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)

We report the case of a 21-year-old man who had been developing acute renal failure with Methicillin-resistant Staphylococcus aureus (MRSA) colitis and sepsis. He was admitted for consciousness disturbance, nausea, vomiting, and diarrhea. Oliguria was also observed and his serum creatinine level was elevated to 10 mg/dl. Urinary protein was positive and an abundance of hyaline cast were seen in urinary sedimentation. Diarrhea and pyrexia were prolonged and serum C-reactive proteins were elevated, but lymphocyte and leukocyte counts temporarily decreased from the 3rd to the 6th hospital day and remained low until normalizing after the 14th day. His clinical symptoms improved with hemodialysis (HD) and effective antibiotic therapies. An MRSA strain producing toxic shock syndrome toxin-1 (TSST-1), a super antigen which specifically stimulates human V beta 2-positive T cells, was separated from his feces and blood. To ascertain the cause of his renal dysfunction, a renal biopsy was performed on the 8th day. His renal histology revealed acute interstitial nephritis with severe inflammatory cell infiltration around the medullary areas without glomerular changes. Most of the infiltrated cells were small monocytes, and lymphoid cells were rich in the interstitium. With immunohistochemical staining, over 70% of T-cells were V beta 2-positive. TSST-1-producing MRSA was detected in his blood specimen. Furthermore, V beta 2-positive T cells were accumulated in the renal intersititium, and transient lymphocytopenia was observed. These data suggested the following possible pathogenesis for interstitial nephritis: TSST-1 acts as a super antigen in the renal interstitium where major histocompatibility complex (MHC) is class-2-positive, thereby resulting in interstitial nephritis with T cell migration.
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PMID:[A case of interstitial nephritis induced by a super antigen produced by methicillin-resistant Staphylococcus aureus (MRSA) presenting as acute renal failure]. 1036 25

We report a 73-year-old Japanese woman with familial Parkinson's disease. The patient was well until her 67 years of the age, when she noted rest tremor in her right hand. Soon after her gait became short stepped. She visited our clinic on October 6, 1992 when she was 68 years old. She was alert and well oriented without dementia. She showed masked face, small voice, small stepped gait, retropulsion, resting tremor in her right hand, rigidity in the neck, and bradykinesia. She was treated with 400 mg/day of levodopa-carbidopa, which improved her symptoms, however, she developed wearing off phenomenon 3 years after the initiation of levodopa treatment. On August 26, 1998, she developed abdominal pain, diarrhea, and vomiting. She was admitted to another hospital, where abdominal plain x-ray revealed an evidence of intestinal obstruction (ileus). She was treated with nasogastric suction and intravenous fluid. Her condition did not improve and she was transferred to our hospital on August 29, 1998. Her family history revealed no consanguineous marriage. She had two elder brothers and three elder sisters. One of her brothers had been diagnosed as Parkinson's disease. Her husband also suffered from Parkinson's disease, however, her parents apparently did not have Parkinson's disease. On admission, she appeared to be drowsy. Her blood pressure was 102/70 mmHg, body temperature 36.2 degrees C. The lungs were clear and no cardiac murmur was present. Abdomen was flat and bowel sound was audible. No abnormal mass was palpable. Neurologic examination revealed mild consciousness disturbance, masked face, and small voice. No motor paralysis was noted. Muscle tone was hypotonic. No abnormal involuntary movement was noted. Abnormal laboratory findings on admission were as follows; WBC 11,300/microliter, amylase 1,373 IU/l, CK 446 IU/l, BUN 50 mg/dl, creatinine 1.17 mg/dl, CRP 22.7 mg/ dl, Na 134 mEq/l, K 3.1 mEq/l, and Cl 81 mEq/l. A chest x-ray film revealed pneumonic shadows in both lower lung fields. She was treated by nasointestinal suction, intravenous fluids, and chemotherapy for her infection. Her BP started to drop on September 2 and she developed cardiac arrest on the same day. She was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had a form of autosomal dominant familial Parkinson's disease. As parents did not have Parkinson's disease, some of the participants raised the possibility of autosomal recessive inheritance. But the age of onset was too late for autosomal recessive inheritance. Majority thought that the mode of inheritance was autosomal dominant with low penetrance. alpha-Synuclein mutation causes an autosomal dominant familial Parkinson's disease, but this type is very rare in non-Greek populations and the penetrance is high. Chromosome 2-linked autosomal dominant familial Parkinson's disease shows low penetrance. There are many other autosomal dominant forms of familial Parkinson's disease linked to yet unknown chromosome loci. Majority thought that this patient also had a form of Lewy-body positive autosomal dominant familial Parkinson's disease of unknown chromosome locus. Post mortem examination revealed ischemic intestinal lesion with strangulation. This was thought to be the cause of her death. In the central nervous system, the brain appeared to be normal by inspection. In the coronal sections, the substantia nigra and the locus coeruleus showed marked depigmentation. Histologic examination revealed marked neuronal loss and Lewy body formation in the remaining neurons. Pathologic examination was consistent with Parkinson's disease. Mutational analysis for the parkin gene was negative.
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PMID:[A 73-year-old woman with familial Parkinson's disease]. 1065 9

