Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 49-year-old man with an 11 year history of NIDDM presented hypercalcemic and with acute on chronic renal failure. His only symptoms were mild anorexia and nausea. Four years previously he had been diagnosed as having lipoid pneumonia, with classical histological findings. On this admission, serum parathyroid hormone was suppressed and 1,25 dihydroxyvitamin D levels elevated. The cause of his hypercalcemia presumably was ectopic 1 hydroxylation of 25 hydroxyvitamin D in the chronic granulomata in his lungs. It should be emphasised that any chronic granulomatous disease, and not just sarcoidosis, may be a cause of hypercalcemia.
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PMID:Hypercalcemia and lipoid pneumonia. 263 65

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

We reported a 41-year-old male with paramedian thalamic and midbrain infarcts due to cerebral embolism from bilateral pulmonary arterio-venous fistula and primary medullary hemorrhage. The patient had an episode of sudden onset consciousness disturbance with left Weber's syndrome (right hemiplegia and left oculomotor palsy) and vertical gaze palsy at age of 23. He noticed numbness in the left hand and the left half body under clavicular when he had got up in a morning at age 41. He had headache and left tinnitus on second and third days, and on the 3rd and 4th days, he experienced nausea. He had severe hiccup persisting from the 6th to the 13th days. The 23rd days he was admitted to our hospital. He showed dysesthesia and paresthesia in left half body under clavicular, dysesthesia in left hand and vertical gaze palsy and convergence disturbance. MRI performed on the 18th and 24th days, disclosed hyperdense mass in T1 and T2-weighted images in dorsal site of medulla, but the 70th days MRI showed no abnormal lesions. Therefore we diagnosed the high intensity mass as primary medullary hemorrhage. Cerebral angiography showed no abnormal vasculature. Many members of his family had history of sever nasal bleeding. He had skin hemangioma and mucosal hemangioma in esophagus, stomach, colon and rectum, and bilateral pulmonary arterio-venous fistula which had been operated at age 39. His mother also had skin hemangioma and pulmonary arterio-venous fistula. Therefore this family was diagnosed Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasia). MRI also disclosed multiple cerebral infarctions in bilateral thalamus, left cerebral peduncle and left cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Rendu-Osler-Weber syndrome presented paramedian thalamic and midbrain infarcts and primary medullary hemorrhage: a case report]. 269 33

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 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

Fenestration of basilar artery is an uncommon vascular anomaly that is usually an incidental product on autopsy or angiography. None of the cases in the literature had clinical symptoms associated with this anomaly except for subarachnoid hemorrhage when accompanied with saccular aneurysm. We report a rare case of the basilar artery fenestration associated with clinical symptoms without any aneurysm. A 71-years-old male, who had been treated for labile hypertension and had had recurrent attacks of vertigo, nausea, sometimes diplopia or unsteady gait, for 5 years, was referred to our hospital on Sept. 13, 1985. One day prior to admission, he suddenly felt diplopia and vertigo and unsteady gait. His family noticed he was dysarthric. On admission, he was alert and normotensive. He complained of dysesthesia on the right half of the perioral region and his right fingers. A neurological examination showed a mild weakness and hyperactive deep tendon reflexes on his right leg. His motor coordination was almost normal, but he was unsteady when he stood on one foot with his eyes closed. Laboratory examinations were normal except for an elevated serum uric acid level. A chest x-ray film showed a sclerotic change of aorta and mild cardiomegaly. Left ventricular hypertrophy was observed on his ECG. His CT scans showed multiple lacunae and mild brain atrophy. On cerebral angiography, his basilar artery (BA) had a fenestration almost in its total length that divided the BA, like a duplication, into two components with a smaller diameter than normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of basilar artery fenestration with recurrent attacks of vertebrobasilar insufficiency]. 344 54

