Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four male volunteers were given obidoxime tablets in quantities ranging from 1.84-3.58 g in a single dose, or 7.36 g divided into 4 equal doses. With the lowest dose, average peak plasma level of the drug was 1.9 mug/ml and after the highest single dose it was 5.6 mug/ml, both attained 1.5 h after administration. In the multiple-dosed individuals, plasma levels of the oxime increased gradually following each additional dose, reaching a peak of 3.5 mug/ml after the last dose. Thirteen individuals complained of one or more of the following side effects: pallor, nausea, pyrosis, headache, generalized weakness, sore throat, and paresthesia of the face muscles. Activities of blood cholinesterase, glutamic oxalacetic transaminase, glutamic pyruvic transaminase, as well as hematocrit values, heart rate, and blood pressure were not affected. It is postulated that due to the undesirable side effects, the general use of obidoxime tablets should not be recommended. However, prophylactic oral treatment with obidoxime could be considered for persons at high risk of organophosphate poisoning or when parenteral administration might not be feasible.
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PMID:Administration of obidoxime tablets to man. Plasma levels and side reactions. 78 81

1. Three oral glucose tolerance tests were performed in each of 32 symptomatic postprandial hypoglycaemic patients (before placebo, before doxepin therapy and after doxepin therapy). Plasma neurotransmitters were determined in parallel with assays of plasma insulin and glucose levels. 2. Three different types of patients were distinguished. Type I showed a low noradrenaline/adrenaline ratio, high dopamine levels and low platelet 5-hydroxytryptamine (serotonin) levels during basal periods. After a glucose load, late peaks of dopamine and free 5-hydroxytryptamine, which coincided with the symptoms but not with the nadir of plasma glucose, were observed. Type II showed a low basal plasma noradrenaline/adrenaline ratio. After a glucose load, progressive increases in adrenaline and decreases in glucose were seen. Adrenergic symptoms coincided with the nadir of glucose. Although type III patients showed hyperinsulinaemia after a glucose load similar to the other types of patient, they did not show hyperglycaemia, but rather exhibited a sustained and progressive reduction in plasma glucose. These patients were characterized by a high basal plasma noradrenaline/adrenaline ratio, high basal plasma levels of 4-hydroxy-3-methoxyphenylethyleneglycol and high basal levels of platelet 5-hydroxytryptamine, all of which increased after a glucose load. Systolic and diastolic blood pressure decreases paralleled reductions in heart rate and glucose. The nadir of plasma glucose occurred simultaneously with the appearance of symptoms (weakness, heartburn, oppressive chest pain, tension headache, abdominal cramps, dizziness, etc.). Therapy with doxepin led to disappearance of the symptoms within 3-4 weeks. Normalization of all other disordered variables (cardiovascular, metabolic and neurochemical, and the clonidine test) paralleled the disappearance of the symptoms. 3. Symptoms varied in the three types of patients and we conclude that they are related to hypoglycaemia-induced disorders of plasma neurotransmitters, rather than to hypoglycaemia per se. We postulate that an uncoping stress situation (type I and II patients) and depression (type III patients) underlie the physiopathological mechanisms.
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PMID:Doxepin therapy for postprandial symptomatic hypoglycaemic patients: neurochemical, hormonal and metabolic disturbances. 167 82