Three cases of chronic subdural hematoma (CSH) associated with malignancy are reported. Case 1; A one-year-old girl was referred for vomiting and convulsions. Left CSH was removed, and her symptoms disappeared. Cytological examination of chronic subdural hematoma revealed abnormal white blood cells. A clinical diagnosis of acute monocytic leukemia was made after the laboratory examination. Remission was achieved by chemotherapy, but she died one year after the operation. Case 2; A 72-year-old woman was referred for right hemiparesis and urinary incontinence. Left CSH was irrigated, and her clinical symptoms immediately disappeared. Cytological examination of chronic subdural hematoma revealed abnormal white blood cells. A clinical diagnosis of chronic lymphocytic leukemia was made after the laboratory examination. No treatment was given since there were no clinical symptoms of chronic lymphocytic leukemia. Case 3; A 70-year-old woman who had been affected with early gastric cancer and mammary cancer for the previous two years was admitted to our clinic because of headache, right hemiparesis and consciousness disturbance. Left CSH was irrigated, and her clinical symptoms improved. However, there was a tendency to bleed because disseminated intravascular coagulation had occurred, and CT showed bilateral subdural hematoma. A second irrigation was performed, but her symptoms did not improve. Left acute subdural hematoma, which was removed by craniotomy, occurred three days after the second operation. Pathological examination of the outer membrane of the subdural hematoma revealed invasion of adenocarcinoma. She died three days after the third operation. It is recommended that both the cytological and the histological examinations be performed when possible, since they are simple to perform and very useful in some cases.
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PMID:[Chronic subdural hematoma associated with malignancy: report of three cases]. 1066 38

Holocarboxylase synthetase (HCS) is responsible for the biotinylation of pyruvate carboxylase, propionyl coenzyme A (CoA) carboxylase, beta-methylcrotonoyl CoA carboxylase, and acetyl CoA carboxylase. We report on a patient with HCS deficiency resulting in a rare metabolic disease. The patient, a 2-year-old boy, presented with vomiting, consciousness disturbance, and dyspnea. Laboratory examinations showed hyperglycemia, hyperammonemia, lactic acidosis, and excretion of large amounts of beta-hydroxyisovalerate and beta-methylcrotonylglycine in the urine. After 10 days of treatment with biotin 5 mg.kg-1.day-1, the abnormal organic acids in his urine had almost completely disappeared. There were no subsequent attacks, and his growth and development remained normal during 1 year of follow-up. Nucleotide sequence analysis of the HCS cDNA of the patient revealed a homozygous 1809C-->T (R508W) mutation. The R508W mutation is found worldwide, and might be associated with higher residual HCS activity than other mutations. Late-onset HCS deficiency cannot be differentiated clinically from biotinidase deficiency. Prompt and correct diagnosis is important for these biotin-responsive disorders.
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PMID:Late-onset holocarboxylase synthetase deficiency with homologous R508W mutation. 1077 35

Gliomatosis cerebri (GC) is a rare disease loosely defined as a diffusely infiltrating glioma involving extensive areas of the brain. The prognosis is poor and no definite treatment has proven effective for GC. Little information exists regarding the role of radiation therapy (RT) for GC, but some researchers have suggested that it is a good choice of treatment from their limited experience. In this report, we present a case with imaging and histological diagnosis of GC and demonstrate the treatment results of RT. The patient was a 39-year-old woman with progressive symptoms of dizziness, unsteady gait, headache, vomiting, and consciousness disturbance for 6 months. She received a series of radiographic examinations and surgical interventions for diagnosis. The definite diagnosis of GC was made by a combination of magnetic resonance imaging (MRI) findings and histological examinations. Forty Gray (Gy) of whole brain irradiation followed by 14 Gy reduced-field boosts were given to her. The MRI, following treatment, showed regressive changes, and clinical symptoms were slightly improved. The patient survived 19 months after the diagnosis, which is longer than the average survival time of patients without treatment.
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PMID:Diagnosis and results of treatment with radiation therapy in gliomatosis cerebri patient: case report. 1135 88

