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 47-year-old man had an episode of severe respiratory failure after acute intoxication with arsenic. Features of the initial clinical presentation included nausea, vomiting, and diarrhea, acute psychosis, diffuse skin rash, and marked pancytopenia. A peripheral neuropathy then developed which resulted in severe weakness of all muscles of the limbs, the shoulder and pelvis girdles, and the trunk. The neuropathy continued to progress despite treatment with dimercaprol (BAL in oil). Five weeks after the initial exposure, the patient was no longer able to maintain adquate ventilation and required mechanical ventilatory support. Improvement in the patient's neuromuscular status permitted successful weaning from the ventilator after one month of mechanical ventilation. Long-term follow-up revealed no further respiratory difficulty and slow improvement in the strength of the peripheral muscles.
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PMID:Acute respiratory failure following severe arsenic poisoning. 22 46

An acute respiratory distress syndrome in 10 adult dogs was usually preceded by vomiting, anorexia and lethargy followed, after a short interval, by dyspnoea. The dyspnoea became increasingly severe, despite oxygen therapy, and cyanotic respiratory failure ensued. All 10 dogs died or were killed after illnesses lasting between one and eight days. Necropsies revealed pulmonary congestion, oedema, collapse and haemorrhage with loss of alveolar epithelial cells. Early alveolar fibrosis was also found. Paraquat was identified in post mortem samples from four of the 10 dogs.
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PMID:Acute respiratory distress in the dog associated with paraquat poisoning. 86 Mar 82

Hereditary coproporphyria is biochemically distinct from the other porphyrias and is characterized by excessive excretion of coproporphyrin in faeces and usually in urine. The laboratory findings in 28 patients with this disease are presented and the clinical details of eight patients who have been in attack summarised. The remaining 20 patients were latent for the disease. In all patients studied the activity of delta-aminolaevulinic acid synthase was raised and coproporphyrinogen oxidase depressed in the leucocyte. This indicates the partial enzyme block in the haem biosynthetic pathway in this disease. The activities of the other enzymes in the pathway, leucocyte ferrochelatase and erythrocyte delta-aminolaevulinic acid dehydratase, porphobilinogen deaminase and uroporphyrinogen decarboxylase showed no consistent change. On review of 111 cases, 35 per cent presented in acute attack: 80 per cent had abdominal pain, 34 per cent vomiting, 29 per cent solar sensitivity, 23 per cent neurological involvement, 23 per cent psychiatric symptoms and 20 per cent severe constipation. Only two fatalities have been published, both from respiratory failure. There was a female preponderance of cases in attack of 2-5:1 and in the latent cases of 1-5:1 suggesting hormonal provocation in the uncovering of the disease. Drugs were implicated as precipitating 54 per cent of acute attacks and in 34 per cent of cases, these were barbiturates. This study demonstrates the reduction in activity of coproporphyrinogen oxidase in the haem biosynthetic pathway and the elevation of delta-aminolaevulinic acid synthase in the peripheral blood. These features, together with the typical abnormal porphyrin excretion pattern, appear to be diagnostic of hereditary coproporphyria whether in attack, remission, or in the latent form.
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PMID:Hereditary coproporphyria. Demonstration of the abnormalities in haem biosynthesis in peripheral blood. 86 76

These agents act as anticholinesterases. Signs of toxicity are: overactivity of the parasympathetic nervous system, nausea, vomiting, diarrhea, sweating, abdominal cramps and copious secretions. Large doses may cause sustained depolarization of the motor end plate, leading to muscular paralysis. Death may ensue from respiratory failure. The extensive and often careless use of insecticides, fungicides and pesticides makes organophosphates a particular pediatric hazard. Atropine and pralidoxime chloride are effective for therapy.
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PMID:Organophosphates--a pediatric hazard. 113 Feb 47

The clinical and pathological features of 28 fatal cases of acute uncomplicated massive cerebellar infarction are reviewed. Although infarcts may involve any portion of the cerebellum, they predominantly involve the posteroinferior half of one cerebellar hemisphere. The frequency of acute uncomplicated fatal cerebellar infarction is much greater than previously appreciated, approximating that of acute fatal cerebellar hemorrhage. All patients were past middle age. Atherosclerosis and acute vertebral artery occlusion were the most common etiological factors. The onset was sudden in most cases, with vomiting, dizziness, vertigo, and cerebellar dysfunction. All patients died with progressive brain stem dysfunction and medullary respiratory failure secondary to compression by a swollen cerebellum. Death usually occurred between the third and sixth days following the onset of symptoms, but only six to 30 hours after the onset of obtundation; therefore, decompressive therapy must be instituted promptly.
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PMID:Cerebellar infarction. A clinicopathological study. 113 Oct 69

