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 7-year-old boy presented with a 4-week history of daily headache. His parents reported that he was unable to attend school the week prior to presentation. Intermittent nausea without vomiting was reported, but no blurred vision, photophobia, or diplopia were described. There was no history of trauma or recent systemic illness. The physical examination showed mild neck discomfort, no papilledema, and normal cranial nerve, motor and sensory functioning. Both a CT scan of the sinuses and an MRI of the brain were normal. Although the opening pressure was elevated, the cerebrospinal fluid was also normal. In previous accounts of idiopathic intracranial hypertension in children, concomitant papilledema, visual symptoms and/or palsy of the sixth cranial nerve are described. This case demonstrates that idiopathic intracranial hypertension in a young child can present as a daily headache without any visual symptoms or signs.
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PMID:Idiopathic intracranial hypertension in a young child without visual symptoms or signs. 891 68

A 25-year-old man developed nausea, vomiting, severe headache, and confusion. He had a past history of hyperuricemia and mild renal dysfunction. On admission he had somatic growth retardation, hypertrichosis, and bilateral auditory impairment. A cranial CT scan showed a small area of low density in the left temporal lobe and cerebellar atrophy. Five days later, he developed right homonymous hemianopia, sensory aphasia, and sensory inattention, and a new, large area of low density in the left occipital lobe on a cranial CT scan. On laboratory examination, lactate, pyruvate, and the lactate-to-pyruvate ratio were elevated in both the serum and cerebrospinal fluid. The biopsied muscle showed ragged red fibers and strongly SDH-reactive blood vessels. Gene analysis revealed the presence of the A 3243 G point mutation of the mitochondrial tRNA(Leu) gene in his blood leucocytes and muscle. Serum concentrations of BUN and creatinine were elevated to 46 mg/dl and 2.2 mg/dl, respectively. Creatinine clearance was 14.1 ml/min. An abdominal CT scan disclosed atrophy of his left kidney with subcapsular calcification and the findings of his abdominal ultrasonography were compatible with chronic renal failure. His mother, who suffered from renal failure and became dialysis dependent in her late forties also bore the A 3243 G mutation of the mitochondrial tRNA(Leu) gene in her circulating leucocytes. Though the association between MELAS and renal dysfunction still remains obscure, we speculate that renal failure can be a manifestation of MELAS.
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PMID:[Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with chronic renal failure: report of mother-child cases]. 897 30

A 15-year-old man was admitted because of diplopia and bilateral ptosis which occurred a few days after initial clinical signs, such as fever up, nausea, vomiting and headache. His pupils were anisocoric (Rt. phi 3.5 mm < Lt. phi 6.0 mm). In his left eye, light reflex was absent and its movements were limited in all directions. Brain MRI revealed the findings of paranasal sinusitis in bilateral ethmoidal and sphenoidal sinuses and swelling of bilateral cavernous sinus. Combination of intravenous antibiotic therapy and drainage improved his clinical symptoms and MRI findings. It was diagnosed as the inflammation originated in the sphenoid and ethmoid sinuses, which extended to the cavernous sinus and then involved III, IV, and VI cranial nerves. In conclusion, MRI was very useful to detect the cavernous sinusitis secondary to sphenoidal sinusitis.
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PMID:[A case of paranasal sinusitis-cavernous sinusitis with ophthalmoplegia externa]. 899 45

We describe a 30 year-old man who presented with an abdominal abscess as an unusual complication of endoscopic retrograde cholangiopancreatography with papillotomy. His presenting symptom was recurrent vomiting, while fever, abdominal pain, and leukocytosis were not significant. The abscess was observed with repeated computerized tomographic scans and completely regressed with intravenous antibiotic treatment over a three week period, leading to complete remission.
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PMID:Conservative therapy in an ERCP-induced abdominal abscess. 936 Sep 41

We experienced a patient with panhypopituitarism which occurred following extensive brainstem and cerebellar infarction due to dissection of basilar artery (BAD). Panhypopituitarism followed by BAD has not yet been reported in the literature. The patient was a 67-years-old man who was admitted to our hospital because of a sudden onset of consciousness disturbance and vomiting. On the day of admission, he was drowsy and had left IIIrd nerve palsy, skew deviation, occular bobbing, and left hemiparesis. His neurological state was rapidly deteriorated, and fell almost into apneic state, requiring artificial ventilation for a week. Cerebral angiography demonstrated a double lumen sign of the basilar artery confirming the diagnosis of dissection. There were extensive hypodensities in the brainstem and bilateral cerebellar hemispheres on CT. On day 20, he suddenly became shocked following infection. Even after the effective and successful treatment of infection, severe hypotension continued that required administration of chatecholamine agents. Laboratory examinations revealed that he had panhypopituitarism. Supplement therapy with adrenocortical hormones made his circulatory state improved, and could finally be stopped on day 100. In the present case, subclinical hypopituitarism was considered to occur mainly from compression of the pituitary stalk and hypothalamus by the enlarged BAD. Increased intracranial pressure and upward herniation may also have made the pituitary function worse, and the infection finally triggered the adrenal crisis. The BAD occurs more frequently than previously considered, and should be kept in mind as a cause of secondary panhypopituitarism.
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PMID:[Panhypopituitarism following basilar artery dissection with extensive brainstem and cerebellar infarction: a case report]. 961 74

