Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acetazolamide is a useful prophylactic for acute mountain sickness causing marked reduction in headache, nausea, vomiting, weakness, etc. Improvements correlate with increased arterial oxygen concentrations, reduction in proteinuria and peripheral oedema and other objective measures of acute mountain sickness. Evidence that Acetazolamide is beneficial for pulmonary oedema or cerebral oedema is scanty because of the lower frequency of these severe forms of mountain sickness. Dexamethasone, used prophylactically, also reduces the symptoms of acute mountain sickness partly due to its euphoric effect. Use of Acetazolamide as a treatment for established acute mountain sickness has been investigated. Large doses of Acetazolamide increase arterial oxygen levels over a few hours and this leads to a reduction of symptoms but data is limited and faster acting carbonic anhydrides inhibitors such as Methazolamide may be preferable in an emergency situation. There is no comparison of the effectiveness of Acetazolamide with other drugs used for treating acute mountain sickness such as steroids and calcium channel blocking drugs. Also, there is no data on drug combinations which could have additive effects and thereby be more beneficial than individual drugs.
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PMID:Acetazolamide and high altitude diseases. 148 96

Pregnancy-induced hypertension is a disorder of unknown etiology unique to pregnant women. Classic clinical manifestations include hypertension, proteinuria, and edema. Early recognition and proper management of this disease may serve to avoid serious maternal complications. Ultimate maternal treatment depends on delivery of the fetus and placenta. Advanced stages of this disease result in multi-organ system dysfunction that may be life-threatening to the mother and her fetus. Such maternal complications of PIH include severe hypertension, oliguria or anuria, HELLP syndrome, eclamptic seizures, liver rupture, pulmonary edema, cerebral edema, and abruptio placentae. A multidisciplinary approach of the critical care team often will effect a reduction in maternal morbidity and mortality.
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PMID:Management of severe preeclampsia and eclampsia. 174 3

In 7 years (1981-1988) at the Kenyatta National Hospital (KNH), Nairobi the diagnosis of systemic lupus erythematosus (SLE) was made in 67 patients. In 23 of these patients lupus nephritis complicated the SLE. Lupus nephritis was diagnosed through renal biopsy, haematuria and proteinuria in urine with positive lupus erythematosus (LE) cell phenomenon. The histology found in these patients included 5 patients with minimal lesion, 7 patients with membranous, 3 with focal, 4 with diffuse, 3 with crescenteric and one with membranoproliferative glomerulonephritis. While patients with minimal, membranous and focal nephritis had general good outlook on low dose maintenance or intermittent high dose steroid therapy the others with diffuse, crescenteric and membranoproliferative nephritis had poor prognosis. Patients with diffuse proliferative, membranoproliferative and crescenteric nephritis tended to have septicaemia, pulmonary oedema, fluid overload and chronic renal failure with poor prognosis. These patients responded poorly to oral and parenteral steroid therapy whether high or low dose.
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PMID:Management of lupus nephritis at the Kenyatta National Hospital. 227 66

During a 12-year period, 254 cases of eclampsia were managed at this center. Eighty patients (32%) did not have edema, 58 (23%) had "relative hypertension," and 49 (19%) did not have proteinuria at the time of convulsions. Eclampsia developed at less than or equal to 20 weeks in 6 patients and beyond 48 hours post partum in 40 (16%). Convulsions developed in 33 while they were receiving standard doses of magnesium sulfate for preeclampsia during or after birth, and subsequent seizures developed in 36 (14%) after magnesium sulfate therapy was started. There was one maternal death (0.4%) and morbidity was frequent (acute renal failure, 4.7%; pulmonary edema, 4.3%; cardiorespiratory arrest, 3.1%; and aspiration, 2%. The use of multiple drug therapy was associated with significant maternal and neonatal complications. The total perinatal mortality was 11.8%, with the majority of them related to either abruptio placentae or extreme prematurity. These findings emphasize the need for intensive monitoring of women with preeclampsia throughout hospitalization and underscore the importance of maternal stabilization before and during transfer.
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PMID:Eclampsia. VI. Maternal-perinatal outcome in 254 consecutive cases. 240 30

