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

In the etiology of premature labor prostaglandins fulfill a significant role. It is known that indomethacin is a strong inhibitor of prostaglandin synthesis. The effect of indomethacin on premature labor was studied in a prospective randomized double-blind study in 36 patients. Eighteen patients received indomethacin and eighteen received placebo. 200-300 mg of indomethacin was the total dosage in a 24 hours period. The activity of the uterus was monitored with a cardiotocograph. The mean duration of pregnancy and the mean birth weight in indomethacin group (36.4 weeks, 2833 g) were both significantly greater (p less than 0.001) than that in placebo group (31.2 weeks, 2028 g). In the indomethacin group 3 children weighted less than 2500 g compared with 14 in placebo group. In 15 of 18 indomethacin treated patients (83.3%) premature labor was arrested after indomethacin treatment compared with 4 of 18 in the placebo group (22.2%). The indomethacin group had a mean 1 minute APGAR score of 9.3 +/- 0.2 whereas the placebo group showed a score of 7.8 +/- 0.5 (p less than 0.01). Three infants died from respiratory distress syndrome; one in the indomethacin group (1810 g) and two in the placebo group (600 and 1450 g). Autopsies in the infants demonstrated a typical picture of pulmonary atelectasis and hyaline membranes. There was no evidence of premature closure of the ductus arteriosus or pulmonary hypertension. 2 mothers in the indomethacin group suffered minor discomfort i.e. nausea, vomiting and vertigo.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Further study of the inhibition of premature labor by indomethacin. Part II double-blind study. 637 98

Prostacyclin (PGI2) is a bioactive substance produced by vascular endothelial cells, which exerts powerful vasodilative and anti-platelet actions. Patients with pulmonary hypertension have an imbalance between vasodilative PGI2 and vasoconstrictive thromboxane B2 (TXB2). Treatment with vasodilative agents is essential for such patients. Continuous intravenous infusion of PGI2 is an effective treatment of primary pulmonary hypertension in terms of exercise capacity and survival rate. We tested a new stable PGI2 analogue, beraprost sodium (Procyclin, Dornar) suitable for oral administration, in patients with primary and secondary pulmonary hypertension. A short-term study of cardiac catheterization in four patients with primary pulmonary hypertension showed a 15 +/- 12% reduction in mean pulmonary artery pressure in three of the four patients, and a 24 +/- 22% decrease in pulmonary vascular resistance in all four patients. Cardiac index increased by 27 +/- 14% in three of the four patients. Among three patients with secondary pulmonary hypertension, there was a 7% reduction in pulmonary artery pressure in one patient, and a 24 +/- 14% decrease in pulmonary vascular resistance in all three patients. In a long-term study (23 +/- 11 months), NYHA functional class improved from 3.0 +/- 0.7 to 2.4 +/- 0.5 in two of the five patients with primary pulmonary hypertension. Although the radiographic cardiothoracic ratio was not significantly improved, cardiac index increased by 78 +/- 60% in four of the five patients. Only two patients, one with primary and one with secondary pulmonary hypertension, died during the long-term follow-up period. Plasma TXB2/6-keto prostaglandin F1 alpha ratio decreased from 8.1 +/- 8.7 to 1.5 +/- 0.4. The optimal dose remains uncertain, but the initial dosage of 40-60 micrograms/day given in three to four doses for adult patients is considered to be acceptable. Side effects such as flushing face, headache, vomiting, and nausea were mild and resolved when the dose was reduced. Oral PGI2, beraprost, appears to be an effective and possibly adequate substitute for intravenous vasodilators in pulmonary hypertension for both short- and long-term management.
 ...
PMID:[Short- and long-term effects of the new oral prostacyclin analogue, beraprost sodium, in patients with severe pulmonary hypertension]. 864 6

In July 1996 a 43-year-old illiterate Hispanic woman presented with uncontrollable vomiting, palpitations and confusion. In 1994, despite several hospitalisations in other medical centres where a cerebral CT-scan, oesogastroduodenoscopy, colonoscopy and abdominal ultrasound were performed, no satisfactory diagnosis could be found. A psychiatric origin was finally considered. On admission, the laboratory findings showed severe metabolic alkalosis with associated hypokalaemia, confirmatory evidence of vomiting. The ECG showed tremendous P waves (5 mV) in the standard derivations, which can be explained by the hypokalaemia, with multiple supraventricular extrasystoles. Echocardiography and pulmonary scintigraphy ruled out pulmonary hypertension and a pulmonary embolus. After additional discussion with her daughter we discovered that the patient had been treating chronic headaches for years with 4-5 Cafergot-PB suppositories per day. This drug contains 2 mg ergotamine tartrate, 100 mg butalbital, 100 mg caffeine and 0.25 mg belladona alkaloids. As is known, vomiting is a classical symptom of ergotamine intoxication. After rehydration we discovered a megaloblastic anaemia with a folate deficiency compatible with chronic barbiturate intoxication. Folate and iron supplementation allowed a rapid normalisation of the haemoglobin values. Five months after having stopped the Cafergot-PB, the patient was well and did not vomit anymore. The headaches were treated with chlorpromazine with a good result. Despite sophisticated technical means, the diagnosis could only be established after a thorough history taking. This message should be heard in times when high tech medicine tends to obscure the place of a good history taking!
 ...
PMID:[Intractable vomiting, convulsions and megaloblastic anemia: anamnesis, key to diagnosis]. 1043 23

