at nicotinic cholinergic synapses is inhibition of ACh-esterase. Their interactions with the nicotinic ACh receptor are with its "receptor" as well as allosteric "channel" sites, but they differ in their effects. Neo and Pyr act mainly as partial agonists, while Phy is mostly an inhibitor of the channel in the activated receptor conformation.
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There were two Class 1 certificate holders (for professional flying) and six Class 2 certificate holders (for private pilot flying) and three air traffic controllers. The mean and median ages at diagnosis were 53 and 57 yr, respectively, with a range of 28-67 yr. The mean and median intervals from diagnosis to loss of certification were 22 and 11 mo, respectively, with a range of 0 to 108 mo.
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Fifty-two consecutive patients undergoing thymectomies for myasthenia gravis (MG) were evaluated.
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Soman reduced blood and brain cholinesterase (ChE) activity to less than 15% and increased cerebral acetylcholine (ACh) levels to 137.4% of control. When pyridostigmine (P) was used as a prophylactic adjunct, it reduced blood ChE activity to 31.6% of control, failed to significantly alter brain ChE activity, and protected more than 70% of the blood (but not brain enzyme) from phosphonylation by soman. Benactyzine (B) was more effective than atropine (A) in reducing cerebral ACh concentrations, while a combination of the two was more effective than either alone. A prophylaxis of P + A + B was effective in controlling ACh levels in rats poisoned with one LD50 dose of Soman. Since P did not diminish the effects of the cholinolytics on cerebral ACh, this (together with the enzyme data) suggests that the two cholinolytics alone provided the central protection.
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Pyridostigmine without atropine, pyridostigmine with atropine or neostigmine with atropine were used to antagonise neuro-muscular blockade induced by d-tubocurarine in forty otherwise healthy, female patients recovering from gynaecological surgery. Pulse rates fell significantly (P less than 0.01, control heart rate 72 +/- 18 beats/min (M +/- SD) to 55 +/- 13 beats/min) at ten minutes after pyridostigmine (10 mg/70 kg), necessitating administration of atropine (1.25 mg/70 kg) by fifteen minutes after pyridostigmine. After an initial rise in rate, pulse rates also fell significantly (P less than 0.01, control heart rate 70 +/- 12 beats/min to 44 +/- 11 beats/min) at fifteen minutes after injection of neostigmine (2.5 mg/70 kg) with atropine (1.25 mg/70 kg). By contrast when pyridostigmine and atropine were used together, pulse rates rose and then fell, but mean values never fell below control during a twenty-minute observation period. It was concluded that pyridostigmine should not be given alone, but requires the use of atropine to prevent bradycardia. This combination may, however, provide a more stable heart rate than that seen with neostigmine and atropine in usual doses, when these drugs are used to antagonise d-tubocurarine.
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Thousands of soldiers who served in the Gulf War have symptoms that have been collectively termed Gulf War Illness (GWI). It has been suggested that a combination of operational stress and pyridostigmine, a drug given as a pretreatment to protect soldiers against the effects of exposure to nerve agents, might have had unexpected adverse health effects causing these symptoms. Our laboratory has previously modeled operational stress in rats using a paradigm of around-the-clock intermittent signalled footshock. In the present studies, this model was used to investigate the potential synergistic effects of chronic stress and pyridostigmine on physiology and behavior. Seventy-two rats were trained to perform an alternation lever pressing task to earn their entire daily food intake. The rats were then implanted with osmotic minipumps containing vehicle, pyridostigmine (25 mg/ml pyridostigmine bromide) or physostigmine (20 mg/ml eserine hemisulfate). The pumps delivered 1 microl/h, which resulted in a cumulative dosing of approximately 1.5 mg/kg/day of pyridostigmine or 1.2 mg/kg/day of physostigmine, equimolar doses of the two drugs. The rats were then returned to their home cages where performance continued to be measured 24 h/day. After 4 days, 24 of the 72 rats were trained to escape signalled footshock (avoidance-escape group) and 24 other rats (yoked-stressed group) were each paired to a rat in the avoidance-escape group. The remaining 24 rats were not subjected to footshock (unstressed group). Shock trials were intermittently presented in the home cage 24 h/day for 3 days, while alternation performance continued to be measured. Since only 12 test cages were available, each condition was repeated to achieve a final n of six rats per group. Pyridostigmine and physostigmine each decreased blood acetylcholinesterase levels by approximately 50%. Physostigmine also decreased brain cortical acetylcholinesterase levels by approximately 50%, while pyridostigmine had no effect on cortical acetylcholinesterase activity. Alternation performance was impaired on the first day of stress and then recovered. Neither pyridostigmine nor physostigmine affected performance in the absence of stress or increased the effects of stress alone. Corticosterone was significantly increased in the yoked stress group compared to unstressed controls. These data suggest that pyridostigmine does not exacerbate the effects of stress on performance or levels of stress hormones. Furthermore, these data do not suggest that stress enables pyridostigmine to cross the blood brain barrier.
