Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is now quite well accepted that laboratory test results are indispensable or of primary significance to accurately diagnose a new patient's disease. Furthermore, most doctors recently find difficulty in appropriately selecting and ordering necessary but not excess laboratory tests and to read and interpret all the given test results correctly. In our hospital the system of the outpatient clinic will be changed basically on a specialty clinic system. In order to operate such a specialty clinic system effectively, it appears quite important to set up a unit to discriminate new unspecified patients properly and to consult them to an appropriate specialty clinic. As a preliminary trial, we opened a new patient clinic in July, 1992. The aim of this clinic is to accurately diagnose the new patients' disease immediately and to send them to the specialty clinic on the day of their first visit. Prior to history taking and physical examination by the attending doctor, the patients are instructed to take a set of laboratory tests. These include urinalysis, chest X-P, ECG, hematological examinations (RBC, WBC, Ht, Hb, PLT and ESR) and biochemical tests (AST, ALT, ALP, gamma GTP, LDH, CPK, Chol, T-Bil, TP, Alb, TG, BUN, Cr, Glu, Na, K, Ca, P and CRP). These results are transferred to the clinic within one hour so that the doctor is able to make the diagnosis effectively and to refer the patients to an appropriate clinic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Roles of department of laboratory medicine on the new patient clinic]. 828 94

A case of a 73-year-old woman with acute renal failure due to toxic shock syndrome (TSS) is reported. The patient was admitted to our hospital with the complaints of high fever, disturbance of consciousness and shock. Laboratory findings on admission were; CRP 25.11 mg/dl, WBC 35000/ microl, Plt 1.6 x 10(4)/ microl, GOT 155 U/l, GPT 65 U/l, CPK 4202 U/l (CPK-MM 96%), BUN 123 mg/dl and SCr 7.0 mg/dl. Because of anuria, hemodialysis was performed. This patient was treated with dopamine, methyl prednisolone (MP), frozen fresh plasma, AT III, antibiotics, and platelet transfusion. The bacterial cultures of blood and cerebrospinal fluid were negative, but MRSA was isolated subsequently from the pharynx and vagina. We investigated the production of toxic shock syndrome toxin 1 (TSST-1) and staphylococcal enterotoxins (SE). The isolated MRSA produced TSST-1, SEB and SEC. Accordingly, we made the diagnosis of TSS. After improvement of acute renal failure and the patient's general condition, MRSA persisted and TSST-1 was still found in the patient's blood. Finally we eradicated the MRSA and TSST-1 after administration of ciprofloxacin hydrochloride (CPFX) and Rifampicin (RFP).
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PMID:[A case of toxic shock syndrome (TSS) induced by methicillin-resistant staphylococcus aureus (MRSA) presenting as acute renal failure with disseminated intravascular coagulation]. 885 34

We report a 56-year-old man who developed progressive paraparesis. He was apparently well, except for left Bell's palsy which developed on May 9 of 1994, for which he received stellate ganglion block on the left side more than ten times until July 2nd of 1994, when he noted pain in his left shoulder and in his lumbar region. On July 5th, he noted some difficulty in urination. On July 6th, he noted tingling sensation in his four extremities and difficulty in gait. He was admitted to another hospital where he was treated with intravenous infusion of glycerol. After this treatment, his gait and sensory disturbance showed some improvement, however, on July 7th, his shoulder and lumbar pain worsened, and he became unable to stand. His temperature went up to 39 degrees C on the next day. Lumbar CSF on that day contained 119 cells/microliters, 112 mg/dl of protein, and 53 mg/dl of sugar. He was transferred to our hospital on July 14th. His past medical history revealed that he had suffered from frequent bouts of osteomyelitis since the age of 13 years. He was operated on several times on osteomyelitis. He had been treated on his tooth ache until shortly before the onset of the present illness. He also received steroid hormone for his Bell's palsy. On admission, his consciousness varied from alert to stupor. His BP was 150/100 mmHg, HR 98/min and regular, BT 39.4 degrees C. The bulbar conjunctiva appeared somewhat icteric. Otherwise, general physical examination was unremarkable. On neurologic examination, there was no apparent dementia. Higher cerebral functions appeared intact. The optic discs were flat. Pupils were round and isocoric reacting to light and accommodation promptly. Ocular movements were full without nystagmus. Some exophthalmos was noted bilaterally. The sensation of the face and facial muscles were intact. The remaining cranial nerves also appeared intact. Nuchal rigidity was present. He was unable to stand or walk. Muscle strength was markedly diminished in all four limbs; manual muscle testing revealed 1 to 2/5 weakness in both upper and lower extremities bilaterally. Muscle stretch reflexes were decreased or lost in both upper and lower limbs, but the plantar response was extensor on the right. Sensation appeared to be diminished in legs, but detail was not clear because of disturbance of consciousness. Pertinent laboratory findings were as follows: WBC 12,800/microliter, GPT 58 IU/l, total bilirubin 2.65 mg/dl, and CRP 16.8 mg/dl. Cerebrospinal fluid contained 34 cells/microliter (approximately two thirds were neutrophils), RBC 1,110/microliter, 2,949 mg/dl of protein, and 119 mg/dl of glucose; stapylococcus aureus was cultured from the CSF. Myelogram showed a filling defect in the anterior epidural space between the low thoracic and the upper lumbar region. The patient was treated with cephotaxim, aminobenzyl penicillin, and chloramphenicol. On the second hospital day, his BT was still 39 degrees C and he was agitated His weakness was worse than the previous day. Spinal MRI was attempted; as he was agitated 5 mg of diazepam was given intravenously at 4 PM. His respiration was rapid and somewhat shallow. At 6 PM, gadolinium DTPA was injected intravenously; at that time, he was breathing and pupils were 3 mm on both sides. At 6:35 PM, an examiner noted that he stopped breathing; the left pupil was dilated to 5 mm. Cardiopulmonary resuscitation was initiated immediately, and intubation was performed. He was placed on a respirator. His blood pressure did not reach 100 mmHg; he was in deep coma. Cardiac arrest occurred at 8:53 AM on the next morning. The patient was discussed in a neurological CPC. Most of the participants thought that the patient had either spinal epidural empyema or spinal subdural abscess. The question was what might be the original focus of infection. Three possibilities were considered, i.e., stellate ganglion block, teeth infection, and osteomyelitis...
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PMID:[A 56-year-old man with fever, backache and tetraparesis]. 896 86

