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 36-yr-old man was admitted to our hospital complaining of severe vomiting and diarrhea. Upper gastrointestinal series showed deformity of the duodenum. Serum gastrin level was very high (1,829 pg/ml) and secretin provocative test presented a positive result (peak 4,535 pg/ml). We diagnosed his illness as Zollinger-Ellison syndrome, but failed to identify the site of tumor. His symptoms were controlled with cimetidine 1,600 mg qid, but serum gastrin level was increasing. A year after the first admission, computed tomographic scan and selective angiography demonstrated the tumor, and surgery was performed. A solitary 2-cm tumor was noted at the surface of mesenterium of the duodenum. Frozen and paraffin section of the tumor revealed islet cell tumor apparently within a lymph node. Immunohistological examination revealed positive staining for gastrin alone. No other tumors were detectable by inspection and palpation during the operation. After excision of the tumor, serum gastrin and secretion test were normalized, and the patient remains asymptomatic 1 yr after surgery.
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PMID:Gastrinoma in a mesenteric lymph node. 265 53

Histamine poisoning results from the consumption of foods, typically certain types of fish and cheeses, that contain unusually high levels of histamine. Spoiled fish of the families, Scombridae and Scomberesocidae (e.g. tuna, mackerel, bonito), are commonly implicated in incidents of histamine poisoning, which leads to the common usage of the term, "scombroid fish poisoning", to describe this illness. However, certain non-scombroid fish, most notably mahi-mahi, bluefish, and sardines, when spoiled are also commonly implicated in histamine poisoning. Also, on rare occasions, cheeses especially Swiss cheese, can be implicated in histamine poisoning. The symptoms of histamine poisoning generally resemble the symptoms encountered with IgE-mediated food allergies. The symptoms include nausea, vomiting, diarrhea, an oral burning sensation or peppery taste, hives, itching, red rash, and hypotension. The onset of the symptoms usually occurs within a few minutes after ingestion of the implicated food, and the duration of symptoms ranges from a few hours to 24 h. Antihistamines can be used effectively to treat this intoxication. Histamine is formed in foods by certain bacteria that are able to decarboxylate the amino acid, histidine. However, foods containing unusually high levels of histamine may not appear to be outwardly spoiled. Foods with histamine concentrations exceeding 50 mg per 100 g of food are generally considered to be hazardous. Histamine formation in fish can be prevented by proper handling and refrigerated storage while the control of histamine formation in cheese seems dependent on insuring that histamine-producing bacteria are not present in significant numbers in the raw milk.
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PMID:Histamine poisoning (scombroid fish poisoning): an allergy-like intoxication. 268 58

A 12-year-old boy with corticosteroid-responsive mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) is described. His mother proved to have an asymptomatic mitochondrial myopathy on examination of a muscle biopsy specimen. Three weeks after the onset of vomiting, headache, ataxia and visual and speech impairment, he presented with a background of somatic growth retardation, deafness and school failure. Examination revealed disorientation, dysphasia, dyspraxia, optic atrophy, hemianopia, hemiparesis and sensory inattention. A cranial computed tomographic scan disclosed a large, low-density area, which was consistent with infarction, in the left posterior hemisphere and marked calcification of the basal ganglia bilaterally. Within two weeks of the commencement of corticosteroid treatment, the neurological dysfunction resolved. Attempts to decrease the dosage of dexamethasone caused an exacerbation of symptoms repeatedly. Two weeks after ceasing corticosteroid therapy, the patient developed a serious neurological relapse and a new, large, low-density area, which resembled an infarction, in the right posterior hemisphere on a computed tomographic scan. The reintroduction of corticosteroid therapy again resulted in the rapid resolution of all symptoms. It became evident that the patient had an exquisitely sensitive corticosteroid dependency, whereby a reduction in the dexamethasone dosage of even 0.25 mg a day caused confusion, headaches and increasing lactic acidaemia. Although it is difficult to assess the impact of various therapies in MELAS because of the episodic natural course of the disease, this remarkable corticosteroid responsiveness also has been noted in four previously reported patients with MELAS syndrome; therefore, it would seem reasonable to suggest that corticosteroid therapy now should be considered as standard treatment for this condition. However, corticosteroid therapy in other forms of mitochondrial disorders still awaits careful evaluation.
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PMID:Mitochondrial encephalomyopathy with corticosteroid dependence. 273 98