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We have studied the effect of increased cholinergic tone on the GH response to growth hormone-releasing hormone (GHRH) and on GH feedback, using pyridostigmine, an acetylcholinesterase inhibitor. In six healthy male adult volunteers 120 mg oral pyridostigmine increased basal GH secretion compared to placebo and augmented the GH response to 100 micrograms i.v. GHRH (1-29) NH2; the effect was more than the additive effect of pyridostigmine and GHRH when each was given alone. Pretreatment with 2 IU methionyl-hGH given i.v. abolished the serum GH response to GHRH given 3 h later, demonstrating a negative feedback loop of GH on the response to GHRH; this inhibited response to GHRH was restored in subjects given pyridostigmine as well as methionyl-hGH. The data demonstrate that enhanced cholinergic tone releases GH, augments the serum GH response to GHRH and unblocks the negative feedback effect of methionyl-hGH pretreatment on the GH response to GHRH. These results suggest that GH negative feedback effects on its own secretion occur predominantly through increased hypothalamic somatostatin secretion; this somatostatin secretion is under inhibitory cholinergic control.
A coronary patient with myasthenia gravis with a previous myocardial infarction presented with severe ventricular arrhythmias after the replacement of neostigmine by pyridostigmine for the treatment of the myasthenia. These arrhythmias were resistant to antiarrhythmic therapy associating betablockers and amiodarone throughout treatment with pyridostigmine but regressed when this drug was withdrawn. A test of reintroduction of pyridostigmine under medical surveillance led to the reappearance of the ventricular hyperexcitability, so confirming the responsibility of this drug. This would seem to be the first reported case of severe ventricular arrhythmias due to a proarrhythmic effect of pyridostigmine. The possible mechanisms of this effect are discussed.
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Our results indicate that the GH releasable pool is reduced in obesity and, to an even greater extent, in Cushing's syndrome. The inability of pyridostigmine and arginine to restore a normal GH response to GHRH in these conditions makes the existence of a hypothalamic somatostatinergic hyperactivity unlikely.
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Pyridostigmine, which does not cross the blood-brain barrier, increased cardiac vagal tone, and reduced cardiomyocyte diameter and collagen density, but did not affect the AP and plasma cytokine levels. Donepezil, which crosses the blood-brain barrier, attenuated the development of hypertension, increased cardiac vagal tone, and improved AP and PI variability. Likewise, donepezil reduced the plasma levels of tumor necrosis factor-α, interleukin 6, and interferon γ, besides reducing cardiomyocyte diameter and collagen density.
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Randomized, double-blind, placebo-controlled study.
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Somatostatin tone was examined by manipulating cholinergic tone in young adults with radiation-induced GH deficiency and a control population. Each individual underwent three separate studies: the GH response to 100 micrograms GHRH-(1-29)-NH2 was assessed alone, and 60 minutes after pyridostigmine or pirenzepine.
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A good knowledge of the basic mechanisms of acute toxicity of organophosphorus compounds has lead to the development of specific antidotes able to counteract their acute toxic effects. Unfortunately, there are still some highly toxic organophosphorus compounds, called nerve agents, that are resistant to standard antidotal treatment. Relatively unsatisfactory antidotal treatment of acute poisonings with some nerve agents has prompted studies of pretreatment possibilities that would increase the resistance of organisms exposed to nerve agents. Current protection against nerve agent poisoning is pyridostigmine, but its prophylactic efficacy is rather limited. To increase the effectiveness of pharmacological pretreatment of soman or tabun poisoning, a prophylactic mixture called PANPAL and consisting of pyridostigmine and two anticholinergic drugs - benactyzine and trihexyphenidyle was developed, produced and introduced into the Czech Army to protect soldiers against nerve agent exposure. This review describes the evaluation of the potency of PANPAL to counteract acute soman or tabun poisoning and to increase the therapeutic and neuroprotective efficacy of current post-exposure antidotal treatment in comparison with pyridostigmine given alone as pretreatment.
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Compared to phase 1, the addition of carbenoxolone (with or without concurrent fludrocortisone administration) produced statistically significant decreases of 20-50% in mean plasma 17-hydroxyprogesterone, androstenedione, and renin activity. Since carbenoxolone also decreased the apparent metabolic clearance rate of cortisol by 20%, other measures of systemic glucocorticoid activity were examined. Carbenoxolone did not produce a cushingoid appearance or increase body weight, blood pressure, blood glucose or plasma insulin levels. Carbenoxolone also did not suppress stimulated GH levels, but did decrease TRH-stimulated TSH levels by approximately 20% (P < 0.05).
Pyridostigmine was first used extensively during Operation Desert Storm for prophylaxis against the effects of nerve agents. After initial reports of asthma exacerbations following its use, we gave 10 asthmatic and 6 non-asthmatic soldiers a 30-mg dose of pyridostigmine. We found no changes in forced vital capacity in any of the soldiers, but observed exacerbation of asthma symptoms in seven of the asthmatics. Severity of the exacerbation correlated best with severity of asthma in the desert and inversely with body weight. The irritant effect of the dust may predispose asthmatics to worsen after pyridostigmine, an effect not seen in the laboratory.
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These preliminary data suggest that PYRIDO is safe and may be effective at ameliorating the orthostatic fall in BP in select individuals with SCI.