A rare case with the episodes of vertebrobasilar TIAs which were caused by carotid ulcerative lesion and by persistence of proatlantal intersegmental artery is reported. This 69-year-old man was admitted on 14th Feb. 1985 with complaints of three attacks of vertigo, diplopia, nausea, vomiting and dysequilibrium lasting about 1 hour. His past history and family history were unremarkable. On admission, physical and neurological examinations revealed nothing particular, except bilateral carotid bruits. On the right side, innocent low pitched bruit was detected, however on the left side, carotid bruit was high pitched and was regarded as pathological. Blood pressure was 180/80 mmHg. Pulse rate was 66/min and cardiac arrhythmia was not detected by EKG. He also had no history of cardiac arrhythmia as mentioned above. CT scans and MRI showed only mild brain atrophy and no brain stem nor cerebellar lesions. Left carotid angiogram revealed ulcerative lesion of the common carotid bifurcation which was compatible with high pitched bruit. And at the level of the C2 vertebra, persistent proatlantal intersegmental artery originated from the left internal carotid artery which, after running upward, joined to the horizontal portion of the left vertebral artery above the atlas. Internal carotid and the vertebrobasilar vasculature beyond the proatlantal intersegmental artery were normal except slight irregularity of carotid siphon. Right carotid and vertebral angiograms revealed no abnormality and basilar artery was opacified clearly again via right vertebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of transient cerebral ischemia of the vertebrobasilar system caused by carotid ulcerative lesion and persistent proatlantal intersegmental artery: a case report]. 360 Sep 93

A case of postoperative neuroleptic malignant syndrome is presented. A healthy 23-year-old male underwent a shoulder repair under uneventful fentanyl, halothane, nitrous oxide and oxygen anaesthesia. He received droperidol 5 mg IV and metoclopramide 10 mg IV intraoperatively to prevent postoperative nausea. Postoperatively, the patient developed autonomic instability, fever and generalized muscle rigidity. His level of consciousness was depressed. These findings were consistent with the diagnosis of neuroleptic malignant syndrome. The supportive treatment of the patient included active cooling measures, muscle relaxation and mechanical ventilation. The ability of anti-dopaminergic agents, including metoclopramide and droperidol, to precipitate the neuroleptic malignant syndrome is discussed. Treatment of the neuroleptic malignant syndrome is briefly discussed.
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PMID:Postoperative neuroleptic malignant syndrome. A case report. 366 20

Scombroid poisoning has become an almost world-wide medical problem. It is probably the most common cause of fish poisoning, although frequently misdiagnosed as "Salmonella infection'. While there remains some question as to the definitive etiology, there is little doubt that the poisoning is caused by the ingestion of certain mackerel-like fishes whose tissues have undergone a number of changes provoked by bacteria, and involving the conversion of histidine to histamine, potentiated by diamines. Improper storage of the fishes, usually at temperatures above 20 degrees C, appears to be the most important predisposing factor. The organisms most commonly involved are Proteus sp., Clostridium sp., Escherichia sp., Salmonella sp. and Shigella sp. Twenty-five cases of scombroid poisoning are presented. The clinical manifestations were very similar in most cases, consisting of: alterations in taste; anxiety; hyperemia, particularly of the face and neck; nausea; pruritus; headache; certain other symptoms and signs. Most patients responded to antihistamitics, and all cases were self-limiting.
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PMID:Scombroid poisoning: mini-review with case histories. 382 4

Unexpected differences in clinical and biochemical findings in two brothers occupationally exposed to the same source of lead for dissimilar lengths of time are presented. Only the brother with the shorter period of lead exposure was anemic and afflicted by nausea, vomiting, abdominal colic and arthralgia. His urinary PBG output yielded the high orders of magnitude found in acute intermittent porphyria in relapse. Prior to administration of a single dose of EDTA (1 g of the calcium disodium salt given intravenously in 325 mL 0.15 mol/L NaCl), his blood lead levels averaged 3.6 mumol/L. The amount of chelatable lead retrieved from his urine, 31 mumol/day, was more than twice that found in his asymptomatic counterpart who was exposed to lead for 13 months and whose pre-EDTA blood lead levels averaged 4.0 mumol/L. Not only the activity of delta-aminolaevulinic acid dehydratase, but also that of uroporphyrinogen I synthetase, was markedly inhibited by lead in red cells of both brothers. These activities were restored to normal levels in vitro by addition to the assay system of zinc and dithiothreitol. This ruled out a coexisting genetic deficiency of either enzyme. The anemia of the symptomatic brother with the shorter period of lead exposure was alleviated by folic acid, 15 mg/day. The differences in findings between the two brothers point to differential susceptibility to lead and illustrate the extent to which symptomatic lead poisoning may mimic biochemical and clinical features of the acute porphyrias.
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PMID:Occupational lead exposure: studies in two brothers showing differential susceptibility to lead. 401 20


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