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)

Previous studies have shown that age at onset of primary haemolytic uraemic syndrome (HUS) is a feature of prognostic significance, the disease being of much better outcome in paediatric patients younger than 3 years than in older children. In an attempt to find an explanation for such a difference, we analysed the clinical and pathological features of 42 children over 3 years of age who presented with HUS between 1955 and 1990 in our department. On the basis of the presence of a prodromal diarrhoea, we divided our patients into two groups: 21 children presented with the diarrhoea-associated (typical or D+) form of HUS, whereas 21 had the non-diarrhoea-associated (atypical or D-) form. Of the 42 children, 20 (47.5%) progressed to end-stage renal failure. However, our study shows that age at onset of HUS is not a prognostic feature per se. The difference in outcome between children and infants is most likely related to the high incidence of the atypical subset of HUS in children over 3 years, a subset that is very uncommon in infants. The ominous features which characterise this form of the disease are: (1) the absence of a diarrhoeal prodrome, (2) normal urine output, (3) marked proteinuria, (4) hypertension, (5) the occurrence of relapses or recurrences and (6) the presence of widespread and severe arteriolar changes on renal biopsy. The poor prognosis of the atypical form of HUS warrants the use of fresh-frozen plasma infusions and/or plasma exchange as early as possible in the course of the disease.
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PMID:Haemolytic uraemic syndrome: prognostic factors in children over 3 years of age. 774 17

Paraneoplastic manifestations are signs and symptoms observed in patients with cancer, distant from the tumour or its metastases and not caused by invasion, obstruction or bulk mass. In children with cancer, paraneoplastic manifestations are rare and distinct from those observed in adults. Knowledge about paraneoplastic manifestations can be of great clinical importance because they may be the presenting sign of a tumour or its recurrence and hence facilitate early diagnosis. In contrast, they sometimes mask the symptoms of a tumour and cause diagnostic delay. In this review, paraneoplastic manifestations in children are described, including hypercalcaemia, Cushing syndrome, precocious puberty, opsoclonus/myoclonus, acquired von Willebrand disease, watery diarrhoea syndrome, and hypertension. The mechanisms causing these manifestations are also discussed.
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PMID:Paraneoplastic manifestations in children. 784 90

Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura is known to occur as a secondary complication of primary renal diseases, specifically of lupus nephritis, membranous glomerulonephritis, and focal segmental glomerulosclerosis. In a patient without a family history of hemolytic uremic syndrome/thrombotic thrombocytopenic purpura we observed biopsy-confirmed postinfectious glomerulonephritis with humps, with simultaneous subendothelial hyaline deposits and fibrinoid thrombi in arterioles. The patient had a history of febrile pharyngitis with diarrhea 10 days prior to renal biopsy. He presented with transient elevation of serum creatinine, a nephritic sediment, and hypertension not exceeding 160/100 mm Hg. The patient also had purpura, transient thrombocytopenia, and signs of intravascular hemolysis. Results of verocytotoxin serology were negative. With the exception of isolated microhematuria, all findings reverted to normal within 8 weeks without any specific treatment. This case illustrates that hemolytic uremic syndrome/thrombotic thrombocytopenic purpura may complicate primary postinfectious glomerulonephritis in adults.
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PMID:Hemolytic uremic syndrome complicating postinfectious glomerulonephritis in the adult. 784 62

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin I2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.
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PMID:Magnesium deficiency in alcoholism: possible contribution to osteoporosis and cardiovascular disease in alcoholics. 784 87

Thirty-one children with diarrhea-associated hemolytic uremic syndrome were retrospectively studied to determine if expression of the P1 blood type was related to the severity of the acute illness or to the prognosis. No differences were found in the clinical variables studied in the patients who were P1 positive compared to the patients who were P1 negative. The clinical variables studied included the age, hemoglobin, white blood cell count (WBC), and presence of central nervous system involvement at presentation, the duration of elevated WBC, thrombocytopenia, hemorrhagic colitis, and anuria, and the follow-up incidence of proteinuria, hypertension and decreased GFR. Expression of the P1 phenotype does not appear to exert a protective influence in patients with D+ HUS.
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PMID:The P1 blood group and the severity of diarrhea-associated hemolytic uremic syndrome. 785 Oct 28

