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)

Recombinant Tumour Necrosis Factor (rHuTNF) was locally applied to 18 patients with gynaecological tumours and recurrent malignant pleural effusions. Twenty-nine administrations with doses between 0.10 mg and 0.50 mg were carried out. Side-effects were flu-like symptoms (41%), fever/chill (34%), fatigue/malaise (28%), nausea/vomiting (10%), chest pain (14%). A dose-toxicity or dose-response relationship could not be established. Eighty-eight percent of the patients treated with rHuTNF did not suffer from any recurrent effusion within 4 weeks after treatment. Regarding the total survival time after therapy with rHuTNF 78% of all patients did not require any further pleural aspiration. Instillation of rHuTNF appears to be an effective method which can be used for pleurodesis with relatively few side-effects. It is a treatment which can also be applied to patients who are in a poor general state of health. It is especially recommendable since it can be successfully applied even after other pleurodesis devices have failed.
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PMID:Pleurodesis with recombinant tumour necrosis factor in gynaecological neoplasms. 961 Oct 46

A 28-year-old woman presented to the emergency department for evaluation of acute chest pain. She lacked risk factors for coronary artery disease and her initial electrocardiogram (ECG) was nondiagnostic. Within 45 minutes of presentation she developed nausea, vomiting, restrosternal chest pain, and ECG changes compatible with an acute inferoposterior myocardial infarction. Emergent cardiac catheterization revealed three-vessel coronary artery ectasia and two-vessel occlusion. She underwent emergency coronary artery bypass grafting. Her myocardial ischemia was believed to have been induced by methergine, which she had been taking over the preceding 3 days. The etiology and pathophysiology of coronary artery ectasia, as well as the cardiovascular effects of methergine and a related drug, ergotamine, are discussed.
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PMID:Postpartum myocardial infarction induced by methergine. 972 66

Psittacosis, also referred to as ornithosis, is a disease primarily of birds, which may be transmitted to humans. Psittacosis is caused by Chlamydia psittaci, an obligate intracellular parasite found worldwide. Humans are infected with C. psittaci when the organism enters the blood stream, usually through inhalation of dried excrement from diseased birds or through wound contamination with infected avian secretions. C. psittaci replicates in the liver and spleen and infects the lung and other organs hematogenously.1 The clinical manifestations of human psittacosis range from a mild respiratory infection to a severe systemic illness.1,2 Symptoms are frequently described as flu-like with fever, headache, body aches, and dry or productive cough. Sore throat, chest pain, abdominal pain, vomiting, and diarrhea are variably present. Physical findings may include a pulse-temperature dissociation, localized lung crackles, hepatomegaly, splenomegaly, and a pale macular skin rash. Chest radiographs may demonstrate lesions that are atelectatic, patchy, miliary, nodular, or consolidated in one or both lungs. White cell counts, erythrocyte sedimentation rates, and liver function tests are usually normal. In severe illness, signs and symptoms of liver dysfunction, neurological impairment, and respiratory and renal failure may be present. Since 1879 when psittacosis was recognized as a disease entity, cases have been reported in North and South America, Europe, Asia, and Australia. However, reports of psittacosis in Africa have been rare. An Ethiopian group, studying community-acquired pneumonia, published what they claimed to be the first report of psittacosis in Africa in 1994.3 The report published here is believed to be the first documented case of human psittacosis in Egypt.
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PMID:Psittacosis in Egypt: A Case Study. 981 79

We experienced a case of spontaneous rupture of the esophagus after gastrointestinal examination using barium. A 48-year-old male experienced severe chest pain after vomiting following gastrointestinal examination. Chest X-ray revealed a right pneumothorax and pleural effusion by barium. We diagnosed spontaneous rupture of the esophagus and performed right thoracotomy 6 hours after onset of symptoms. At 10 cm above the diaphragm, there was a vertical perforation 3 cm in length. Following saline lavage, the ruptured esophageal wall was directly closed by the layer to layer method. The post operative course was uneventful and the patient was discharged 3 weeks after surgery. Cases of spontaneous rupture of the esophagus into the right thoracic cavity induced by gastrointestinal examination are extremely rare.
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PMID:[Spontaneous esophageal rupture after gastrointestinal examination using barium]. 988 74