Enprostil (E), is a semisynthetic E2 prostaglandin with wide-range antisecretory properties. Administered orally E reduced mucosal injury in rats exposed to NSAID and gastric acid. The aim of the present study was to analyze the cytoprotective effect of 7 micrograms of E on the aspirin-induced (500 mg) decrease in gastric transepithelial difference of potential (DP) in a) five healthy volunteers and b) five patients with epigastric heartburn, normal endoscopy and a low gastric DP (mucosal barrier weakness). Aspirin-induced decrease of gastric DP was measured during two four hour periods separated by an interval of two days: a) during a one hour basal period and after three hours after 7 micrograms of E, and b) during a second basal period and one hour after aspirin, E, and then aspirin again. The following parameters were analyzed: maximal drop of DP DP Max (mV), area under the curve of DP drop, AUC (mV.min), and time to return to basal values, TRB (min). In the control group, when E was administered after aspirin, the decrease in DP Max (11.4 +/- 2.3 vs 6.6 +/- 2.1) and in AUC (68 +/- 22 vs 35 +/- 11) was significant (p less than 0.05) as compared with values obtained after aspirin alone. In the patient group, E produced a significant decrease in aspirin-induced DP Max (11.8 +/- 1.9 vs 6.8 +/- 2.4) (p less than 0.003) and in AUC (117 +/- vs 48 less than 22) (p less than 0.006) as well as in TRB (52 +/- 2 vs 37 +/- 10) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of enprostil on changes in the gastric transepithelial potential differential induced by aspirin]. 313 Feb 80

Many patients, who suffer of heartburn or non ulcerous dyspepsia, seem to have a normal gastric mucosa (gastroscopy or histology). Potential difference is a measurement of the efficacity of mucosal barrier, and it drops when healthy volunteers ingest aspirin. By this method it is shown that patients with non ulcerous dyspepsia have a weakness of gastric mucosal barrier. Compare to controls or irritable bowel syndrome, basal potential difference is lower and time to return to basal value after aspirin is longer. This test shows that a trouble of the mucosal barrier exists even if the mucosa seems to be normal at gastroscopy and histology.
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PMID:[Weakened condition of gastric mucosa barrier and hypersthenic dyspepsia]. 396 38

This review examines the interaction of pyridoxal phosphate with select neuroendocrine and neuropharmacological systems and their health related therapeutic implications. Vitamin B6 and its vitamers can be involved in many interactions with a number of drugs as well as the actions of various endocrines and neurotransmitters. Nutritional deficiencies, particularly of vitamins and proteins, can affect the manner in which drugs undergo biotransformation and thus may modify the therapeutic efficacy of certain drugs. In addition to pyridoxine deficiency adversely affecting drug actions, improper supplementation with viatmin B6 can in some instances also adversely affect drug efficacy. A decrease by pyridocxine in the efficacy of levodopa used in the treatment of Parkinsonism is an example. The interrelationships and enzymatic interconversions amony pyridoxine vitamers, both phosphorylated and nonphosphorylated, are briefly discussed, particularly concerning their pharmacokinetic properties. The chronic administration of isoniazid for the prevention or treatment of tuberculosis can produce peripheral neuropathy which can be prevented by the concurrent administration of pyridoxine. An acute toxic overdose of isoniazid causes generalized convulsions, and the intravenous administration of pryidoxine hydrochloride prevents or stops these seizures. The acute ingestion of excessive monosodium glutamate will, in some persons, cause a group of symptoms, including headache, weakness, stiffness, and heartburn, collectively known as the "Chinese Restaurant Syndrome." These symptoms can be prevented by prior supplementation with vitamin B6. It is postulated that the intestinal absorption of zinc is facilitated by picolinic acid, a metabolite of tryptophan. The derivation of picolinic acid from tryptophan depends on the action of the enzyme kynureninase, which is dependent on pyridoxal phosphate. Therefore, the adequate absorption of zinc is indirectly dependent on an adequate supply of vitamin B6. The formation of pyridoxal phospate appears to be indirectly dependent on Zn2++ which activates pyridoxal kinase. Treatment with daily pyridoxine can reverse a state of depression induced in women who take oral contraceptives (OCs). 1 hypothesis to explain this effect is that the OC is somehow causing a deficiency of seroton serotonin in the brain and that the vitamin B6 helps to overcome this deficiency through the stimulation of 5-hydroxytryptophan decarboxylase by pyridoxal phosphate. In sum, the stimulation of 5-hydroxytryptophan decarboxylase by pyridoxal phosphate. In sum, pyridoxal phosphate in physiological concentrations seems to function as an endogenous "down regulator" of several receptor sites, including estrogen, progesterone, and androgen.
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PMID:Drug-pyridoxal phosphate interactions. 608 25