Interstitial lung diseases comprise a heterogeneous group of pulmonary conditions that cause restrictive lung disease of poor prognosis, especially if growth failure, pulmonary hypertension and fibrosis appears. We report on the case of a girl of 11 years of age who suffered from severe nonallergic asthma in early childhood and who developed severe interstitial pulmonary disease caused by gastro-oesophageal reflux at the age of 8 years. This diagnosis was established by lung biopsy, bronchoalveolar lavage and a high amount of lipid-laden alveolar macrophages, 2-level pH measurement and oesophageal biopsy. Because therapy with oral and inhaled steroids failed and Omeprazol showed benificial effects, hemifundoplication according to THAL was performed. At present the lung function is clearly normal and there is no need of any medicaments. Following the history, we can assume the pathological gastro-oesophageal reflux to be the cause of the disease. It is important to state that there were no typical symptoms at any time pointing to gastro-oesophageal reflux disease. The development of pulmonary disease by pathological reflux is very often caused by "silent aspiration". Very typically there are no symptoms such as vomiting, heartburn and pain but only signs of chronic lung disease.
 ...
PMID:[Severe interstitial lung disease from pathologic gastroesophageal reflux in children]. 1044 54

Fetal and neonatal hyperthyroidism are usually produced by transplacental passage of thyroid-stimulating immunoglobulins. Most commonly, the thyroid-stimulating immunoglobulins are a component of active maternal Graves' disease. However, such antibodies may continue to be produced after ablation of the thyroid by surgery, radioiodine, or by the immune mechanisms of Hashimoto's thyroiditis. Other mechanisms that have produced fetal and neonatal hyperthyroidism include activating mutations of the stimulatory G protein in McCune-Albright syndrome and activating mutations of the thyrotropin (TSH) receptor. Fetal hyperthyroidism may be associated with intrauterine growth retardation, nonimmune fetal hydrops, craniosynostosis, and intrauterine death. Features of this condition in the neonate include hyperkinesis, diarrhea, poor weight gain, vomiting, ophthalmopathy, cardiac failure and arrhythmias, systemic and pulmonary hypertension, hepatosplenomegaly, jaundice, hyperviscosity syndrome, thrombocytopenia, and craniosynostosis. The time course of thyrotoxicosis depends on etiology. Remission by 20 weeks is most common in neonatal Graves' disease; remission by 48 weeks is nearly always seen. A subset of these patients may have persistent disease when there is a strong family history of Graves' diseases. Disease persistence is characteristic of patients with activating mutations of the TSH receptor. Treatment of fetal hyperthyroidism comprises administration of antithyroid drugs to the mother. Fetal heart rate and fetal growth should be monitored. Ultrasonography may reveal changes in thyroid size. At times, cordocentesis may be useful for monitoring fetal thyroid function. Hyperthyroid neonates may be treated with antithyroid drugs, beta-adrenergic receptor blocking agents, iodine, or iodinated contrast agents, and at times, with glucocorticoids and digoxin. Nonremitting causes of neonatal hyperthyroidism require ablative treatments such as thyroidectomy.
 ...
PMID:Fetal and neonatal hyperthyroidism. 1044 21

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
 ...
PMID:[Mountaineering and altitude sickness]. 1144 1