This report reviews the biological effects and case reports of suicidal or accidental ingestion of, and occupational exposure to sodium azide. Ingested doses of sodium azide were estimated for the 6 survival and 4 fatal cases studied. The lowest dose among survival cases was 5-10 mg. The patient reported headache, sweating, and faintness within approximately 5 minutes of ingestion. Four victims ingested 20 to 40 mg and recovered within 2 hours. However, a man who took 80 mg reported chest pain for 6 months after ingestion. The smallest doses among fatal cases were 0.7-0.8 g for women and 1.2-2 g for men. All victims suffered from hypotension, tachycardia, hyperventilation, diaphoresis, vomiting, nausea, and diarrhea. There is no antidote for sodium azide. Detoxicants for cyanide such as sodium nitrite or thiosulfate were tried, but were unfortunately, ineffective. Sodium nitrite may worsen the hypotension caused by sodium azide, and is not recommended. Occupational exposure to sodium azide is thought to be common, however, fatal exposure is rare. NIOSH "Recommended Exposure Limits" for sodium azide is 0.3 mg/m3.
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PMID:[Sodium azide: a review of biological effects and case reports]. 1019 13

Spontaneous intramural hematoma of the esophagus (SIHE) is a rare condition, usually presenting with severe acute chest pain. Vomiting, dysphagia, odynophagia, and hematemesis may appear later. We herein report a case of this disease in a patient treated with low doses of aspirin, and review the literature for possible etiologies for this condition. In addition, we compare the utility of the various diagnostic modalities in this uncommon condition.
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PMID:Spontaneous intramural hematoma of the esophagus. 1044 63

We designed a study to determine the efficacy and safety of amlodipine given once daily in the pediatric population. Twenty-one patients (mean age 13.1 years) with either essential (n=160) or renal (n=5) hypertension, and newly diagnosed (n=15) or poorly controlled or intolerant on existing antihypertensive therapy (n=6), were included. Patients received amlodipine once daily at a starting mean dose of 0.07+/-0.04 mg/kg per day. The total daily dose of amlodipine was increased 25%-50% every 5-7 days if the mean home blood pressure measurements (HBPM) were above the 95th percentile for age and gender. A baseline followed by a repeat 24-h ambulatory blood pressure monitor study (ABPM) was performed in 20 patients when the mean HBPM was below the 95th percentile goal. The mean titrated dose required to control BP was 0.29+/-0.11 mg/kg per day for those < 13 years, 0.16+/-0.11 mg/kg per day for those > or = 13 years, 0.23+/-0.14 mg/kg per day for essential, hypertension and 0.24+/-0.13 mg/kg per day for renal hypertension. The ABPM demonstrated that amlodipine provided effective BP control as primary therapy in 14 essential patients. Adverse effects included fatigue (n=6), headache (n=5), facial flushing (n=4), dizziness (n=3), edema (n=3), abdominal pain (n=3), chest pain (n=2), nausea (n=1), and vomiting (n=1). Quality of life appeared to improve during therapy. Amlodipine was an effective once daily antihypertensive agent with an acceptable safety profile. Higher doses of amlodipine were required for younger patients, and monotherapy was effective in patients with essential hypertension.
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PMID:Efficacy of amlodipine in pediatric patients with hypertension. 1045 79

There are three clinical presentations of anthrax in humans: cutaneous (>95% of cases), orogastric and inhalational. The infectious form, the spore, enters the body and is thought to germinate within macrophages either at the site of inoculation (cutaneous or orogastric) or in the regional lymph node (inhalational). The bacillus then synthesizes its antiphagocytic capsule and the lethal and oedema toxins which interfere with the non-specific host defences leading to the characteristic locally destructive lesion and spread by lymphatics to the systemic circulation and other organs. The cutaneous form begins as a papule which progresses over several days to a vesicle and then ulcerates. There is often oedema, sometimes massive, probably due to the oedema toxin that surrounds the lesions which then develop a characteristic black eschar. The patient may be febrile with mild to severe systemic symptoms of malaise, headache and toxicity. Oropharyngeal anthrax presents with severe sore throat or an ulcer in the oropharyngeal cavity associated with neck swelling, fever, toxicity and dysphagia. Gastrointestinal anthrax begins with anorexia, nausea, vomiting and abdominal pain which may be similar to an acute abdomen. There may be diarrhoea and ascites, both of which may be haemorrhagic. Inhalational anthrax begins with non-specific symptoms of malaise, fever, myalgia and non-productive cough. After a period of 2-3 days, this is followed by a sudden onset of severe respiratory distress associated with diaphoresis, cyanosis and increased chest pain. There may be a widened mediastinum and pleural effusions on chest X-ray. Death follows in 24-36 h from respiratory failure, sepsis and shock. The diagnosis of anthrax is easy if it is considered. The organism is readily observed by Gram or Wright stain in local lesions or blood smear and can be easily cultured from the blood and other body fluids. However, because of its rarity, it is not often included in the differential diagnosis and in inhalational disease the diagnosis is rarely made until the patient is moribund. More rapid diagnostic tests are under development. Penicillin, combined with supportive care, remains the mainstay of treatment, although the organism is susceptible in vitro to many antibiotics. In recent years, there have been significant advances in our knowledge of the organism and its toxins and it is anticipated that similar progress will be made in the future in developing more rapid diagnostic tests and new modalities of treatment.
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PMID:Clinical aspects, diagnosis and treatment of anthrax 1047 74

