Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The number of changes in some maternal serum biochemical parameters for some congenital malformations are presented. In all pregnancies we observed low levels of LAT, AST, CPK, HBD, AP and high levels of GGTP, THY, amylase. These data demonstrate total depression in metabolism of women with an affected fetus. The biological basis of altered levels of enzymes in pregnancies with affected fetus is unclear.
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PMID:[Various biochemical parameters in serum of pregnant women carrying fetuses with various congenital defects of development]. 830 59

To assess the significance of ST segment shift during the acute phase of non-Q myocardial infarction we studied the clinic echocardiographic, ergometric and coronarographic findings of 46 patients with a first non-Q wave myocardial infarction. The study population was subdivided in 2 subgroups on the basis of acute electrocardiographic change (Group I with ST elevation, Group II with ST depression). Patients with ST elevation had little myocardial infarction with enzymatic (early CPK peak) and coronarographic (low prevalence of coronary occlusion) signs of early spontaneous fibrinolysis. The second group had more diffuse myocardial infraction, higher prevalence of multivessel coronary disease and positive stress test. The ECG changes in this subgroup an probably due to subendocardial necrosis for the presence of collateral flow. The worse intrahospital prognosis of patients with ST segment depression may be related to cardiac function and age.
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PMID:[A non-Q wave myocardial infarct with an up or down shift of the ST segment in the acute phase: the clinical, echocardiographic, ergometric and coronary angiographic correlates]. 832 71

A 53-year-old woman was admitted to the hospital for chest pain with headache, nausea and vomiting, two and a half hours after an intramuscular injection of 6 x 10(6) units of IFN (interferon) alpha 2a, in the 11th week of IFN treatment for chronic hepatitis C. The electrocardiogram (ECG) showed ST depression and T inversion in leads II, III, aVF and V3-V6, as commonly seen in myocardial ischemia. However, emergency coronary angiography (CAG) did not show stenosis or spasms clearly, serum CPK was always within the normal limits, Tc-99m PYP scintigraphy and T1-201 scintigraphy did not show any abnormal uptake or defect, and the echocardiogram did not show any abnormality. She recovered from chest pain and the ischemia-like changes seen on the ECG, after IFN treatment was stopped, and she rested for 7 days from this treatment and other treatment using nitrites and a calcium-antagonist. After recovery, the ECG during exercise and hyperventilation showed changes similar to those seen on admission. From these findings, this case was considered to be precipitated by spasms of coronary microvessels, which were not noticeable in CAG. The cause was thought to be complicated by IFN treatment, because this episode appeared after IFN injection, and improved after stopping IFN treatment.
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PMID:[A case of chronic hepatitis C complicated by ischemia-like changes seen on the electrocardiogram during interferon treatment]. 835 43

A 77-year-old male had been noticing progressive weakness of the legs for three years. By the age of 75 he had difficulty in climbing stairs. On admission, serum level of CPK was moderately high. There were weakness and atrophy of the proximal muscles. Deep tendon reflexes were depressed. Sensation was normal. The electromyogram and the biopsy of the femoral quadriceps muscles showed nonspecific changes. In 1989, he developed difficulty in walking and had congestive heart failure. On the second admission, moist rales were heard over the chest, and pitting edema was present in the lower extremities. The chest roentgenogram showed a cardiothoracic ratio of 63% and bilateral pleural effusion. The electrocardiogram showed atrial flutter with 2:1 conduction, QS in V1-3, rS in V4, and ST depression and T inversion in V5,6. The echocardiogram revealed a thick left ventricular wall and impaired left ventricular contraction (EF 22%). Macroglossia, hepatosplenomegaly and renal dysfunction were not noted. Congestive heart failure progressed and he suddenly died of ventricular tachycardia in December 1989. At autopsy, skeletal muscle fibers varied in size and showed fiber splitting. A cellular infiltration was observed in the stroma. Amyloid deposit was positively stained with Congo red. The heart weight was 570 g with marked left ventricular hypertrophy and moderate bilateral atrial dilatation. In both atria and ventricles, extensive amyloid deposition was found around myocardial fibers as well as in perivascular spaces. Amyloid was present also in the liver, the kidneys, the gastrointestinal tracts, and the other organs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of primary systemic amyloidosis with skeletal muscle atrophy and congestive heart failure]. 848 88