We compared the severity of clinical symptoms and laboratory test results of tsutsugamushi disease patients in Oita Prefecture according to the serotype of infected R. tsutsugamushi. Of the 45 patients, except one with the Karp-type, who were suffering in Oita Prefecture between 1992 and 1994, 20 were the Irie-type and 24 were the Hirano-type. There was no apparent difference with regard to clinical symptoms between the two groups of patients. Laboratory tests showed that CRP increased almost equally in the two groups. The ESR level was slightly higher in the Irie-type patients than in the Hirano-type, but did not differ significantly between the two groups. Both leukocyte count in the acute stage and platelet count decreased in the Hirano-type, as compared with those of normal ranges in the Irie-type. GPT values elevated in proportion to the day of illness in the acute stage. This trend continued after the initiation of specific chemotherapy in the Hirano-type. The median GOT, GPT and LDH values were 71, 65 and 709 IU/l for the patients in the Hirano-type, as compared with 37, 36.5 and 546.5 for the patients in the Irie-type, respectively. Above results show that the Hirano-type rickettsiae produces a more severe illness than the Irie-type ricketsia. Platelet count had a significant correlation with ESR, suggesting the pathophysiologic changes leading to disseminated intravascular coagulation, a symptom of severe tsutsugamushi disease. There may be common causes in leukopenia and thrombopenia, as being suggested by the significant correlation between leukocyte count and platelet count.
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PMID:[Analysis of clinical severity of tsutsugamushi disease according to the serotype of pathogenic rickettsia]. 916 83

We have characterized clinical and diagnostic features in 18 cases of Legionella pneumonia. Age average of patients was 62.0 years old (male:female = 14:4) and underlying diseases were observed in 12 patients. Legionella pneumonia were diagnosed in 3, 5, 8 and 9 cases by culture, serum antibody measurement, urinary antigen detection and PCR, respectively. Sixteen cases were caused by L. pneumophila, while the other 2 cases were L. bozemanii pneumonia and L. pneumophila or L. dumoffii pneumonia. Chest X-rays of those patients showed multiple pneumonia shadows in 14 cases, alveolar shadows in 10 cases, pleural effusion in 5 cases. Blood-gas analysis on admission indicated hypoxemia in all cases with abnormal A-a DO2. Laboratory findings showed abnormal data in WBC, CRP, LDH, CPK and liver function tests (ex. GOT, GPT) in most cases. Serum antibody testing showed positive by 5 weeks after onset of pneumonia, but 10 cases of Legionella pneumonia diagnosed by other techniques were judged to be negative. In urinary antigen detection test, 6 and 2 cases showed positive 1 and 4 weeks after onset of pneumonia, respectively. Macrolide antibiotics were administered in all cases during the episode, but delay of macrolide administration was observed in 3 of 4 cases of dead outcome. Serum antibody measurement, urinary antigen detection and PCR, in addition to culture to bacteria, may be required for exact diagnosis of Legionella infection.
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PMID:[Clinical and diagnostic characteristics of Legionella pneumonia]. 928 39