In order to evaluate the influence of cigarette smoking on health conditions, the authors analyzed results of the THI (Todai Health Index) questionnaire, which was administered to male employees of a large-sized enterprise in Osaka between 1984 and 1990. The smoking rate of male employees decreased over this period of time from 62.4% (1984) to 58.3% (1990) in this enterprise. Complaints regarding "respiratory organ", "digestive organ", "circulatory organ", "irregularity of daily life", "impulsiveness", and "many subjective symptoms" significantly increased with the amount of smoking. Many items of physical complaints in the THI questionnaire were also associated with smoking. These were coughing, sore throat, sputum, nausea when brushing teeth, loss of appetite, stomach pain, stomach problems, diarrhea, heartburn, gum problems, bad breath, heavy eyelids, itchy skin, face looked pale, shortness of breath, palpitation, feeling flushed or feverish, back pain, going to bed late and getting up late, weakness or fatigue, irregular meals, irritation, sensitive or nervous, eating salty or greasy food, and heavy drinker. It is therefore important in the health education of individual smokers to put special emphasis not only on the many diseases associated with smoking but also these physical complaints.
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PMID:[Relationship between cigarette smoking and physical complaints]. 831 11

Dysphagia is related to the impairment of food passage from the mouth to the stomach. Globus pharyngis implies the frequent and often painful sensation of a lump in the throat that usually does not interfere with swallowing and may even be relieved by food intake. The diagnosis is based upon a careful history, clinical examination, endoscopy, dynamic imaging (videofluoroscopy, cinematography, videosonography) and electrophysiologic procedures (including pharyngoesophageal manometry, electromyography and pH determinations). Structural lesions of the cervical spine such as diffuse idiopathic skeletal hyperostosis are rare causes of dysphagia. Dysphagia following anterior cervical fusion as well as globus and dysphonia due to dysfunction of the vertebral joints are more likely. Symptoms with swallowing fluids indicate a neurogenic origin. Dyscoordinated swallowing, nasal reflux, dysphonia or general weakness may also occur. Chronic aspiration with respiratory compromize is the main consequence in a variety of neurological disorders as well as in cases of postsurgical dysphagia. Relaxation of the upper esophageal sphincter indicates coordinated muscle movement between the pharynx and esophagus. Dysfunction of the pharyngoesophageal segment may lead to cricopharyngeal achalasia. A dyskinetic sphincter commonly represents an extrapharyngeal cause: i.e., disease associated with gastroesophageal reflux. Disorders of the esophageal phase of deglutition can produce retrosternal pain, heartburn, regurgitation and vomiting, as well as laryngeal and respiratory signs. Esophageal motility disorders include lower achalasia, tumors, peptic strictures, inflammatory diseases, drug-induced ulcers, rings and webs. Motility disorders present with aperistaltic, spontaneous contractions, diffuse esophagospasm, or a hypermotile esophagus. Gastroesophageal reflux with esophagitis must always be excluded, especially in patients with a globus sensation. The multiple features of the appearance of the symptoms of dysphagia and globus makes multidisciplinary approach necessary in order to establish a diagnosis and begin effective treatment.
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PMID:[Deglutition disorders]. 977 28

Four hundred consecutive patients who were referred to a home palliative care program were prospectively surveyed to estimate the prevalence and severity of common symptoms according to the changes in the performance status. Patients were admitted for the presence of different symptoms and psychosocial support. Common symptoms included in a standard form were rated for severity (absent 0, mild 1, moderate 2, severe 3) for each visit. Pain intensity was rated on a numerical scale (0-10). For each level of Karnofsky performance score (K), the frequency and the worse symptom intensity were recorded until patient's death. Data from 370 patients were analyzed. Pain was effectively controlled. In the final stage, it was also less frequently observed, despite the use of lower analgesic doses in the last days of life. The peak of opioid consumption and symptom frequency and severity was found at K40. This was also the most frequent K level at admission. Some symptoms, such as nausea and vomiting, dry mouth, gastric pyrosis, and diarrhea reached a peak in frequency and severity, then decreased with the advanced stage of the disease. Other symptoms, such as dyspnea, drowsiness, weakness, and confusion tended to further increase and to have a peak at the lowest levels of K. Dysphagia and constipation progressively increased in frequency and intensity, but decreased at the end. These findings clarify the actual frequency and intensity of symptoms in a non-selected home care population with advanced cancer.
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PMID:The course of symptom frequency and intensity in advanced cancer patients followed at home. 1098 48