The aim of this prospective, randomized, controlled clinical trial was to define the opioid analgesic requirement after a remifentanil (REMI)-based anesthetic with spinal anesthetic blockade (SAB+REMI) or without (REMI) spinal blockade for open-heart surgery in children. We enrolled 45 patients who were candidates for tracheal extubation in the operating room after cardiac surgery. Exclusion criteria included age <3 mo and >6 yr, pulmonary hypertension, congestive heart failure, contraindication to SAB, and failure to obtain informed consent. All patients had an inhaled induction with sevoflurane and maintenance of anesthesia with REMI and isoflurane (0.3% end-tidal). In addition, patients assigned to the SAB+REMI group received SAB with tetracaine (0.5-2.0 mg/kg) and morphine (7 mug/kg). After tracheal extubation in the operating room, patients received fentanyl 0.3 mug/kg IV every 10 min by patient-controlled analgesia for pain score = 4. Pain scores and fentanyl doses were recorded every hour for 24 h or until the patient was ready for discharge from the intensive care unit. Patients in the SAB+REMI group had significantly lower pain scores (P = 0.046 for the first 8 h; P =0.05 for 24 h) and received less IV fentanyl (P = 0.003 for the first 8 h; P = 0.004 for 24 h) than those in the REMI group. There were no intergroup differences in adverse effects, including hypotension, bradycardia, highest PaCO(2), lowest pH, episodes of oxygen desaturation, pruritus, and vomiting.
 ...
PMID:Postoperative analgesia after spinal blockade in infants and children undergoing cardiac surgery. 1584 70

Cor triatriatum is a rare congenital cardiac anomaly in which the left atrium is divided into proximal (dorsal or upper) and distal (ventral or lower) chambers by a fibromuscular septum. The upper chamber receives the pulmonary veins and the lower chamber contains the atrial appendage and the mitral valve. The 2 chambers communicate through a defect in the membrane. Cor triatriatum is often associated with other congenital cardiac anomalies. Most frequently, the upper chamber communicates with the right atrium through a patent foramen ovale or atrial septal defect, and the clinical symptoms simulate anomalous pulmonary venous return. Less commonly, the foramen ovale communicates with the distal chamber and the clinical features mimic mitral stenosis. When cor triatriatum is the only abnormality, the clinical findings are also similar to mitral stenosis with development of pulmonary hypertension and subsequent right ventricular hypertrophy and atrial enlargement. The diagnosis is usually made in infancy or childhood, and the lack of treatment results in death in 75% of patients. We report the case of a woman who presented much later in life. The patient was a 57-year-old female with a clinical history of chronic atrial fibrillation who presented to the emergency department because of a "funny sensation" in her chest, though she denied chest pain, nausea, vomiting, or diaphoresis. EKG revealed atrial fibrillation with a rapid ventricular response and a tachycardic rate of 157. She had a therapeutic level of digoxin, and cardiac enzymes were normal. The patient was admitted and placed on Cardizem drip. Serial EKGs remained normal and heart rate control was achieved. On hospital day 2, the patient became dyspneic and cyanotic. She went into cardiac arrest and died.Autopsy revealed cardiomegaly (610 g) with 4-chamber dilatation. A septum divided the left atrium into 2 chambers. The defect in the dividing membrane measured 1 cm in diameter. No other congenital defects were noted. The large size of the defect in the membrane likely accounted for the late onset of symptoms that allowed this patient to survive into adulthood without previous diagnosis or surgical intervention (which is usually required in childhood).
 ...
PMID:Cor triatriatum sinistrum: a rare congenital cardiac anomaly presenting in an adult with chronic atrial fibrillation. 1612 Oct 87

Nesiritide is a synthetic form of B-type natriuretic peptide. It is approved for the treatment of acute exacerbations of congestive heart failure in hospitalized adult patients. It is currently under investigation for use in other settings and other patient populations. This article describes administration of nesiritide to an infant patient with severe pulmonary hypertension and cor pulmonale. No adverse reactions occurred during administration of the drug. Specifically, there was no hypertension, vomiting, arrhythmia, or changes in renal function. No changes in renal function occurred in the months subsequent to treatment. This case report illustrates that nesiritide can be safely administered to critically ill infants with pulmonary hypertension and cor pulmonale. Our patient experienced a decrease in pulmonary pressure and improved clinical condition during and after the infusion. However, further study is required to fully evaluate the safety and efficacy of nesiritide for these patients.
 ...
PMID:Nesiritide for the treatment of pulmonary hypertension and cor pulmonale in an infant. 1737 50

We describe a 3-year-old Hispanic male with cblC-type methylmalonic aciduria and homocystinuria who presented to the emergency department with progressive tachypnea, vomiting, and edema secondary to pulmonary embolism and cor pulmonale. With aggressive medical management, there was complete resolution of right heart failure and pulmonary hypertension after 3 months. Pulmonary embolism is rare in the pediatric population. Children with cblC-type methylmalonic aciduria and homocystinuria may be at increased risk for thrombus formation and pulmonary embolism due to chronic hyperhomocystinemia, a risk factor for thrombus formation in the adult population. Aspirin therapy may be indicated in children with inborn errors of metabolism that predispose to hyperhomocystinemia.
 ...
PMID:Resolution of cor pulmonale after medical management in a patient with cblC-type methylmalonic aciduria and homocystinuria: a case report. 1983 91


1 2 3 Next >>