Excessive stimulation of serotonin 5HT1A receptors causes a syndrome of serotonin excess that consists of shivering, muscle rigidity, salivation, confusion, agitation and hyperthermia. The most common cause of this syndrome is an interaction between a monoamine oxidase inhibitor (MAOI) and a specific serotonin reuptake inhibitor. Venlafaxine is a new antidepressant agent that inhibits the reuptake of serotonin and norepinephrine. We report a venlafaxine-MAOI interaction that resulted in the serotonin syndrome in a 23-y-old male who was taking tranylcypromine for depression. He had been well until the morning of presentation when he took 1/2 tab of venlafaxine. Within 2 h he became confused with jerking movements of his extremities, tremors and rigidity. He was brought directly to a hospital where he was found to be agitated and confused with shivering, myoclonic jerks, rigidity, salivation and diaphoresis. His pupils were 7 mm and sluggishly reactive to light. Vital signs were: blood pressure 120/67 mm Hg, heart rate 127/min, respiratory rate 28/min, and temperature 97 F. After 180 mg of diazepam i.v. he remained tremulous with muscle rigidity and clenched jaws. He was intubated for airway protection and because of hypoventilation, and was paralyzed to control muscle rigidity. His subsequent course was remarkable for non-immune thrombocytopenia which resolved. The patient's maximal temperature was 101.2 F and his CPK remained < 500 units/L with no other evidence of rhabdomyolysis. His mental status normalized and he was transferred to a psychiatry ward. This patient survived without sequelae due to the aggressive sedation and neuromuscular paralysis.
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PMID:Serotonin syndrome from venlafaxine-tranylcypromine interaction. 888 41

Although lupus cardiomyopathy is thought to be clinically uncommon, we encountered 6 patients with systemic lupus erythematosus (SLE) over a 10 year period who had severe left ventricular dysfunction and showed remarkable improvement in their cardiac function after cytotoxic therapy. All patients met the American College of Rheumatology criteria for classification of SLE and presented with signs of severe biventricular failure relatively early in their disease. Concurrent manifestations of SLE at the time of cardiomyopathy included rash, arthritis, myalgias, pleuritis, pericarditis, and nephritis. Four of the 6 patients were taking prednisone 20 mg/day at the time heart failure developed. In all cases the CPK were normal. Evaluation of cardiac function by echocardiogram and/or radionuclide gated blood pool scintigraphy revealed a severe depression of ventricular function with initial left ventricular ejection fraction (LVEF) ranging from 11 to 34% (mean 19%). Within 6 months of initiation of cytotoxic treatment all patients showed a dramatic response: the post-treatment LVEF ranged from 25 to 55%. This series of patients suggests that cardiomyopathy may be a more common complication of SLE than previously reported. Cardiomyopathy occurs relatively early in the course of SLE, may lead to severe cardiac dysfunction despite corticosteroid therapy, and appears to be responsive to cytotoxic therapy.
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PMID:Dramatic improvement of left ventricular function after cytotoxic therapy in lupus patients with acute cardiomyopathy: report of 6 cases. 1052 51

Melia azedarach fruits were administered at single doses ranging from 5 to 30 g/kg bw to 10 calves. The animals dosed with 25 g/kg bw and 30 g/ kg bw died, as well as 1/2 cattle that received 15 g/kg bw. Clinical signs were depression, ruminal stasis, anorexia, diarrhea, incoordination, muscle tremors, difficulty to stand, sternal recumbence, hypothermia and dyspnea. Serum AST and CPK were increased. Signs appeared 4 to 24 h after dosing and the clinical manifestations continued for 20 to 72 h. Macroscopic findings included congestion of the intestine, focal or diffuseyellow discoloration of the liver, and brain congestion. LiQuid content was in rumen, reticulum and intestines. The liver had swollen and vacuolated hepatocytes, and necrotic hepatocytes were scattered throughout the parenchyma or concentrated in the periacinar zone. Degenerative and necrotic changes were in the epithelium of the forestomachs. There was also necrosis of lymphoid tissue. Skeletal muscles had hyaline degeneration and fiber necrosis.
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PMID:Intoxication of cattle by the fruits of Melia azedarach. 1204 65