Subtypes of functional dyspepsia (FD), including refluxlike dyspepsia, ulcerlike dyspepsia, dysmotility-like dyspepsia, and nonspecific dyspepsia, have been described and are widely used clinically. However, these symptom patterns often overlap, and the terms are insufficient for indicating all FD symptoms. In this study, we divided 71 FD patients into two groups: patients with or without pain. Group I, the pain dyspepsia group, included patients in whom the main symptoms were epigastralgia and/or chest pain. Group II, the painless dyspepsia group, included patients without pain, in whom the symptoms were nausea, vomiting, and heartburn. We examined the relationship between esophageal function and psychiatric factors in the test groups and compared them with a control group. Of the FD patients, 19.7% [8 (25%) of 32 group I patients, 6 (15.4%) of 39 group II patients] had esophageal motility disorders, such as nutcracker esophagus and diffuse esophageal spasm. The LES pressure of group I was higher than that of group II by esophageal manometry (P < 0.05). In 17 (53.1%) of 32 group I patients and 31 (79.5%) of 39 group II patients, psychiatric disorders (38.0% had depressive disorder and 21.1% had an anxiety disorder) were diagnosed following DSM III-R criteria. Group II tended to be more depressive than group I (P = 0.0508). Psychological assessment scores, STAI-I and STAI-II, were higher in groups I and II than in the control group (P < 0.001). Long-term distress, anxiety, and depression seem to influence the symptoms of FD patients. Esophageal dysmotility may be an important functional abnormality of FD.
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PMID:Esophageal motility and psychiatric factors in functional dyspepsia patients with or without pain. 1054 63

There is no consensus regarding the specific management of HIV-associated nephrotic syndrome. We report a child whose first manifestation of human immunodeficiency virus type 1 (HIV-1) infection was nephropathy and wasting syndrome associated with profound immunodeficiency. The patient had a dramatic clinical and immunologic response to triple antiretroviral therapy delivered through a gastrostomy tube, with complete resolution of nephrotic syndrome. A 51/2-year-old African-American girl presented with a 2-week history of cough, chest pain, vomiting, loose stools, abdominal distention, anorexia, and fever. In addition, she had recurrent oral thrush. Her weight and height were below the 5th percentile. She was chronically ill, appearing with oropharyngeal thrush and pitting edema in lower extremities. She had scattered rhonchi and decreased breath sounds on both lung bases. Her abdomen was distended and diffusely tender. A chest radiograph showed consolidation of the right upper and left lower lobes with bilateral pleural effusion. Admission laboratories were consistent with nephrotic syndrome. Streptococcus pneumoniae grew from the blood culture and the child responded well to treatment with intravenous ceftriaxone. She was found to be HIV-infected, her CD4(+) cell count was 3 cells/mcL and her plasma HIV-1 RNA was >750 000 copies/mL. A percutaneous gastrostomy tube was placed for supplemental nutrition. She was treated with stavudine, lamivudine, and nelfinavir via gastrostomy tube with good clinical response. Twenty-one months after instituting antiretroviral therapy, her weight and height had increased to the 50th and 10th percentile respectively, and she had complete resolution of her nephrotic syndrome. Her CD4(+) cell count increased to 1116 cells/mcL and her viral load has remained undetectable. HIV-1 associated nephrotic syndrome has been described in children with profound immunodeficiency. The course of untreated HIV-associated nephrotic syndrome is rapid progression to renal failure in up to 40% of the children. Regardless of the presence of renal insufficiency, if untreated, it is uniformly fatal. A modest improvement of HIV-1 associated nephrotic syndrome has been observed in patients treated with zidovudine. Steroid and cyclosporine treatment have resulted in improved renal function but long-term use of immunosuppressive therapy has raised concerns about safety. We have described, to our knowledge, the first child with HIV-associated nephrotic syndrome who had a remarkable clinical, immunologic, and virologic response to triple-drug combination therapy given by gastrostomy tube, with complete resolution of proteinuria and normalization of the serum albumin. She also had a striking improvement in weight, height, and quality-of-life. Whether the presence of a gastrostomy tube contributed to the excellent response because of improved compliance is unknown, but warrants systematic evaluation.
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PMID:Resolution of HIV-associated nephrotic syndrome with highly active antiretroviral therapy delivered by gastrostomy tube. 1058 95


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