We report on a 13 years 7 months old boy who ingested 650 mg azathioprine in a suicide attempt. His baseline medication was azathioprine and methotrexate for control of juvenile chronic polyarthritis. After the induction of vomiting by ipecacuanha sirup and administration of charcoal (1 g/kg), he was closely followed for haematological, hepatic, and renal side effects. During the following days, no serious adverse events were noted except that the thrombocyte (from 403,000 down to 199,000/microliter) and total leukocyte count decreased moderately (from 12,000 down to 7100/microliter). On the basis of this case report and the available literature, the potential acute toxicity of azathioprine and possible treatment modalities are discussed.
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PMID:[Azathioprine ingestion with suicidal intent by an adolescent with chronic juvenile polyarthritis]. 962 49

A 38-year-old homosexual male with AIDS suffered four neurological episodes including headaches, confusion, visual impairment, memory disturbances, and dysarthria which resolved spontaneously in a few days. He was admitted to hospital during a fifth episode. Neurological examination revealed a cerebellar syndrome. General examination was normal. CD4 count was 90. CSF contained two WBCs/mm(3) and 12.30 mg/dL protein. MRI revealed diffuse ill defined increased signal on T2-weighted images in the white matter. His condition worsened rapidly with vomiting and he died 1 month after admission. Neuropathological examination revealed diffuse brain oedema with ventricular compression, central diencephalic herniation and bilateral tonsilar herniation in the absence of a focal lesion. Microscopical examination revealed predominant involvement of the white matter with diffuse myelin pallor and massive perivascular dilatation containing an exudate expressing serum proteins and occasional macrophages. The same exudate was also diffuse in the leptomeninges. Parenchymal damage predominated around the perivascular spaces and included loosening of tissue, axonal damage with spheroids and reactive astrocytosis. There was no evidence of productive HIV encephalitis, no multinucleated giant cells; p24 immunostaining and RT-PCR for HIV genome were negative. There was neither significant inflammation nor microglial activation. In this illustrative case, the relapsing course of the neurological signs, the diffuse topography of the blood-brain barrier breakdown and the absence of local cause make it likely that the diffuse leak and axonal damage could be related to circulating factors.
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PMID:Acute, relapsing brain oedema with diffuse blood-brain barrier alteration and axonal damage in the acquired immunodeficiency syndrome. 971 86

Pelizaeus-Merzbacher disease (PMD) is a hereditary disorder with myelin dysplasia in the central nervous system. The connatal type is a more severe form compared to the classical type and shows developmental arrest or deterioration, nystagmus, spasticity, and/or convulsions in the neonatal period. A 1 1/4-year-old Japanese boy diagnosed as connatal type PMD is reported here. Soon after his birth, he demonstrated horizontal and rotatory nystagmus and opisthotonic posture. At the age of 10 months, he had difficulty in feeding. At the age of 1 year, he presented more severe opisthotonic posture and frequent vomiting. He showed deterioration in gross motor development. His chromosome analysis showed a normal male karyotype. Electroencephalogram did not show a sleep spindle. Auditory evoked brainstem responses (ABR) showed only wave I on both sides. Visual evoked potentials (VEP) showed prolongation of latencies. These results were compatible with PMD. Nuclear magnetic resonance imaging (MRI) demonstrated in the white matter of cerebrum and brainstem no high intensities on T1-weighted images and diffuse high intensities on T2-weighted images. Such absence of myelination including the brainstem was characteristic to the connatal type PMD. The diffuse disturbance of myelination appeared to correlate with the severity of clinical symptoms.
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PMID:[Connatal type of Pelizaeus-Merzbacher disease: a case report]. 1019 41

A young adult presenting with 11 months history of fever, headache, vomiting was found to have CSF lymphocytic pleocytosis with increased protein. His serum tested strongly positive for Brucella (standard tube agglutination titre 1: 320) whereas CSF was weakly positive. He became asymptomatic on treatment with tetracycline, rifampicin and streptomycin with significant CSF response. This case is reported because of its rarity.
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PMID:Systemic brucellosis with chronic meningitis: A case report. 1033 11

An 11 1/2-year-old African-American male presented with a 3-day history of abdominal pain that was constant, dull, and localized to the right lower quadrant. It was associated with anorexia, bile-stained vomiting, and enema-relieved constipation. His white blood cell count was elevated and the serum was lipemic. He had an immediate appendectomy, which revealed purosanguinous fluid in the peritoneal cavity. Postoperatively his triglycerides and total cholesterol were markedly elevated, and his pancreas was enlarged and poorly delineated, with no pseudocysts. He was diagnosed with type V primary hyperlipidemia and placed on gemfibrozil regimen. He was compliant with medication and made dietary changes, which all contributed to lower cholesterol and triglyceride levels.
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PMID:Beware of Cloudy Serum. 1035 90


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