The outcome is described for 106 patients with severe hypertension in pregnancy requiring delivery between 26 and 34 weeks. Management was with methyldopa, hydralazine when required and delivery by caesarean section when indicated. Most patients were delivered for cardiotocographic fetal distress or unstable maternal blood pressure. Eighty-five babies (80%) survived and were well at follow-up at 1 year; the perinatal mortality was 123/1000 total births. One patient had postpartum eclampsia, one had pulmonary oedema and one had transient renal failure, but all mothers left hospital well. Stepwise logistic regression analysis showed that the primary positive factor for survival of a healthy baby was gestational age, which was strongly correlated with birthweight. The need for caesarean section as an emergency, hypotension after parenteral hydralazine, intrauterine growth retardation, and severe proteinuria were adverse factors. Intraventricular haemorrhage had a major adverse effect on neonatal survival; it was predisposed to by prolonged maternal hypertension and by low gestational age.
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PMID:Outcome of pregnancies complicated by severe hypertension and delivered before 34 weeks; stepwise logistic regression analysis of prognostic factors. 259 Jun 53

Based on earlier studies in rats, phospholipase C (PLC) seemed to be a very promising prophylactic agent for certain types of thrombo-embolic disease. Recent studies in rabbits have, however, demonstrated that phospholipase C is more toxic than expected from the previous data. To gain more knowledge about its toxicity in larger animals we have studied its effect in sheep. Estimated LD50 for the enzyme in sheep was between 0.4 and 0.2 mg PLC/kg given as a 23 min infusion and below 0.2 mg/kg given as a bolus. Cellular necrosis was a common feature in several tissues of sheep dying from PLC. This explained the pulmonary oedema, decreased oxygen tension and renal failure with haematuria, proteinuria and glucosuria which occurred. PLC was probably filtered out in the glomeruli and totally reabsorbed in the tubuli until they were destroyed by PLC. An increase in different plasma enzymes suggested that PLC exerted a toxic effect on both muscle cells and hepatocytes. The blood glucose level remained about 20% lower in the PLC-treated animals than in the controls for more than 2 weeks. Pulmonary oedema and renal failure were the probable causes of death.
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PMID:The effect of phospholipase C in sheep. 664 29

Eight patients with Legionnaires' disease were seen at one hospital in the summer of 1979. They presented in the same 12-day period with an illness of rapid onset characterized by fever, chills, malaise, profuse sweating and neurologic symptoms. Neutrophilia, a high erythrocyte sedimentation rate, proteinuria, hypoalbuminemia, hyponatremia, hypochloremia and abnormal liver enzyme levels in the serum were usually noted. The roentgenographic findings in the lungs ranged from segmental interstitial infiltration to panlobar pneumonia. Seven patients responded to erythromycin treatment, though one died suddenly, presumably of unrelated cardiac disease. The other patient died of a combination of renal and respiratory failure, with pulmonary edema.
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PMID:Eight cases of Legionnaires' disease. 700 76

To assess the course and prognosis of salicylate-induced pulmonary edema, we reviewed the records of 36 consecutive patients admitted with serum salicylate levels greater than 30 mg/dL. Pulmonary edema developed in eight patients, and pulmonary infiltrates were never seen in 28 patients. Several features distinguished the two patient groups. Persons with pulmonary edema were older, ingested salicylates chronically, and had a history of smoking. They also were more likely to present with neurologic abnormalities. proteinuria, and serum salicylate levels greater than 40 mg/dL. The severity of pulmonary edema ranged from moderate (no assisted ventilation) to severe (characteristics of adult respiratory distress syndrome requiring assisted ventilation with positive end-expiratory pressure). Pulmonary edema resolved concomitant with a decline in serum salicylate levels. We conclude that certain patients are at increased risk for salicylate pulmonary edema, which responds to measures that lower serum salicylate levels.
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PMID:Salicylate-induced pulmonary edema. Clinical features and prognosis. 728 90