In 1980, a 10-year-old boy was admitted to the authors' hospital with consciousness disturbance and vomiting. Computerized tomography (CT) scans revealed a pineal mass lesion and hydrocephalus. The tumor was totally removed and a ventriculoperitoneal (VP) shunt was inserted. Histological investigation of a surgical specimen revealed that it was a teratoma. Five years later, the patient was readmitted to the same institution with polyuria. Magnetic resonance (MR) imaging revealed a mass lesion in the suprasellar region. The patient received systemic chemotherapy, and the tumor disappeared; however, 2 years after the chemotherapy, MR imaging demonstrated a right lateral ventricular mass. The tumor was totally resected, and histopathological investigation revealed a teratocarcinoma. Three years after the chemotherapy, CT scanning revealed suprasellar and right lateral ventricular tumor recurrences, for which the patient received irradiation and chemotherapy. The tumors disappeared and the patient achieved complete remission that lasted longer than 10 years. On January 25, 2000, however, he noticed hip pain. Lumbar MR imaging demonstrated a spinal tumor below L-4 and also an abdominal tumor. The abdominal tumor was totally removed, and the histological findings identified it as a germinoma. The patient received systemic chemotherapy and the tumor disappeared completely. The authors believe that the suprasellar tumor was a metachronous germinoma and that it had metastasized through the intrathecal route and the VP shunt.
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PMID:Intrathecal and intraperitoneal germinomas occurring 20 years after total removal of a pineal teratoma. Case report. 1183 13

Human infections due to Yersinia enterocolitica have been reported worldwide, predominantly in Europe. However, there have been few reports of Yersinia enterocolitica infection in Taiwan. We report a case of Y. enterocolitica sepsis in a 15-year-old Taiwanese girl with Cooley's anemia and insulin-dependent diabetes mellitus. She presented at admission with fever, shock and consciousness disturbance. She had symptoms of abdominal pain, vomiting and diarrhea for three days before admission. Blood pressure stabilized after intravenous normal saline rescue. Blood culture yielded Y. enterocolitica 2 days later and ceftriaxone was administered according to the results of sensitivity tests. She recovered well after a course of antibiotic treatment. Though Y. enterocolitica sepsis is rare in Taiwan, clinicians should be aware of its tendency to develop in patients with Cooley's anemia, fever and enterocolitis and that its clinical course may include sepsis leading to shock.
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PMID:Yersinia enterocolitica sepsis in an adolescent with Cooley's anemia. 1278 40

The aims of this study were to identify the generator of the paroxysmal partial discharges in Panayiotopoulos syndrome by means of magnetoencephalography and to determine the significance of these formations in the epileptogenesis of the developing nervous system. We report magnetoencephalographic data for two cases of Panayiotopoulos syndrome showing the rapid generalization of the source of interictal spikes that explains extraoccipital manifestations such as ictal vomiting and consciousness disturbance.
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PMID:Magnetoencephalographic analysis in children with Panayiotopoulos syndrome. 1615 32

A 60-year-old female patient with a therapy-resistant Bence-Jones (BJ) lambda-type multiple myeloma was treated with bortezomib. She had been treated with tandem autologous stem cell transplantations and achieved complete remission before her disease relapsed. Sixteen hours after the first administration of bortezomib, an episode of fever, slight consciousness disturbance and vomiting occurred, which was accompanied by a remarkable elevation of LDH (3608 IU/l). Serum levels of creatinine, uric acid, and AST were also transiently elevated. Serum interleukin-6 level was also increased after the administration of bortezomib. The symptoms disappeared rapidly within 48 hours. Bortezomib at a 25%-reduced dose was administered again along with dexamethasone 26 days later, which caused a moderate increase in LDH levels, but no other symptoms. Further treatment caused no increase in LDH. The treatment was very effective and eradicated both urinary BJ protein and bone marrow myeloma cells after 8 sessions of bortezomib administration. These findings suggest that a bortezomib-induced rapid reduction in tumor burden led to tumor lysis syndrome, for which caution is needed when treating myeloma patients with this very effective agent.
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PMID:[Bortezomib-induced tumor lysis syndrome with a remarkable elevation of LDH in a case of relapsed and therapy-resistant multiple myeloma]. 1698 18

We report a very rare case of Japanese encephalitis (JE) presenting with reversible stereotyped movement in the subacute stage. A 58-year-old woman presented with high fever, headache, nausea, vomiting, and consciousness disturbance. Cranial magnetic resonance imaging (MRI) of fluid attenuated inversion recovery (FLAIR) and T2-weighted image (WI) showed high intensity areas in the bilateral thalamus, caudate nucleus and hippocampus. She developed coma, convulsion, and ballism in the acute stage. One month after onset, she showed rhythmic, stereotyped, repetitive movements with hypoperfusion in the thalamus and frontal cortex on single photon emission computed tomography (SPECT). Three months later, her stereotyped movement improved accompanied by recovery of hypoperfusion in the thalamus and frontal cortex on SPECT. We speculated that her stereotyped movement was clonic perseveration due to frontal dysfunction induced by thalamofrontal disconnection.
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PMID:Clonic perseveration in the subacute stage of Japanese encephalitis. 1709 12


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