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 32-year-old man was diagnosed as having pseudo-Bartter syndrome due to surreptitious habitual vomiting and to maldigestion related to decayed teeth. His chief complaints were muscle pain and weakness. In this case, metabolic alkalosis, hypokalemia, hypochloremia, increased plasma renin activity and aldosterone levels were noticed with marked decreases in urinary chloride excretion. Creatinine clearance (GFR) and renal plasma flow (RPF) were also decreased. Blood pressure was normal, but the pressor response to angiotensin II was attenuated. Before treatment with 0.9% saline infusion, plasma vasopressin (AVP) was not suppressed sufficiently by lowering the plasma osmolality (Posm) with an oral water load (WL), but it normally responded to a rise in Posm due to hypertonic saline infusion. Moreover, plasma AVP was normally suppressed by WL after the replenishment of saline. Plasma atrial natriuretic peptide (ANP) was low before WL, but increased normally in response to WL. However, inconsistent with the normal response in this case, decreases in plasma AVP failed to dilute urinary osmolality and to increase urine flow, irrespective of the levels of plasma ANP. These results indicate that chronic inanition due to surreptitious vomiting causes impaired renal diluting ability through decreases in GFR and RPF, irrespective of the levels of plasma AVP and ANP.
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PMID:Impaired water diuresis in a patient with pseudo-Bartter syndrome. 153 41

Because of the increasing preference for natural products intoxications induced by consumption of honey will reappear, especially with products bought directly from the beekeeper. In the hospital of Trapezunt about 8 cases of intoxications induced by honey were reported per year. The courses observed appear to be identical to those already described by Xenophon 2400 years ago. Symptoms begin acutely but last rarely for more than 24 hours. Fatal cases are extremely rare. Most prominent symptoms are loss of consciousness, weakness, severe salivation, sweating, vomiting and diarrhea. Beside these symptoms circumoral paresthesias and bradyarrhythmia may occur. Intoxication is induced by certain diterpenes, so called gray-anotoxins, that appear in flowers of different species of rhododendron. Next to close surveillance only symptomatic therapy is generally necessary.
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PMID:[Honey-induced poisoning]. 157 79

In 1983, a previously healthy 21-year old mother came to University Hospital in Dijon, France feeling weak and had a severe frontal headache with vomiting. Clinical and biochemical tests were normal. She smoked 20 cigarettes/day and used a high dosed combined oral contraceptive (OC) (ethinyl estradiol and cyproterone acetate). 15 days later, the headache returned and she could not understand spoken words and the bilateral section of the brain had slowed. Yet her mental status was normal as were cerebrospinal fluid and cerebral computerized tomography tests. The antiherpes virus drug, vidabarine, did not alleviate symptoms. At least 1 month later, a severe left pulmonary embolism caused acute right heart failure. She also had a prethrombotic left iliac vein, so physicians began heparin therapy, adding nifedipine and buflomedil to control the spasms in the right internal iliac artery and both external iliac arteries. Acute ischemia of the lower limbs eased within a week but sensory disorders remained for 2 months. Satisfactory collaterality transpired due to a blocked left external iliac artery and left iliac vein. The following signs and symptoms indicated her condition to be homocystinuria: blond hair with deep blue eyes, macrocytic anemia, factor VII deficit (51%), strong positive Brandt's reaction, cystine homocystine in the plasma, and presence of homocystine, cystathionine, and methionine in the urine. Physicians took her off the OC and discharged her on vitamin B6/day, folic acid/day, betaine citrate/day, and the anticoagulant Coumadin. A subsequent check of her 19-year old sister found she had it too. They assessed the patient's condition yearly. In 1988, her left leg developed edema and she limped when not using elastic stockings. Effects of iliac vein phlebitis were evident. She no longer suffered from headaches. Since plasma methionine was within the normal range and homocystine no longer was present in plasma and urine, the physicians halted the anticoagulant therapy. In conclusion, the OC precipitated this partial form of homocystinuria.
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PMID:Vascular manifestations in homocystinuria. 161 Jun 63