We report our experience with 90 neurologically impaired children treated with gastrostomy and Nissen fundoplication. Malnutrition was the main problem, followed by aspiration, recurrent pneumonia, and vomiting. The symptomatology was caused by swallowing incoordination and gastroesophageal reflux. The diagnosis of gastroesophageal reflux was confirmed by upper gastrointestinal series and pH probe. Nissen fundoplication was performed following a standard technique with preservation of the vagus nerves and its branches, repair of the diaphragmatic crura, reconstruction of the angle of His, and a 360 degree wrap. A gastrostomy and pyloroplasty or pyloric dilatation were part of the operative procedure. There were no deaths and few complications related to the surgical procedure. Marked nutritional improvement was seen in most cases with an average weight gain of 3.2 kg/patient 3 months following surgery. There was also improvement in milestones and seizure control. The majority of parents were very satisfied and would recommend the procedure to other parents with similar problems.
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PMID:Gastrostomy and Nissen fundoplication in neurologically impaired children. 280 49

A case of primary cerebral malignant lymphoma associated with hydrocephalus is reported. The patient was a 54 year-old male who enjoyed good health until the onset of headache and vomiting 4 weeks before admission. His consciousness was alert and neurological examination revealed severe papilloedema with retinal hemorrhage. No lymph node or abdominal tumor enlargement were noted. CT scan and MR images revealed no abnormal lesion except mild ventriculomegaly. CSF study revealed mild elevation of protein and sugar and cell count was 66/3. CSF cytology revealed atypical lymphoid cell with irregular nuclear contour and large nucleolus. Immunological marker studies of the tumor cell revealed increasing of anti J-5 (CD10), anti B-4 (CD19) and OKT-IA1. The patient was treated by a whole brain irradiation and chemotherapy after V-P shunt. It is 12 months since the operation, and the patient's condition is still good.
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PMID:[A case of primary malignant lymphoma of the brain associated with acute hydrocephalus]. 281 71

A boy aged 6 months who presented with poor weight gain, diarrhoea, and infection with Pneumocystis carinii was found to have congenital hypogammaglobulinaemia, which did not improve despite monthly treatment with intravenous gammaglobulin. At the age of 3 years and 2 months he developed severe vomiting and diarrhoea due to cryptosporidiosis, which failed to respond to conventional treatment. Infusion of hyperimmune bovine colostrum produced against parasite antigen, given by nasogastric tube, was started after symptoms had persisted for three weeks. His vomiting and diarrhoea resolved within five days of treatment, and oocysts were no longer seen in the stools after eight days. Later, however, he developed a rare complication, and oocysts were found in the common bile duct. Hyperimmune bovine colostrum may be useful in the treatment of many patients with immunodeficiency disorders.
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PMID:Remission of diarrhoea due to cryptosporidiosis in an immunodeficient child treated with hyperimmune bovine colostrum. 309 62

A 44-year-old man with acquired immunodeficiency syndrome (AIDS) and Pneumocystis carinii pneumonia (PCP) who suffered adverse effects from treatment with trimethoprim-sulfamethoxazole (TMP-SMX) and was then treated with pentamidine isethionate is described, and approved and investigational drugs used in the management of PCP in the AIDS patient are discussed. After taking TMP-SMX, 240 mg trimethoprim and 1200 mg sulfamethoxazole, four times a day orally for 10 days at home, the patient was hospitalized complaining of nausea, vomiting, diarrhea, and fever. Intravenous TMP-SMX was begun at a dosage of 18 mg/kg/day of trimethoprim. Four days later, his condition had deteriorated and he had elevations of liver enzymes and a decrease in white blood cell (WBC) count. TMP-SMX was discontinued and pentamidine isethionate was started at a dosage of 4 mg/kg/day i.v. His symptoms and fever subsided and his liver enzyme levels and WBC count improved. After nine days of pentamidine his WBC count decreased; pentamidine was suspected as the cause and discontinued; no further therapy was needed. PCP was the initial infection that established this patient's diagnosis of AIDS. The patient did not have exertional dyspnea and nonproductive cough, which are usually seen in AIDS patients with PCP. TMP-SMX 20 mg/kg/day, based on the trimethoprim content, is the usual initial treatment for PCP. Adverse effects of TMP-SMX develop more frequently in AIDS patients than in non-AIDS patients with PCP. The recommended dose of pentamidine isethionate for the treatment of PCP is 4 mg/kg/day, im. or i.v. A few studies have shown good response to aerosolized pentamidine. Trials of investigational agents have excluded patients with severely compromised respiratory status; eflornithine, dapsone in combination with trimethoprim, and trimetrexate have been used. Corticosteroids should be considered a last effort until additional data are available. TMP-SMX may be used to prevent recurrence of PCP or to prevent the initial occurrence of PCP in AIDS patients. Intravenous or aerosol doses of pentamidine may be effective as prophylaxis. Sulfadoxine-pyrimethamine tried as prophylaxis produced adverse reactions. Despite its higher incidence of serious adverse effects in the AIDS population, TMP-SMX is considered preferable to pentamidine for initial therapy. Pentamidine is preferred for patients with documented allergy to TMP-SMX or failure to respond to a five- to seven-day course of TMP-SMX.
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PMID:Treatment of Pneumocystis carinii pneumonia in patients with AIDS. 313 63