We present a 54-yr-old woman with ectopic corticotropin syndrome caused by a neuroendocrine tumor of the pancreas. At initial presentation, the patient suffered from diarrhea, heartburn, and nonspecific abdominal pain. There was no evidence of Cushing's syndrome. A neuroendocrine tumor in the head of the pancreas with metastases into peripancreatic lymph nodes was diagnosed and completely resected. Fourteen months later, abdominal computed tomography and scintigraphy with (111)In-labeled octreotide suggested relapse of the tumor. The patient again had no evidence of Cushing's syndrome. A second in toto tumor resection was performed. Another 8 months later, the patient developed forgetfulness, depressive episodes, muscle weakness, new-onset hypertension, hypokalemia, plethora, diabetes mellitus, polyuria, and weight loss. Endocrine testing suggested a source of ectopic ACTH production. An octreotide scan showed an intense uptake ventromedial of the left kidney, an area that showed a mass lateral of the superior mesenteric artery on abdominal magnetic resonance imaging. A complete pancreatectomy with splenectomy and left-sided adrenalectomy were performed. At this second relapse, this neuroendocrine tumor clinically had changed its hormonal profile. Immunohistochemically, in contrast to primary tumor and first relapse, we found strong immunostaining for ACTH in tumor cells of the second relapse and a MIB-1 index greater than 20%. To our knowledge, this is the first report describing a pancreatic neuroendocrine tumor that started to secrete ACTH de novo at the time of the second relapse after two former complete tumor resections. This case underscores the pluripotency of neuroendocrine tumor cells and the importance of keeping in mind a possible shift in hormone production during tumor evolution and progression.
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PMID:Pancreatic neuroendocrine tumor with ectopic adrenocorticotropin production upon second recurrence. 1529 97

Myotonic dystrophy (MD) is characterized by myotonic phenomena and progressive muscular weakness. Involvement of the gastrointestinal tract is frequent and may occur at any level. The clinical manifestations have previously been attributed to motility disorders caused by smooth muscle damage, but histologic evidence of alterations has been scarce and conflicting. A neural factor has also been hypothesized. In the upper digestive tract, dysphagia, heartburn, regurgitation and dyspepsia are the most common complaints, while in the lower tract, abdominal pain, bloating and changes in bowel habits are often reported. Digestive symptoms may be the first sign of dystrophic disease and may precede the musculo-skeletal features. The impairment of gastrointestinal function may be sometimes so gradual that the patients adapt to it with little awareness of symptoms. In such cases routine endoscopic and ultrasonographic evaluations are not sufficient and targeted techniques (electrogastrography, manometry, electromyography, functional ultrasonography, scintigraphy, etc.) are needed. There is a low correlation between the degree of skeletal muscle involvement and the presence and severity of gastrointestinal disturbances whereas a positive correlation with the duration of the skeletal muscle disease has been reported. The drugs recommended for treating the gastrointestinal complaints such as prokinetic, anti-dyspeptic drugs and laxatives, are mainly aimed at correcting the motility disorders. Gastrointestinal involvement in MD remains a complex and intriguing condition since many important problems are still unsolved. Further studies concentrating on genetic aspects, early diagnostic techniques and the development of new therapeutic strategies are needed to improve our management of the gastrointestinal manifestations of MD.
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PMID:Gastrointestinal manifestations in myotonic muscular dystrophy. 1660 87


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