Two hundred dogs with pituitary dependent hyperadrenocorticism (PDH) were treated with mitotane at an initial daily dosage of 21 to 69 mg/kg (mean = 45.2 mg/kg) for 5 to 14 days. During the induction period, 194 of the dogs also were given daily maintenance dosages of a glucocorticoid. Fifty of the dogs exhibited one or more adverse effects during initial induction, including weakness, vomiting, anorexia, diarrhea, and ataxia. After completion of the induction period, repeat ACTH stimulation testing revealed significant decreases in mean serum cortisol concentrations when compared with initial values. Twenty-five dogs, however, still responded to exogenous ACTH with serum cortisol concentrations above normal resting range, necessitating daily treatment for an additional 5 to 55 days. In contrast, 70 of the 200 dogs had low post-ACTH serum cortisol concentrations after the induction period. These subnormal serum cortisol concentrations generally increased spontaneously to within normal resting range 2 to 6 weeks after cessation of mitotane. In 184 dogs, mitotane was continued at an initial mean maintenance dosage of 49 mg/kg administered weekly in two to three divided doses. Of these dogs, 107 had one or more relapses of hyperadrenocorticism during treatment. In the 75 dogs that had one relapse, the median maintenance dosage was increased by approximately 35%, whereas the median maintenance dosage in the 32 dogs having two or more relapses was eventually increased by 225% over the initial dosage. After a mean maintenance treatment time of 2.0 years, the final maintenance dosage required in the 184 dogs ranged from 26.8 to 330 mg/kg/week.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitotane (o,p'-DDD) treatment of 200 dogs with pituitary-dependent hyperadrenocorticism. 165 32

Barium intoxication, a rare cause of hypokalemia, can sometimes result in respiratory paralysis and ventricular tachyarrhythmia. Herein, we report one such case. A 29-year-old man swallowed barium-contaminated fried flour-coated sweet potatoes. Then, abdominal discomfort, vomiting, diarrhea, progressive muscular weakness, apnea and ventricular tachycardia developed and laboratory data revealed profound hypokalemia. He regained his health after mechanical ventilation, anti-arrhythmic agent and aggressive potassium chloride supplement. Analysis of blood, urine and contaminated flour showed the presence of barium carbonate. Barium intoxication is a medical emergency which requires rapid therapy to prevent mortality.
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PMID:[Barium intoxication: a case report]. 168 96

On the 1st of April in 1988, we identified 26 children with Fukuyama type congenital muscular dystrophy (FCMD) among 1,227,000 children in Tokyo whose ages ranged from 6 to 14 years. The prevalence rate of FCMD was 2.1 per 100,000. All affected children attended special school for crippled children. Mean absence from school on account of illness was 33.9 days in a year. Fifteen among 26 affected children had ability of verbal communication. The loss of gross motor function started at ages 6-7 years but muscle weakness might have occurred earlier. Ten affected children were treated with antiepileptic drugs. Six affected children needed to be hospitalized for the treatment of vomiting with dehydration, acute bronchitis, or pertussis infection during one year until the 1st of April in 1989. Two cases among 26 with FCMD died of respiratory complications shortly after admission.
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PMID:[Survey of Fukuyama type congenital muscular dystrophy in Tokyo]. 173 25

Twenty-eight patients with refractory advanced malignancies were treated with a 24 hr infusion of 5-fluorouracil (5-FU), Leucovorin (LV), and N-(phosphonacetyl)-L-aspartic acid (PALA) weekly. Twenty-seven patients were evaluable for the assessment of toxicity and anti-tumor activity. PALA was administered as intravenous bolus over 15 min at a fixed dose, 250 mg/m2 24 hr before the start of 5-FU and LV infusions. 5-FU was initially administered at 750 mg/m2 and was incrementally increased to 2600 mg/m2. LV was administered in a fixed dose of 500 mg/m2 concurrently with 5-FU over a 24-hr period. The course was repeated weekly. Diarrhea, stomatitis, nausea, and vomiting were among dose-limiting toxic effects. Other toxicities observed were hand-foot syndrome, hair loss of scalp/eyelashes, overall weakness, rhinitis, and chemical conjunctivitis. Maximum tolerated dose (MTD) of 5-FU in this combination and schedule was 2600 mg/m2. Seven of 14 patients treated at 2600 mg/m2 were able to tolerate the chemotherapy on a weekly basis without interruption. The other seven patients required dose de-escalation, a majority of whom contained 5-FU at a dose of 2100 mg/m2. Twenty-three of 27 patients had been previously treated. Eight patients achieved a partial response, all of whom were previously treated, except three patients. A complete response was observed in a patient with pancreatic carcinoma, previously untreated. Overall response rate for the patients who were treated at the 5-FU dose of 2100 mg/m2 or 2600 mg/m2 is 9 of 18 patients (50%).
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PMID:Phase I study of high dose 5-fluorouracil and high dose Leucovorin with low dose phosphonacetyl-L-aspartic acid in patients with advanced malignancies. 173 89

