Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A now 10 month old female infant suffered from persistent non ketotic neonatal hypoglycemia despite continuous intravenous application of glucose (greater than 10 mg/kg/min). There was only a transient response of blood glucose after intravenous administration of glucagon and prednisolon. Biochemical findings indicated hyperinsulinismus (insulin level of 26 mE/ml during hypoglycemia). Oral diazoxid treatment in high doses (22 mg/kg) stopped hypoglycemia episodes for several days but the newborn remained glucose infusion depended. Finally the treatment had to be interrupted because of vomiting. At the age of 4 1/2 weeks a subtotal pancreatectomy was performed. The histological examination of the pancreas confirmed the clinically suspected diagnosis of nesidioblastosis. After pancreatectomy the infant required insulin therapy. Since six months the girl is without insulin in a good condition. Despite periods of arrested head growth before pancreatectomy the psychomotoric development is normal.
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PMID:[Persistent neonatal hypoglycemia in nesidioblastosis of the pancreas]. 232 89

During treatment of four type-1 diabetics (aged 20-46 years) by continuous subcutaneous insulin infusion (CSII) a leak developed in the system which caused severe ketoacidosis. The gastrointestinal symptoms (nausea, vomiting and abdominal pain) were misdiagnosed by both the patients and their doctors because there was only mild hyperglycaemia. These observations highlight the importance of carefully instructing and supervising patients at the beginning of CSII and point to the need of frequent urine testing by the patients, also for urinary keto bodies.
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PMID:[Diabetic ketoacidosis during insulin pump therapy]. 249 65

A 68-yr-old man had developed intractable vomiting soon after recovering from a flu-like illness. The use of Compazine as an antiemetic produced classic dystonic manifestations which resolved rapidly after discontinuation and treatment with Artane. However, he later developed a variety of neurobehavioral disturbances which led to his admission to the hospital. Extensive diagnostic procedures failed to identify any gastrointestinal or neurological causes. His condition unceasingly worsened until hypocortisolemia was serendipitously discovered, and all of his symptoms disappeared rapidly and completely with glucocorticoid replacement. Over the course of hospitalization, other than a single episode of orthostatic hypotension, the patient did not manifest any signs of adrenal insufficiency or endocrinopathy. Although detectable, his plasma ACTH level was markedly low in the presence of hypocortisolemia. His adrenal function was subnormal in the cortisol response to ACTH stimulation. His renin-angiotensin-aldosterone system and catecholamine levels were normal. He had normal pituitary responses to GnRH, TRH, and insulin, with rises in plasma levels of LH, FSH, TSH, PRL, and GH, but no stimulation of ACTH. Repeated CRH tests revealed no stimulation of ACTH and cortisol. No circulating anti-ACTH, antiadrenal, or antipituitary antibody was detected. We conclude that this elderly patient had a rare syndrome of selective corticotroph dysfunction which resulted in secondary adrenal failure and exacerbated his mental and neuromuscular abnormalities. To our knowledge, these symptoms, which clearly relate to hypocortisolism, have not been previously reported.
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PMID:Delirium and neuromuscular symptoms in an elderly man with isolated corticotroph-deficiency syndrome completely reversed with glucocorticoid replacement. 255 16

A 57-year-old white man presenting frequent recurrent chest and precordial pain, heartburn (pyrosis) and post-prandial vomiting for the previous 33 years (one to two years after Bilroth II gastrectomy) was submitted to cardiovascular, endoscopic, radiologic and biochemical studies with negative results. Doctors recommended surgical operation because of an excessively long afferent loop, Several biologic markers were performed at our hospital (intestinal pharmacomanometry, i.m. clonidine test, plasma neurotransmitters plus hormones, oral glucose tolerance test, plasma insulin, etc.), revealing an autonomic nervous system (ANS) imbalance characterized by hyperactivity of the cholinergic plus hypoactivity of the noradrenergic central system. Psychiatric evaluation demonstrated Dysthymic Depression. Treatment with a small daily dose of amitriptyline (a drug which enhances central noradrenergic activity and exerts powerful anticholinergic effects) suppressed symptoms, normalized physiological plus hormonal plus neurochemical parameters and made depressive manifestations disappear. The results suggest that the ANS imbalance was related to depressive syndrome and potentiated by neurohumoral disorders depending on duodenal and jejunal exclusion, and on intestinal post-prandial hyper-osmolarity.
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PMID:Recurrent gastroesophageal symptoms and precordial pain in a gastrectomized man improved by amitriptyline. Physiologic, metabolic, endocrine, neurochemical and psychiatric findings. 257 35