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

Liver dysfunction often occurs during chemotherapy for AML, but the etiologies are many and varied. To determine liver dysfunction that is not related to HCV, liver function during intense therapy for one week after complete remission was studied in eight patients not infected with HCV (38 courses) and six HCV-infected patients (19 courses) with AML. There were remarkable differences in changes of ALT levels among HCV-infected patients. ALT level changes among patients not infected with HCV were similar. Changes in mean serum ALT levels in HCV-infected patients occurred at higher serum levels as compared with those in patients not infected with HCV. The mean serum ALT levels in patients not infected with HCV significantly increased at one week (45 +/- 5 IU/l) and further increased at two (58 +/- 8 IU/l) and three weeks (57 +/- 5 IU/l) as compared with pretreatment levels (24 +/- 21 IU/l) (p < 0.001, p < 0.001, p < 0.0001, respectively). ALT levels returned to normal at four weeks. During 31 of 38 courses (81.6%) in patients not infected with HCV, febrile episodes occurred at three weeks. The mean serum ALT levels in patients with febrile episodes were significantly higher than those in patients without febrile episodes at three weeks, and serum ALT levels at three weeks showed a significant positive correlation with CRP levels at three weeks. These findings indicate that liver dysfunction during chemotherapy for AML is due to hepatocellular injury, and infection or inflammatory cytokine induced by infection results in the worsening of the liver dysfunction.
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PMID:Liver dysfunction in patients with acute myelogenous leukemia: studies on patients not infected with hepatitis C virus during intense therapy. 970 92

We have characterized clinical and diagnostic features in 18 cases of Legionella pneumonia. Age average of patients was 62.0 years old (male: female = 14:4) and underlying diseases were observed in 12 patients. Legionella pneumonia were diagnosed in 3, 5, 7 and 9 cases by culture, serum antibody measurement, urinary antigen detection and PCR, respectively. Sixteen cases were caused by L. pneumophila, while the other 2 cases were due to L. bozemanii and L. pneumophila or L. dumoffii. Chest X-rays of those patients showed multiple pneumonia shadows in 14 cases, alveolar shadows in 10 cases, pleural effusion in 5 cases. Blood-gas analysis on admission indicated hypoxemia in all cases with abnormal A-a DO2. Laboratory findings showed abnormal data in WBC, CRP, LDH, CPK and liver function tests (ex. GOT, GPT) in most cases. Serum antibody testing showed positive by 5 weeks after onset of pneumonia, but 10 cases of Legionella pneumonia diagnosed by other techniques were judged to be negative. In urinary antigen detection test, 6 and 2 cases showed positive 1 and 4 weeks after onset of pneumonia, respectively. Macrolide antibiotics were administered in all cases during the episode, but delay of macrolide administration was observed in 3 of 4 cases of dead outcome. Serum antibody measurement, urinary antigen detection and PCR, in addition to culture of bacteria, may be required for exact diagnosis of Legionella infection.
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PMID:[Legionella pneumonia--epidemiology, clinical characteristics and development of diagnosis]. 979 41

A 70-year-old woman was referred to our hospital for treatment of cholelithiasis. A giant liver cyst (6 cm in diameter) had been diagnosed three years earlier. On admission, she had low grade fever and hepatomegaly. High values were observed for WBC (9900/microliter), CRP (8.9 mg/dl), GPT (45 IU/l), ALP (1399 IU/l), gamma-GTP (333 IU/l) and LAP (249 IU/l). The diagnosis of infected liver cyst (8 cm in diameter) was made based on contrast-enhanced CT scan. Endoscopic retrograde cholangiopancreaticography showed no communication between the cyst and the intrahepatic bile duct. She was successfully managed with antibiotics and discharged without percutaneous aspiration the cyst. On abdominal CT scan 4 months after the discharge, the liver cyst had decreased dramatically in size (1 cm in diameter). The patient remains healthy without symptoms.
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PMID:[An elderly case of giant infected liver cyst that decreased dramatically without percutaneous aspiration]. 1046 56

A 66-year-old male was admitted to our hospital, presenting a high fever and generalized erythema on June 9, 1999. Physical examination revealed many eschars on his legs. Laboratory examinations were as follows: platelet counts, 5.5 x 10(4)/microliter: FDP, 25 micrograms/ml: TAT, 70.9 ng/ml: GOT, 177 IU/l, GPT, 174 IU/l: CRP, 32.3 mg/dl. Based on these findings, he was diagnosed as having rickettsiosis with DIC, and minocycline (200 mg/day) and heparin were started immediately, but had no clinical effect for 3 days. Blood gas analysis showed severe hypoxia and the chest CT scan revealed increased CT value in all lung fields with reticular shadows in the lower fields and pleural effusion, suggested interstitial pneumonia. Methyl-prednisolone pulse therapy was started on June 12, after which he completely recovered. Anti-Rikettia japonica IgM antibody was found to be x8,192 by immunofluorescent test, establishing the diagnosis of Japanese spotted fever. Acute respiratory failure with interstitial pneumonia shadows should be emphasized as a complication of severe rickettsiosis.
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PMID:[Japanese spotted fever complicated by acute respiratory failure]. 1074 Oct 8


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