The clinical and pathologic features of 15 new cases of the uncommon primary or granulomatous angiitis of the central nervous system (PACNS) are described. To date, only 108 such cases have been reported in the English literature. Clinically, most PACNS patients have been young or middle-aged (mean age, 45 years; range, 3 to 96 years), with men outnumbering women slightly by a ratio of 4 to 3. The most frequent presenting complaints are headache, weakness, and confusion; less common complaints are aphasia, dysphasia, nausea or vomiting, loss of memory, and seizure disorder. There is usually no evidence of a systemic disease; the erythrocyte sedimentation rate is almost invariably normal, and there are no diagnostic laboratory tests. The cerebral angiogram usually shows multifocal, segmental stenosis or irregularity of small and medium-sized leptomeningeal and intracranial blood vessels, often with a beading or aneurysmal appearance, and alterations in blood flow in the affected regions. Anatomically, the angiitis is focal and segmental in distribution. An isolated negative biopsy, therefore, does not rule out the disease. Histologically, PACNS may be granulomatous, necrotizing, or lymphocytic in character, and mixed morphologic types often occur. Large- and small-vessel thrombosis is common. Acute lesions frequently coexist with healing or healed lesions. Involvement of extracranial blood vessels occurs only rarely. Past or current herpes zoster infection and Hodgkin's lymphoma are the most noteworthy clinical associations of PACNS, but whether they are causally related remains uncertain.
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PMID:Primary (granulomatous) angiitis of the central nervous system: a clinicopathologic analysis of 15 new cases and a review of the literature. 174 Mar

Pyridostigmine is known as a pre-treatment drug against intoxication with organophosphorus nerve agents. During the Persian Gulf war, we encountered a cluster of nine cases of pyridostigmine self-poisoning, of which three presented with mixed drug poisoning. The clinical and laboratory features of pyridostigmine toxicity are presented. Doses ranged between 390 and 900 mg. Pyridostigmine ingestion resulted in mild to moderate cholinergic symptoms such as abdominal cramps, diarrhea, emesis, nausea, hypersalivation, urinary incontinence, fasciculations, muscle weakness and blurred vision. No central nervous system manifestations were evident. The symptoms developed within several minutes and lasted up to 24 h. All patients underwent gastric emptying followed by administration of activated charcoal. Atropine (1-8 mg) was required in only three patients. Measurement of serum cholinesterase inhibition was found to be a reliable and sensitive diagnostic tool in pyridostigmine poisoning. No clear correlation was found between the extent of cholinesterase inhibition and the incidence or severity of the cholinergic signs. The clinical recovery was faster than the spontaneous recovery of the enzyme. Pyridostigmine intoxication is self-limited and well tolerated by young healthy adults.
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PMID:Acute pyridostigmine overdose: a report of nine cases. 175 42

A female patient who had clinical characteristics of MELAS but with no apparent muscle symptoms was reported. She was in good health until 12 years and 5 months of age when she began to have afebrile generalized tonic-clonic convulsions. Thereafter, she had repeated stroke-like episodes, including headache, vomiting, convulsions, hemiparesis and left ehemianopsia. She had neither muscle weakness, fatigability nor atrophy. Laboratory examinations disclosed elevated lactate and pyruvate levels in the serum and cerebrospinal fluids, transient focal low density areas on brain CT and right sensorineural deafness by audiometry. No ragged-red fibers (RRF) were found in the first biopsy at 13 years and 6 months of age, and two RRF-like fibers containing red granular materials in the subsarcolemnal regions in the second at 15 years and 3 months of age. A biochemical assay on the two biopsied muscles demonstrated normal enzyme activities in the mitochondrial electron transport system. She was diagnosed as having MELAS because of remarkable mitochondrial abnormalities in smooth muscle cells in the intramuscular arterioles which were clearly demonstrated by succinic dehydrogenase (SDH) stain and on electron microscopy. It was suggested that the stroke-like episodes in this patient were induced by a preferential damage to the mitochondria in the blood vessel walls. Thus, we conclude that a simple method of identifying the strongly SDH-reactive blood vessels (SSV) in frozen sections is critical in supporting or making diagnosis of MELAS.
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PMID:[MELAS without ragged-red fibers: a case report]. 176 Feb 9


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