Headaches affecting 117 insulin-dependent diabetic patients were studied. 50 developed 3 varieties of headaches associated with clinical hypoglycaemic episodes: (1) Brief headaches, contemporaneous with cerebral and autonomic symptoms, were relieved within minutes of ingesting carbohydrates (8 patients). (2) Prolonged headaches outlasting hypoglycaemic symptoms by 1-48 (average 4.3) hours, not relieved by food, occurred in 36 patients; 12 of these also had nausea, vomiting or photophobia. (3) Migraine headache. 11 of the 117 patients were migraineurs: in 6 of the 11 their typical migraines (2 classical and 4 common) were induced by hypoglycaemic episodes. 9 of the 50 had 2 types of headaches, easily distinguished by each subject. In the whole series of 117 patients, 9 had never had a headache in their life. The remainder had headaches associated with premenstrual tension, anxiety, alcohol or other causes.
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PMID:Headaches in insulin-dependent diabetic patients. 261 15

Women who are of normal weight and have bulimia nervosa have multiple neuroendocrine disturbances. The reasons for these neuroendocrine abnormalities are not known, but there are reasons to suspect that bingeing and vomiting behavior could be contributory. It is well known that food consumption in healthy volunteers increases plasma insulin, cortisol, and prolactin secretion and suppresses growth hormone secretion, whereas activation of the emetic reflex increases plasma arginine vasopressin (AVP) secretion. The purpose of this study was to investigate the effects of bingeing and vomiting on these hormones. In comparison with healthy control women consuming a large meal, bulimic patients, when bingeing and vomiting, had an exaggerated secretion of either the amount and/or the duration of insulin, cortisol, and prolactin. Vasopressin secretion was not increased during or after bingeing and vomiting, probably because bulimic subjects do not become nauseated. In addition, bulimic patients had significantly reduced baseline plasma prolactin and possibly elevated baseline cortisol compared with controls. In summary, this study supports the presence of neuroendocrine disturbances in bulimia and raises a question as to whether or not excessive and prolonged food consumption (and/or vomiting) are contributory.
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PMID:The effect of bingeing and vomiting on hormonal secretion. 264 57

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.
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PMID:Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis. 267 25

Potassium is one of the most abundant ions in the human body and yet it is difficult to assess potassium balance. Potassium chloride is extensively used as a potassium supplement, both by physicians as a therapeutic modality and by the general public, mostly in the form of salt substitute. Therapeutically, both the oral and intravenous forms of potassium are utilised. Overdose of potassium is not as frequently encountered in clinical practice as hyperkalaemia (excess potassium in the body) due to acute or chronic renal disease. Potassium homeostasis is maintained very delicately and is governed by the daily consumption of potassium and the renal excretion mechanisms. Any change in these or related factors can present as hyperkalaemia. However, potassium overdoses leading to serious consequences do occur. Orally, the dose of potassium has to be large enough so that the normal excretory mechanisms for potassium are overcome and clinical toxicity occurs. It takes a much bigger dose of ingested potassium to produce toxicity in a person with normal renal function than in patients with compromised renal function. Potassium toxicity manifests in significant, characteristic, acute cardiovascular changes with ECG abnormalities. Besides cardiovascular effects, neuromuscular manifestations in the form of general muscular weakness and ascending paralysis occur. Gastrointestinal symptoms manifest as nausea, vomiting, paralytic ileus, and local mucosal necrosis which may lead to perforation. It is imperative when treating hyperkalaemia that the whole clinical picture is taken into account rather than the numerical potassium values. Only the extracellular potassium can be measured in the laboratory, yet 98% of the body potassium is intracellular and cannot be measured. In acute overdose situations due to ingestion of potassium salt, the general principles of treatment for overdoses should be followed. Calcium chloride infusion, dextrose and insulin in water, and correction of acidosis with sodium bicarbonate are helpful in controlling the acute, life-threatening cardiac arrhythmias. These modalities do not remove the excess potassium from the body. That is achieved either by utilising ion-exchange resins or by mechanically removing potassium via haemodialysis. To curtail inadvertent or accidental potassium overdoses, physicians should prescribe any potassium supplements very carefully to their patients and monitor the plasma potassium periodically.
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PMID:Clinical features and management of poisoning due to potassium chloride. 268 36