The immunoconjugate XMMCO-791/RTA consists of ricin A chain bound to a murine monoclonal antibody MoAb 791T. This monoclonal antibody (MoAb) binds to a glycoprotein of 72 kD, which is expressed on human colorectal carcinoma, ovarian carcinoma, and osteogenic sarcoma. XMMCO-791/RTA was tested in a Phase I trial with proposed dose escalation steps of 0.02, 0.04, 0.15, and 0.2 mg/kg per day. Twelve patients with metastatic colorectal carcinoma were treated at 0.02, 0.03, and 0.04 mg/kg per day dose levels administered over 1 hour on days 1-5. Study-related toxicities were hypotension (6 patients); greater than 10% weight gain (6 patients); peripheral edema (9 patients); fever (4 patients); confusion (3 patients); diarrhea (3 patients); proteinuria, as identified by dipstick (3 patients), greater than 0.6 mg/dl decrease in serum albumin (11 patients); greater than 25% decrease in oncotic pressure (10 patients), and a decrease in ionized calcium (8 patients). Six patients received a second course of treatment. HAMA levels developed in 9 patients and titers increased with number of courses administered. Decreased overall toxicity, in comparison to the first course, was noted, but one patient had an allergic-type response (hypotension, crushing chest pain, diaphoresis) after the test dose of the second course (HAMA level > 10,000 IgG). Life-threatening toxicity in the form of fluid shift, resulting in noncardiac pulmonary edema and third-spacing occurred after course 1 in 1 of 3 patients at the 0.04 mg/kg per day level. No further dose escalation was attempted and no antitumor activity was seen.
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PMID:Phase I study of monoclonal antibody-ricin A chain immunoconjugate Xomazyme-791 in patients with metastatic colon cancer. 762 72

The maternal mortality rate associated with eclampsia ranges from 100 to 6000 per 100,000, and the perinatal mortality rate ranges from 150 to 400 per 1000. Both eclampsia and its preceding condition, pregnancy-induced hypertension, occur in varying degrees in different parts of India. The warning signs of imminent eclampsia are 1) systolic blood pressure of 160 mmHg or more on two occasions six hours apart when the patient is on bed rest; 2) proteinuria of 5 g or more in 24 hours or 3 + or more by semiquantitative assay; 3) oliguria or anuria; 4) cerebral or visual disturbances; 5) pulmonary edema or cyanosis; and 6) epigastric/right hypochondriac pain, impaired liver function, and thrombocytopenia and coagulation disorders. Eclampsia is classified as the acute fulminating type, which can occur without warning, and the insidious type. Most cases (61%) show onset of eclampsia during the prenatal period. Treatment of eclampsia involves 1) control of convulsions (through an injection of magnesium sulphate or diazepam or the intravenous administration of phenytoin); 2) correction of hypoxia and acidosis; 3) a gradual lowering of blood pressure with hydralazine hydrochloride, nifedipine, atenolol, labetalol, oxprenolol, or metoprolol); and 4) steps to effect delivery. Diagnosis of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) requires a complete blood count, blood film for platelet count and red blood cell fragmentation, and a coagulation screen for diagnosis of disseminated intravascular coagulation. Efforts to induce delivery in cases of prenatal eclampsia can take place 12-24 hours after convulsions have stopped. There is no reason to prolong pregnancy in the interests of the fetus, and in some cases Cesarean section may be required. Adequate prenatal care should allow the identification of almost every potential case of eclampsia and allow the prompt treatment of pre-eclampsia or termination of pregnancy when necessary. Medical staff must receive proper training to diagnose pre-eclampsia and treat the condition.
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PMID:Eclampsia. 765 39


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