We reported a clinical course and autopsy results of an 8-year-old severely handicapped girl with marked periventricular leukomalacia. She was well until 3 days prior to first admission in local hospital. Two days prior to admission, she began to vomit. Twelve hours later, she was noted to be lethargic and developed malaise with frequent vomiting. At physical examination on admission, she had frequent fits and her posture was decerebrate rigidity. Consciousness disturbance continued for two weeks. Thereafter, she became severely handicapped with spastic quadriplegia, mental retardation and intractable epilepsy. She was transferred to our hospital one month later. We cared her totally and carefully with our rehabilitation staff, but during her course several rare happening occurred; she suffered from subdural hemorrhage due to hypocupremia and received an operation for the release of contracture of her hips. She died of acute cardio-respiratory failure at 8 years and 5 months of age. Her autopsy findings were characteristic of the damage to an immature brain during development; cactus formation of cerebellar cortex and periventricular leukomalacia.
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PMID:[A clinical course and autopsy results of an 8-year-old severely handicapped girl with marked periventricular leukomalacia]. 138 94

The histological and histochemical findings in the respiratory muscles of a patient with severe neonatal nemaline myopathy are described. The patient suffered from frequent pneumonia associated with vomiting due to gastroesophageal reflux and died at 3 months from respiratory failure. The diaphragm was moderately involved and the intercostal muscles mildly involved. Core/targetoid structures were observed in the diaphragm and intercostal muscles.
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PMID:Severe neonatal nemaline myopathy--histological and histochemical studies of respiratory muscles. 162 19

Bleomycin is well recognized as an active antineoplastic agent in the treatment of germ cell tumors. Pulmonary toxicity is the most significant complication of bleomycin administration. In this report, an attempt is made to modify both the incidence and severity of this side effect. One hundred eleven patients with advanced germ cell tumors were treated with a combination chemotherapy program that included the administration of 30 units (U) of bleomycin as a continuous infusion daily for 3 days every 3 weeks rather than a weekly bolus injection of a total of 360 U (mean dose received, 307 U). Also, 31 patients received high-dose steroids, which have been shown to modify bleomycin-induced pulmonary toxicity, for the treatment of chemotherapy-induced emesis. Changes in carbon monoxide diffusion capacity (DLCO) prompting cessation of bleomycin therapy occurred in 15 cases (bleomycin was stopped in one case due to dyspnea and lung infiltrates, and one patient suffered fatal respiratory failure probably due to bleomycin lung toxicity). Thus, probable bleomycin pulmonary toxicity changed the clinical treatment in 15.3% of the cases. On long-term follow-up, only two patients have demonstrated a residual decrease in DLCO. The incidence of a greater than 25% decrease in DLCO was 34% and was not significantly altered by the administration of steroids (P = 0.96). It is possible, however, that the low incidence of clinically significant and fatal pulmonary toxicity, as experienced in this group of patients, may be related to the infusion of bleomycin. It also is possible that the reversibility of the decrease in DLCO in 95% of the patients may be related to the duration and schedule of bleomycin administration. As bleomycin continues to be an important drug in the treatment of advanced germ cell tumors, further studies are warranted to evaluate the role of the continuous infusion of bleomycin as opposed to bolus therapy.
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PMID:The effect of corticosteroid administration on bleomycin lung toxicity. 168 6

A 64-year-old man was admitted to our hospital with leukopenia. On admission, leukocyte count in the peripheral blood was 1,600/microliters, containing 24.5% blasts of lymphoid appearance, which were negative for myeloperoxidase. A bone marrow aspiration showed hypoplasia with increased blasts (31.6%). The blasts were ultrastructurally positive for platelet peroxidase (PPO) and positive for platelet membrane glycoprotein IIb/IIIa complex. A diagnosis of acute megakaryoblastic leukemia was made. Chemotherapy with behenoyl-ara C (BH-AC) (150 mg/day) was transiently effective. However, after three months, numerous nodules without itching appeared over the entire body, particularly on the anterior chest. A biopsy of the skin lesion revealed a diffuse fibrosis with infiltrations of the blasts. Bone marrow aspirations were dry tap, and a bone marrow biopsy showed marked myelofibrosis. Then, severe headache, vomiting, and loss of consciousness developed, and a lumbar puncture revealed infiltrations of blasts. Although methotrexate was intrathecally injected, he died due to the respiratory failure. As far as we know, a case of acute megakaryoblastic leukemia with leukemia cutis and meningeal leukemia is quite rare. In addition, it is interesting that megakaryoblastic leukemia was accompanied with both the fibrosis of skin and the myelofibrosis.
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PMID:[Acute megakaryoblastic leukemia with leukemia cutis, meningeal leukemia, and myelofibrosis]. 175 56

The diagnosis of acute arsenic poisoning should be considered in any patient presenting with severe gastrointestinal complaints. Signs and symptoms include nausea, vomiting, colicky abdominal pain and profuse, watery diarrhea. Hypotension, fluid and electrolyte disturbances, mental status changes, electrocardiographic abnormalities, respiratory failure and death can result. Quantitative measurement of 24-hour urinary arsenic excretion is the only reliable laboratory test to confirm arsenic poisoning. Treatment includes gastric emesis or lavage, chelation therapy, electrolyte and fluid replacement, and cardiorespiratory support.
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PMID:Acute arsenic intoxication. 268 77


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