Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal artery dissection is a rare complication of catheter arteriography. Predisposing factors include atherosclerosis and fibromuscular dysplasia. Optimum management requires aortographic documentation of the extent of vascular obstruction. Dissections causing incomplete obstruction of blood flow can be treated with systemic anticoagulation to prevent downstream thrombosis and should be followed with serial isotope blood flow studies and LDH measurements. Dissection causing complete vascular obstruction usually requires immediate surgery, although spontaneous reestablishment of flow may occur. The 3 patients discussed illustrate a spectrum of findings, including the acute development of renovascular hypertension.
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PMID:Renal artery dissection: a complication of catheter arteriography. 117 54

HELLP syndrome continues to be a clinical entity of difficult diagnosis. Weinstein first defined it in 1982 giving the practicing obstetrician a sequence of useful initials (H = hemolysis; EL = elevated liver enzymes; LP = low platelets). Since then a lot has been written and it has become clear that the syndrome is a form of severe preeclampsia. The American College of Obstetrics and Gynecology does not include HELLP in the description of severe pre-eclampsia as such but does accept each of its components as being part of severe pre-eclampsia. The case presented deals with a 33 year old white female, admitted at 27 weeks gestation with nausea, epigastric pain resembling acute abdomen, nose bleeding and mild hypertension. The analysis revealed an abnormal liver profile with elevated GOT, GPT and LDH, heavy proteinuria (14.4 g/day), decreased platelet count (92000/mm3) and elevated total bilirubin. Pregnancy was terminated by cesarean section 24 hours after admission because the patient's condition was deteriorating. Obviously in pre-eclampsia/eclampsia there is a systematic injury to all tissues. Proof of this is the hypertension as a consequence of vascular spasm and proteinuria due to glomerular injury. In HELLP the sequence of events is probably altered; hepatic injury precedes vascular and renal injury of conventional preeclampsia. The syndrome results from many clinical and pathological symptoms derived from endothelial microvascular injury which determine a rapid platelet activation causing vascular spasm, platelet aggregation and further endothelial injury through a feedback mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Massive proteinuria and HELLP syndrome]. 130 8

From June 1987 to June 1991 at the Belgrade University Children's Hospital 10 patients, 5 males and 4 females, aged 2-16 years, with chronic glomerular disease, were treated with CyA. Seven patients had INS, 2 lupus nephritis and one IgA nephritis. Before initiation of CyA, all but one, were treated with classic immunosuppressive therapy, which had no effect (8/10) and/or had serious adverse effects (9/10). CyA dosage was initiated at 4-6 mg/kg/BW, and was subsequently adjusted to achieve CyA concentrations in blood at range 50-100 ng/ml. Treatment duration was 2-17 months. Patient compliance to CyA therapy was observed in 5/7 INSs: 2 cortico-sensitive (1 with FSGS was cortico-dependent and 1 had frequent relapses) and 3 cortico-resistant patients (2 with FSGS and 1 with minimal histologic changes). After drug withdrawal, only one of the patients who responded, had no relapse. One of the two patients with SLE showed improvement during CyA administration, while no response was observed in the patient with IgA nephritis. Adverse experiences with CyA therapy involved decreased renal function (2/10), arterial hypertension (1/10), hyperbilirubinaemia (1/10), transient LDH increase and hyperuricaemia (1/10).
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PMID:[Cyclosporine in the treatment of glomerular diseases in children]. 146 61

The present study employed enzyme-immunoassay to examine the effect of ethanol on endothelin-1 and/or -2(ET1 + 2) release from human umbilical vein endothelial cells. Thirty minutes of exposure to ethanol increased the release of immunoreactive ET1 + 2 from cultured endothelial cells in a dose-dependent manner. However, ethanol at concentrations of less than 400 mM did not induce any LDH release from the endothelial cells. Trypan blue exclusion test revealed that 400 mM solution of ethanol decreased the cell viability to 7.7%. Thus, ethanol was found to directly stimulate ET1 + 2 release from cultured human umbilical vein endothelial cells. This reaction of vascular endothelial cells against ethanol may be related to ethanol-induced cardiovascular diseases such as hypertension, myocardial infarction and stroke, as well as fatal alcohol syndrome.
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PMID:Ethanol stimulates immunoreactive endothelin-1 and -2 release from cultured human umbilical vein endothelial cells. 159 May 57

The plasma activities of LDH and ASAT isoenzymes as well as of DP IV were studied in patients with essential hypertension and related to blood pressure, haemodynamic indicators of latent heart failure and to ischaemic heart risk indicators. Patients with elevated systolic or diastolic blood pressure showed significantly increased activities of ASAT m. In hypertensives with elevated pulmonary artery pressure markedly increased activities of ASAT, ASAT m, LDH M and DP IV could be observed. Distinctly increased activities of ASAT, ASAT m, LDH M and DP IV were also found in patients with elevated plasma cholesterol. The results obtained suggest that changes of LDH and ASAT isoenzymes as well as of DP IV indirectly reflecting alterations in organ metabolism might provide useful additional information with respect to uncovering hypertension-linked complications.
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PMID:Isoenzyme (lactate dehydrogenase, aspartate aminotransferase) and dipeptidyl peptidase IV activity changes in blood plasma likely indicative of organ involvement due to arterial hypertension. 168 Jun 2

