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 59-year-old man was admitted because of generalized lymphadenopathy with fever and vomiting. His peripheral blood showed leukocytosis with a WBC of 93,500/microliters, and the bone marrow picture revealed a predominance of blast cells. The blasts were negative for peroxidase, alpha-naphthyl butyrate esterase and PAS, and had the phenotype of CD 7, 13 and 33 positive. A diagnosis of AML M0 was made, based on the criteria of the NCI-sponsored workshop in 1988. His initial status had been compromised by acute renal failure which necessitated hemodialysis. He responded partially to chemotherapy consisting of daunorubicin, cytarabine and prednisolone. However leukemia recurred and the patient suffered from various episodes of infection and died six months after admission. The Southern blotting showed the germ line configuration for TCR-beta chain and immunoglobulin heavy chain genes. No messenger RNA was detected for myeloperoxidase, c-myc and c-jun, while c-fms, c-fos and c-myb were expressed on Northern blotting. It is intriguing to detect c-fms and c-fos expression in these poorly differentiated leukemic cells.
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PMID:[A case report of AML M0:CD7, 33 (+) AML M0 case initially presented with cervical lymphadenopathy]. 160 10

A 39-year-old man developed paroxysmal cough, occasional vomiting after cough, and subconjunctival hemorrhage. His illness was complicated by episodes of seizure, with clonic movements of the arms and legs, brief loss of consciousness, and confusion. The episodes were triggered by mild, unremarkable coughing paroxysms. A diagnosis of pertussis was confirmed serologically by measurement of IgG, IgA, and IgM antibodies to pertussis toxin and filamentous hemagglutinin. Serologic studies confirmed the presence of Bordetella pertussis infection in the patient's 10-year-old daughter and suggested that his wife was infected as well. This case report illustrates the occurrence of typical pertussis with serious complications in an adult. Further research is required to determine the scope of this problem and the need for a program of adult immunization against pertussis.
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PMID:Pertussis encephalopathy in an adult: case report and review. 177 35

An 11-year-old boy with asthma had been receiving a controlled release theophylline preparation. He was prescribed fluvoxamine for a depressive disorder and within a week complained of severe headaches, tiredness and vomiting. His serum theophylline concentration had increased from 14.2 mg/L (shortly before fluvoxamine was started) to 27.4 mg/L. Fluvoxamine was withdrawn and theophylline concentrations decreased. Clomipramine was substituted for fluvoxamine with no further problems, and a later theophylline concentration was 13.7 mg/L. Competitive inhibition of hepatic microsomal enzymes by fluvoxamine may have been responsible for the elevated theophylline concentrations and toxicity observed in this case.
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PMID:Toxic interaction between fluvoxamine and sustained release theophylline in an 11-year-old boy. 179 25

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.
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PMID:Management of severe hypercalcemia. 200 13

The need for feeding gastrostomy seems to be increasing in children with neurological impairment and swallowing incoordination. Because gastrostomy can cause or increase gastroesophageal reflux, an antireflux procedure has been advocated at the time of gastrostomy placement in neurologically impaired children. A gastrostomy in the lesser gastric curvature with antirefluxing properties was performed in nine neurologically impaired children. All had severe swallowing incoordination with aspiration and malnutrition. Postoperatively none of the nine patients have demonstrated clinical evidence of vomiting or gastroesophageal reflux. This type of gastrostomy prevents the developement of gastroesophageal reflux by increasing the length of the intraabdominal esophagus and by increasing the acuity of the gastroesophageal angle of His. When compared with an antireflux procedure, it has less complications, shorter postoperative recovery, and is more economical.
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PMID:Gastrostomy with antireflux properties. 226 50

A 31-year-old man being treated for asthma accidently received 3 mg SQ epinephrine. He began retching and vomiting and developed agitation and profuse diaphoresis. He was treated with 5 mg IV labetalol. His symptoms improved significantly, and he required no further treatment. Although he felt a transient increase in his respiratory effort shortly after administration of the drug, he did not develop wheezing or require additional therapy for bronchospasm. The beta-blocking effect of labetalol is greater than the alpha antagonism. The patient exhibited evidence of mild alpha stimulation due to incomplete blockade. This is consistent with previous studies in that labetalol tends to less completely antagonize the alpha effects of a mixed alpha/beta agonist, resulting in a net clinical picture of mild alpha agonism.
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PMID:Labetalol in the treatment of epinephrine overdose. 234 87