A case of ruptured cerebral aneurysm with hemophilia B is reported, and discussion is made concerning the management of mild type hemophilia in surgical operations. A 41-year-old male came to our hospital with complaints of severe headache, vomiting, and transient consciousness disturbance. His dentist said the patient had a mild bleeding tendency when he was 30 years old, however no postoperative hemorrhage was repeated in appendectomy in his childhood. He also had had no episodes of spontaneous bleeding. CT scan on admission showed subarachnoid hemorrhage, and angiography revealed a ruptured aneurysm at the trifurcation of the left middle cerebral artery. His coagulation screening tests (bleeding time, clotting time, prothrombin time, and activated partial thromboplastin time) were normal. An aneurysmal neck clipping was carried out, and operators did not detect any bleeding tendency during the surgery. CT scan on the next day showed no remarkable finding. On the third postoperative day, right hemiparesis occurred. Left putaminal hemorrhage took place. His coagulation tests and FDP were also normal. The hematoma was partially evacuated. After the second operation his condition was good, and rehabilitation program started. On the 15th hospital day his consciousness deteriorated suddenly, and CT scan showed a massive epidural hematoma on the left. His prothrombin time elongated mildly, but other tests were normal. Coagulation factors VIII and IX were examined and the factor IX was 22.5% of control. He was thought to be a patient with mild type hemophilia B. Despite a third operation for hematoma removal he died on the 20th hospital day. Mild type hemophilia B does not bleed spontaneously.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Unusual postoperative hemorrhage in a patient with ruptured aneurysm and hemophilia B]. 321 Dec 77

Neurological manifestations in infantile osteopetrosis are common and varied, and not always attributable to the skeletal pathology. An unusual association of osteopetrosis with neuronal storage of ceroid lipofuscin is reported in two infant brothers born of nonconsanguinous parents. The first child became symptomatic at age 5 days with weight loss and vomiting. He had poor head control, hypertonia, and persistent fisting, and died at age 2 months. In the second infant, the diagnosis of osteopetrosis was confirmed at age 2 days. His neurological symptoms included blindness, deafness, and recurrent seizures. The infant died at 7 months of age. In both cases, autopsy confirmed the diffuse bony sclerosis with hepatosplenomegaly and extramedullary hematopoiesis. Neuropathological examination revealed cerebral atrophy with ventricular dilation, neuronal loss, and astrogliosis. The most striking finding was widespread accumulation of neuronal ceroid lipofuscin associated with formation of axonal spheroids. The optic nerves were compressed at the optic foramina and showed loss of myelinated axons and gliosis. Rapid Golgi impregnations of neurons from the calcarine cortex in the second infant were analyzed quantitatively, showing a reduction in the total dendritic length and number of branches. The primary defect in osteopetrosis is thought to be a lysosomal dysfunction involving the monocyte cell line from which osteoclasts are derived. Thus, the association in two brothers of osteopetrosis with accumulation of neuronal ceroid lipofuscin may not be fortuitous. The neuronal storage disorder in this instance probably reflects lysosomal dysfunction.
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PMID:The association of infantile osteopetrosis and neuronal storage disease in two brothers. 334 81

A case of cryptococcal meningitis in a patient with the acquired immunodeficiency syndrome (AIDS) is described, as well as the epidemiology, pathogenesis, clinical manifestations, diagnosis, and therapeutic management of the disease. In July 1987 a 38-year-old white man was admitted to the hospital because of confusion, disorientation, and headache. His medical history was notable for a positive human immunodeficiency virus test. Culture of the cerebrospinal fluid was positive for Cryptococcus neoformans. The patient was started on amphotericin B 16 mg/day (0.3 mg/kg/day) intravenously and flucytosine 2 g every six hours (150 mg/kg/day) orally. Despite premedication with diphenhydramine and acetaminophen, he experienced rigors that were treated with hydrocortisone and meperidine. Three weeks later he was discharged on flucytosine 2 g orally every six hours and amphotericin B 50 mg intravenously every other day. One week later the patient developed fever and chills; blood cultures were positive for methicillin-sensitive Staphylococcus aureus, and his peripheral leucocyte count was 1.8 X 10(3)/cu mm. Flucytosine was discontinued, and he was treated with intravenous nafcillin while remaining on amphotericin B. In October the patient complained of nausea, vomiting, weakness, and agitation. A CSF latex agglutination titer for cryptococcal antigen was 1:32. He was treated with amphotericin B 50 mg daily until symptoms resolved and then continued on amphotericin B 50 mg twice weekly. Cryptococcosis is the most common life-threatening fungal infection among AIDS patients. In contrast to immunocompetent hosts, this population invariably develops disseminated disease, with 85% having meningeal involvement. The most effective therapy for cryptococcal meningitis in patients with AIDS has not been established.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of cryptococcal meningitis in patients with AIDS. 341 73


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