A clinicofunctional analysis of the heart was made in 50 patients suffering from hemorrhagic fever with renal syndrome (HFRS) in the acute period and at the stage of outpatient rehabilitation. Comparison with healthy subjects was made by physical, ECG, echo-CG data, changes in the levels of creatinphosphokinase (MB-fraction) (CPK-MB), asparagine and alanine aminotransferase in the serum. Clinical symptoms of heart pathology, their incidence rate in different periods of the disease, dynamics of ECG deviations, state of heart chambers and left ventricular systolic function are described. The most manifest changes of the studied parameters were observed in acute disease and depended on the disease severity. The detected changes in the end part of the ventricular complex on ECG associated with a relative depression of left ventricular systolic function as well as a rise in the level of CPK-MB indicate affection of the myocardium. Variants of combination and dynamics of the above disorders allowed to single out the most probable syndromes of heart affection in HFRS.
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PMID:[Clinicofunctional characteristics of the heart in hemorrhagic fever with renal syndrome]. 1247 34

Olanzapine is a new atypical antipsychotic drug acting on different receptors. A variety of pharmacologic effects are responsible for toxicity and the variety of clinical symptoms seen in overdose: tachycardia, agitation or aggression, dysarthria, extrapyramidal dystonic effects, sedation or coma, small pupils, blurred vision, respiratory depression, hypotension. A retrospective analysis of clinical course of eight acute olanzapine intoxication treated at the Department of Clinical Toxicology Jagiellonian University Medical College is presented. CNS symptoms manifested in fluctuations between somnolence/coma and agitation/aggression and miosis were observed in most of the patients. Increased CPK activity was stated in the most of patients. All of the patients recovered, poisoning severity according PSS was moderate and severe.
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PMID:[Clinical course of acute poisoning with olanzapine]. 1622 3

A 74-year-old man with depressive symptoms was admitted to a psychiatric hospital due to insomnia, loss of appetite, exhaustion, and agitation. Medical treatment was initiated at a daily dose of 20 mg paroxetine and 1.2 mg alprazolam. On the 10th day of paroxetine and alprazolam treatment, the patient exhibited marked psychomotor retardation, disorientation, and severe muscle rigidity with tremors. The patient had a fever (38.2 degrees C), fluctuating blood pressure (between 165/90 and 130/70 mg mm Hg), and severe extrapyramidal symptoms. Laboratory tests showed an elevation of creatine phosphokinase (2218 IU/L), aspartate aminotransferase (134 IU/L), alanine aminotransferase (78 IU/L), and BUN (27.9 mg/ml) levels. The patient received bromocriptine and diazepam to treat his symptoms. 7 days later, the fever disappeared and the patient's serum CPK levels were normalized (175 IU/L). This patient presented with symptoms of neuroleptic malignant syndrome (NMS), thus demonstrating that NMS-like symptoms can occur after combined paroxetine and alprazolam treatment. The adverse drug reaction score obtained by the Naranjo algorithm was 6 in our case, indicating a probable relationship between the patient's NMS-like adverse symptoms and the combined treatment used in this case. The involvement of physiologic and environmental aspects specific to this patient was suspected. Several risk factors for NMS should be noted in elderly depressive patients whose symptoms often include dehydration, agitation, malnutrition, and exhaustion. Careful therapeutic intervention is necessary in cases involving elderly patients who suffer from depression.
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PMID:Possible neuroleptic malignant syndrome related to concomitant treatment with paroxetine and alprazolam. 1672 68


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