The study aimed at evaluating an incidence of hypo- and hypernatremia in the elderly and the results of therapy. Hyponatremia. The studies involved 18 patients aged 69.8 +/- 5.9 years with hyponatremia of 126.8 +/- 2.7 mmol/L. The main causes of hyponatremia were: diuretics, diarrhoea, and vomiting. Sodium deficit was calculated prior to the treatment in all patients. An analysis of hyponatremia incidence indicates that hyponatremia was diagnosed in 1.39% of patients over 60 years, hospitalized within 1989-1990. Sodium deficit in this group was 495.5 +/- 167.7 mmol. Sodium chloride solution was given intravenously to 12 patients, according to the "free correction" principle (a mean increase in serum sodium level was 0.17 +/- 0.07 mmol/L per hour). Mortality in such treated patients was 33%. Sodium chloride was not given to 6 out of examined patients. In 12 patients (66.6%) hyponatremia developed prior to hospitalization, in 6 patients (33.3%) during hospitalization. Mortality rate was 16.6% and 50%, respectively. This confirms higher mortality rate of the rapidly developing hyponatremia in the hospitalized elderly patients. In some cases hyponatremia may constitute iatrogenic complication, especially in the elderly given diuretics in an uncontrollable way. Own experience suggests that elderly patients with a risk of hyponatremia require close monitoring and early compensation of the electrolyte disorders. Hypernatremia. The studies involved 20 patients aged 71.4 +/- 7.7 years with hypernatremia of 155.6 +/- 8.4 mmol/L. A total water deficit (DH20) was calculated in this group. An analysis of hypernatremia incidence showed that this state was diagnosed in 1.55% of patients treated at the Department of Arterial Blood Hypertension within 1989-1990. Total water deficit was 3.9 +/- 1.9 L. A 5% glucose was given intravenously to 15 patients whereas oral fluid therapy was carried out in 5 patients. A mean corrected DH2O in the first day was 46.0 +/- 21.0%. Mortality rate in this group was 65%. It is worth mentioning that 37% of patients with chronic hypernatremia which developed prior to hospitalization died while in case of the acute hypernatremia developed in the hospital mortality rate was 83%. A significant effect on the results of therapy plays an early correction of hypernatremia. Mortality rate in case of DH2o supplementation below 30% during the first 24 hours is about 66%., if DH2o supplementation is 31-60%, a mortality rate is 63%, and in DH2o supplementation over 60% mortality rate is 100%. The obtained results suggest that hypernatremia in the elderly is related to the high mortality rate (65%). An early decrease of water deficit increases mortality rate in patients with hypernatremia.
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PMID:[Hyponatremia and hypernatremia in the elderly]. 786 86

In a double-blind controlled trial, 91 middle-aged and elderly women with mild to moderate hypertension who were not on antihypertensive medication were randomly assigned to treatment with magnesium aspartate-HCl (20 mmol Mg/d) or placebo for 6 mo. Magnesium aspartate-HCl in the given dose was well-tolerated and was not associated with an increased frequency of diarrhea compared with placebo. At the end of the study, systolic blood pressure had fallen by 2.7 mm Hg (95% CI -1.2, 6.7; P = 0.18) and diastolic blood pressure by 3.4 mm Hg (1.3, 5.6; P = 0.003) more in the magnesium group than in the placebo group. Blood pressure response was not associated with baseline magnesium status, as measured by dietary magnesium intake and urinary magnesium excretion. Urinary magnesium excretion in the magnesium group increased by 50% during the intervention period. No changes were seen in other biochemical indexes, including serum concentrations of total and high-density-lipoprotein cholesterol. The findings suggest that oral supplementation with magnesium aspartate-HCl may lower blood pressure in subjects with mild to moderate hypertension.
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PMID:Reduction of blood pressure with oral magnesium supplementation in women with mild to moderate hypertension. 801 27