1. Multiple-barreled microelectrodes were used to record from neurons in the area postrema of anesthetized dogs and to test the responses of the neurons to a variety of substances in this structure, which is known to function as the chemoceptive trigger zone for emesis. 2. The neurons in area postrema were silent at rest but could be "found" by virtue of their response to ionophoretic glutamate. The glutamic response was brief and of short latency with high frequency of discharge. 3. Dog area postrema neurons were also excited by over 20 other substances, including acetylcholine, the biogenic amines, several peptides, and at least two hormones. Not all agents were excitatory, however. 4. The responses to all excitatory agents except glutamate were similar and unusual. All responses showed a relatively long latency (3-20 s), a long duration of excitation (30 s to many minutes), and a low discharge frequency (1-3 Hz). 5. There was a good correlation between substances that were excitatory on area postrema neurons and substances known to cause emesis. Because emesis due to intravenous application of these substances is known to be abolished in animals with ablation of the area postrema, it is very likely that recordings were from the neurons which trigger the response. 6. Because so many substances elicit the same type of response there is a possibility that all utilize a common second messenger. Neurons were not excited by ionophoresis of guanosine 3',5'-cyclic monophosphate (cGMP) but were excited by 8-bromo-adenosine 3',5'-cyclic monophosphate (cAMP) and by forskolin, an activator of adenylate cyclase. 7. Behavioral studies were performed looking for emetic responses in awake dogs following intravenous injection of apomorphine, insulin, angiotensin II, and leucine enkephalin. For each a threshold concentration could be determined, which would consistently evoke emesis. 8. Dogs pretreated with phosphodiesterase inhibitors (theophylline, 3-isobutyl-1-methylxanthine, or RO 1724) showed a shift in the threshold concentration of the above substances that triggered emesis, such that emesis was evoked by lower concentrations than in the control. 9. These results suggest that neurons of the dog area postrema trigger the emetic reflex in response to specific receptors for a great variety of transmitters, peptides, and hormones, and that these receptors act through a common second messenger, cAMP.
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PMID:Excitation of area postrema neurons by transmitters, peptides, and cyclic nucleotides. 289 67

In 10 healthy men, we have compared the respective effects of an intravenous injection of glucagon (1 mg) and an oral glucose load (75 G) in eliciting the release of C-peptide and insulin from the pancreas. Serum C-peptide and insulin concentrations increased respectively to median values of 190% and 500% at 6 minutes after glucagon injection, and 344% and 794% at 30 minutes and 268% and 278% at 60 minutes following glucose ingestion. The oral glucose load was as effective as glucagon injection in testing beta cell function and was free from the unpleasant side effects (nausea, vomiting, syncope) commonly associated with glucagon. We conclude that oral glucose loading is probably the test of choice to elicit C-peptide release when screening populations of normal subjects for adequacy of beta cell function.
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PMID:Comparison of oral glucose loading and intravenous glucagon injection as stimuli to C-peptide secretion in normal men. 295 15


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