On the basis of a case history, the clinical and paraclinical manifestations of hypothyroidism are reviewed. Exertion dyspnoea without signs of cardiac insufficiency occurs frequently. The minute and stroke volume and heart rate are reduced. The blood pressure may rise (reversible) and hypertension may occur. The function of the left ventricle is reversibly reduced. A tendency to formation of exudates has been observed. X-ray of the thorax may revial massive relatively asymptomatic pleural exudates and cardiomegaly. Pericardial exudate occurs frequently and is demonstrated best by echocardiography. Inter- and intracellular deposits, infiltrations and fibroses have been demonstrated in the myocardium and these probably contribute to some of the non-specific, reversible ECG changes (low voltage, flattening/inversion of T waves, sinus bradycardia). The plasma concentrations of several different enzymes (including creatine kinase (CK), CK-MB and LDH) may be raised in myxoedema. The reason for this is perhaps compromized membrane function in the skeletal muscle cells. The diagnosis of myocardial infarction in myoedema requires that CK-MB constitutes at least 6% of the total CK and that the increase is transient. In patients with coronary sclerosis, substitution treatment should be initiated carefully because the risk of ischaemic symptoms is otherwise considerably increased. It is not elucidated whether the hypothyroidism per se can increase atheroma formation.
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PMID:[Cardiovascular manifestations of hypothyroidism]. 186 65

A case of microangiopathic hemolytic anemia (MHA) associated with the immunosuppressive agent, cyclosporine, is reported herein. The patient manifested anemia with red blood cell fragmentation, hypertension, thrombocytopenia, elevation of serum LDH levels and glomerular capillary thromboses within a few days of his transplantation. Extensive treatments with urokinase and heparin proved ineffective and graftectomy was performed 7 days after his transplantation. Immunofluorescent staining failed to show immunoglobulin (IgG or IgM) or complement (C3) deposition within the glomeruli, which discriminated MHA from acute humoral-vascular rejection.
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PMID:Cyclosporine-associated microangiopathic hemolytic anemia in a renal transplant recipient. 265 53

1. The authors elaborated an original concept for the interpretation of vasomotor disorders in subjects with an artificial heart. 2. This concept is based on the regeneration of nervous elements in the walls of the atria (in particular the right one) after implantation of the artificial heart and on comparison of their activity with the venous pressure which revealed the interrelationship of the two phenomena. 3. Both therapeutic methods based on this concept, the method of influencing the afferentation and efferentation of vasomotor nervous regulations leading to a reduction of the central venous pressure proved valid and effective. 4. Evaluation of the effectiveness of this therapy is based on regular assessment of the central venous pressure, on the laboratory assay of enzymes (AST, ALT, GMT and LDH), on the assessment of serum albumin and finally on the morphological and histological examination of the liver incl. assessment of the hepatic index. 5. The nervous pathogenesis is closely linked with hormonal factors. The latter are conceived as the participation of associated factors in the pathogenesis of venous hypertension in recipients with an artificial heart.
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PMID:[Therapy of venous hypertension in animals with an artificial heart and long-term survival]. 268 92

To examine the efficacy of magnetic resonance imaging (MRI) in diagnosing hypertrophic cardiomyopathy (HCM), 16 patients with HCM and 14 hypertensives with left ventricular hypertrophy (LDH) were studied using a 0.5 Tesla Siemens MRI apparatus equipped with cardiac gating. In HCM, left ventricular hypertrophy was localized to the septal wall in four, to the apical wall in two, to both the septal and apical walls in two, and to the apical and inferior walls in one, and it was diffuse in seven patients. In hypertensives, LVH was localized to the septal wall in three, to both the septal and anterior walls in two, to the free wall in one, and it was diffuse in eight patients. The distribution of the hypertrophic portion was nearly equal in both groups. The thickest portion of the left ventricular wall was 24.6 +- 4.8 mm in HCM and 21.6 +- 5.4 mm in hypertension, and there was no significant difference between them. The T2 relaxation time of the hypertrophic portion was 52.2 +- 4.8 msec in HCM and 45.3 +- 6.1 msec in hypertension, and there was a significant difference between them (p less than 0.01). However, there were no significant differences between the T2 relaxation times of the hypertrophic and non-hypertrophic portions in both groups. In conclusion, it may be difficult to differentiate HCM from hypertension based on the distribution of hypertrophic portions, but measurements of the T2 relaxation times may be useful for making the differential diagnosis.
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PMID:[Differentiation of hypertrophic cardiomyopathy from left ventricular hypertrophy induced by essential hypertension using magnetic resonance imaging]. 297 2

Six women without hypertension or proteinuria, admitted for severe upper abdominal pain in the third trimester of pregnancy had elevated serum liver enzymes (SGOT, SGPT), markedly increased serum LDH levels, thrombocytopenia and abnormal blood coagulation tests, in particular low antithrombin III levels, indicating disseminated intravascular coagulation (DIC). Liver biopsies showed periportal and/or focal parenchymal lesions with large fibrin deposits, comparable to the liver lesions in eclampsia. Immunofluorescence (IF) showed microthrombi and large fibrin deposits. Three of the six women recovered spontaneously before delivery; in the remaining three all signs and symptoms rapidly disappeared after delivery. Perinatal outcome was poor. Seven women with pregnancy-induced hypertension and elevated serum liver enzymes constituted a reference series. Histopathological examination of liver biopsies in the reference group revealed periportal and/or focal parenchymal lesions in three whereas IF showed fibrin deposition in all seven, but less extensive than in the study group. The present findings indicate that upper abdominal pain in the last trimester of pregnancy can be caused by a syndrome of (pre)-eclamptic liver damage and DIC, even when hypertension and proteinuria are lacking.
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PMID:A syndrome of liver damage and intravascular coagulation in the last trimester of normotensive pregnancy. A clinical and histopathological study. 351 56


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