During normal pregnancy, serum transaminase levels remain within normal limits. An elevated level observed in a pregnant woman always signals a disease process, most often of hepatic origin, but in certain cases, of muscular origin. During the last three months of pregnancy and in the immediate post partum period a large number of liver diseases can cause elevated transaminase levels, depending upon the clinical presentation. In everyday practice, a complete liver battery together with specialized consultation is required for all pregnant women with raised transaminase levels. Toxaemia gravis may be evident in patients with severely raised blood pressure, especially if seizures occur. Epigastric or subcostal pain should suggest hepatic involvement. Hypertension may however be absent and epigastric or left shoulder pain may be the only clinical signs. Acute liver steatosis is 20 to 50 times more rare than toxaemia and may cause nausea and vomiting. Certain non-specific signs such as asthenia, anorexia, polyalgia, abdominal pain, diarrhoea and fever, together with pruritus should suggest acute hepatitis. A 25-fold increase in transaminase level is commonly encountered. The risk of fulminating hepatitis is less than 1/1000 but should always be entertained. All drugs should be stopped and careful research for recent xenobiotic contamination (drugs, infusions, alphamethyldopa, etc.) should be undertaken. Viral hepatitis requires serovaccination of the newborn at birth. Herpetic hepatitis is rare but requires rapid diagnosis (liver biopsy) and treatment with acyclovir in addition to cesarean section and treatment of the newborn at birth. Rare cases of hepatitis E may occur after a stay in North Africa, the Middle-East, Southeast Asia or Mexico. Chronic cases with or without temporary pruritus suggest infectious hepatitis B or C although, in chronic hepatitis C, serum transaminase levels often return to normal during pregnancy. Rare cases of asymptomatic elevations of serum transaminase levels can reveal subclinical chronic hepatitis.
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PMID:[Significance of elevated transaminase levels at the end of pregnancy]. 802 21

The PGE2 vaginal tablet has been introduced for use in term pregnancy. However, its effect in abortion and intrauterine fetal death (IUFD) is still uncertain. So we set up the following processes to research the efficacy of PGE2 in abortion and IUFD. We used PGE2 (3 mg) intravaginally for 12 hours in the patients of the first trimester. Consequently, the induction was achieved in a much shorter period. On the other hand, for patients in the second trimester, we used PGE2 (3 mg) in posterior fornix for 12 hours and PGE2 (1.5 mg) in extra-amnion successively. As a result, the cervical condition ripened more satisfactorily. The time of induction was about 14 to 18 hours in the second trimester, much shorter than the usual time needed. Besides, patients didn't complain of any special symptoms/signs such as nausea, vomiting, diarrhea, tachycardia, or hypertension. Therefore, we prefer to use this method for induction of the first & second trimester pregnancy including IUFD and abortion.
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PMID:Evaluation of the cervical conditions with PGE2 in first and second trimester. 805 9

BMA 031 (Behring Monoclonal Antibody) was given to 25 renal graft recipients with biopsy-proven steroid-resistant rejections. A dose of 50 mg of BMA 031 was given i.v. on 7 consecutive days concomitantly with a standard triple-drug regimen. No premedication was administered before the first BMA 031 dose. After the first dose, 7 patients experienced moderate fever (< 39 degrees C), 5 patients had high fever (> 39 degrees C), 4 patients had nausea/vomiting, 3 diarrhea, 1 headache, and 1 hypertension. These reactions were seen only after the first dose except for 1 patient who developed urticaria on days 3-4. All the rejection episodes were reversed or partially reversed. Twenty-one patients experienced re-rejections 3-46 days after the last BMA 031 dose, and were treated with methylprednisolone and/or rabbit antihuman thymocyte globulin. Seven patients lost their grafts within 1 year (28%), including 2 patients who died of infection with a functioning graft. BMA 031 seems to be a safe drug with only few mild side effects, and it effectively reverses steroid-resistant rejections. Re-rejections were frequent, but mostly reversible.
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PMID:A Scandinavian two-center study of BMA 031 in steroid-resistant rejection of renal grafts. 810 20


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