A 27 year old male with metastatic testicular carcinoma was treated with cisplatin, vinblastine, and bleomycin (PVB) chemotherapy. After receiving a cumulative dose of 500 mg/m2 of cisplatin, he developed severe nausea and vomiting and had clinical evidence of a cisplatin-induced peripheral neuropathy. His vomiting resolved five weeks after discontinuation of cisplatin. We believe this case represents the first report of gastric autonomic neuropathy induced by cisplatin.
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PMID:Cisplatin-induced gastric paresis. 244 37

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

We report a 9 year-old boy with MELAS. High dosed oral thiamine administration and high fat diet induced remarkable neurological and biochemical improvement. His mother had episodic headaches and hemiplegia, probably MELAS. He complained muscle weakness and repeated episodes of vomiting started from 2 years of age. High levels of serum lactate and pyruvate were recognized, but with no metabolic acidosis. He developed generalized muscle weakness, growth retardation, generalized convulsions and stroke-like episodes at 5 years old. Optic nerve atrophy and mental retardation gradually appeared. A muscle biopsy at 5 years old revealed numerous ragged-red fibers with excess accumulation of lipid droplets and glycogen particles. Scattered fibers had no cytochrome c oxidase (CCO) activity representing focal CCO deficiency. An electron microscopy showed markedly increased number of giant mitochondria filled with markedly proliferated complicated cristae. Pyruvate dehydrogenase complex level in the fibroblasts was within normal ranges. Serum carnitine level was normal. With oral administration of thiamine hydrochloride (1000 mg) and high fat diet (60-70%), muscle weakness improved, and lactate and pyruvate levels in the serum reduced to normal ranges, whereas the mental deterioration, muscle atrophy, pes cavus progressed very slowly. He died from cardiac and renal failures at 9 years old. Autopsied muscles showed a marked decrease in cytochrome c oxidase activity (biochemically 12.8% of the normal level), and almost all muscle fibers had no cytochrome c oxidase activity histochemically. The progression of the MELAS was probably in parallel with the decrease in CCO activity.
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PMID:[A case of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) with progressive cytochrome c oxidase deficiency]. 255 13

Spinal subdural abscess is rare, compared with spinal epidural abscess. The first case was reported by Sittig in 1927. Only 43 cases have been reported throughout the literature. We experienced an atypical fulminant case of spinal subdural abscess, following the operation for intracranial aneurysms. The patient was a 48-year-old male, admitted to our hospital on April 9, 1987 with complaining of sudden headache and vomiting. A lumbar puncture proved subarachnoid hemorrhage (S.A.H.), CT scan revealed saccular aneurysms in left middle cerebral artery and left internal carotid-ophthalmic artery. Radical surgical treatment for those aneurysms was undergone successfully. Neither cerebral ventricular nor cisternal drainage was established. His postoperative course was uneventful until the 9th postoperative day. He suddenly complained of pain in his legs and back, followed by paraplegia, respiratory, and cardiac arrests with clinical course of several hours. Antibiotics had been used for eight days after surgery, and there was no clinical evidence of inflammation sign. For his abrupt aggravation, a spinal infarction was suspected. However, the autopsy demonstrated that the dorsal side of the entire spinal cord was covered with masses of pus, and central necrosis and hemorrhage of the spinal cord mainly occupied the central gray matter; so-called Pencilsharped softening. In this case, the cause of spinal subdural abscess was unclear. But the lumbar puncture performed on the day of admission, was most responsible. Also, the reasons why the clinical course of our case was rapid and fulminant were discussed with preference of spinal abscess to primary spinal circular disorder. 44 cases in the literature, including the presented report, was reviewed. Those symptomatology, predisposing factors, pathogenesis, the extent of spinal subdural abscess, clinical diagnosis, treatment, and prognosis were discussed. Among previous cases, this case was one of the most extensive subdural abscess and fulminant clinical course.
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PMID:[Spinal subdural abscess--report of a case and a review of the literature of 43 cases]. 256 85


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