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)

Two hundred fifteen diabetic patients (430 eyes) with early proliferative retinopathy, moderate-to-severe nonproliferative retinopathy, and/or diabetic macular edema in each eye were examined for the presence of white centered retinal hemorrhages (WCRHs). Of the eyes examined, 15.6% demonstrated at least one WCRH and 4.9% showed five or more WCRHs. The prevalence of WCRHs was not significantly related to hypertension, anemia, leukocytosis, thrombocytopenia, thrombocytosis, abnormalities of coagulation, increased serum creatinine, or ingestion of oral contraceptives. Local factors associated with microvascular damage and repair are likely responsible for WCRHs in diabetics. Microaneurysms are at the center of many diabetic WCRHs, and the pale centers of many WCRHs in diabetic retinopathy may be platelet-fibrin aggregates.
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PMID:White centered retinal hemorrhages in diabetic retinopathy. 358 20

The "Hellp syndrome" describes the association of three biological abnormalities (hemolysis, liver abnormalities and thrombocytopenia) establishing the severity of arterial hypertension during pregnancy and requiring the interruption of pregnancy as much for the child as for the mother. This article reports a case of "Hellp syndrome" which was special in that the biological abnormalities preceded the occurrence of pre-eclampsia. The signs, diagnosis, prognosis and treatment of the "Hellp syndrome" are studied in this article.
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PMID:[Hellp syndrome may precede the appearance of arterial hypertension in pregnancy toxemia]. 358 65

IgG and IgM have been identified on the surface of maternal platelets in both autoimmune thrombocytopenia (ATP) and pregnancy-induced hypertension (PIH). IgG is also found on the umbilical cord platelets of patients with ATP and PIH, whereas IgM is only found on the umbilical cord platelets of patients with PIH. The possible maternal or fetal origins of these umbilical cord blood immunoglobulins were investigated by immunoblot analysis of antibodies in paired maternal and umbilical cord blood sera of ATP and PIH patients. Maternal sera contained IgG and IgM antibodies which reacted with several platelet proteins, however, a large amount of patient-to-patient variation was observed in the specific antigens that were identified. Analysis of paired maternal and umbilical cord sera from patients with ATP or PIH showed identical patterns of antigen specificity, which suggested that the IgG antibodies in the fetal circulation were of maternal origin. Circulating IgM antibodies were not observed in the umbilical cord sera of ATP patients. The umbilical cord sera of PIH patients, however, contained IgM antibodies that reacted against a variety of platelet antigens. In addition, most umbilical cord sera from PIH patients had identical patterns and relative intensities of reactivity, which differed from the patterns observed in the paired maternal sera. Antiplatelet IgM in the umbilical cord blood of PIH patients, therefore, appears to be a product of the fetal immune system.
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PMID:Platelet-binding immunoglobulins in pregnancy-induced hypertension. II. Origin of circulating IgG and IgM antiplatelet antibodies in the umbilical cord serum. 362 1

Atypical courses of pregnancy-induced hypertension (PIH) have been reported quite frequently during the last time. They include prepartal coagulation disorders with slight or missing typical symptoms of PIH. In cases of quickly increasing thrombocytopenia during the last trimenon, in company with elevated liver enzymes, PIH must always be taken into account. We give a case report about a nearly asymptomatic secundigravid woman who developed low platelet counts (8,000 platelets/microliter) within a few hours, which later was confirmed to be severe preeclampsia. Transient and moderate thrombocytopenia down to 50,000 platelets/microliter caused by PIH may first be treated conservatively. Progredient symptoms should lead to an early delivery, as neonatal mortality in such cases is high. We give a review about current literature which reflects on differential diagnosis, pathogenesis and therapy of this disease.
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PMID:[Rapidly progressing thrombocytopenia as a threatening form of pre-eclampsia]. 366 Sep 7

Ketanserin, a serotonin antagonist, was used to control blood pressure during cardiopulmonary bypass in 12 patients having cardiac surgery. The drug was administered as a 10 mg bolus followed by a continuous infusion of either 40, 80, or 120 mg/hr to maintain mean arterial blood pressure below 70 mm Hg. There were 16 hypertensive episodes of which 15 (93.7%) were successfully controlled with ketanserin. Mean arterial pressure decreased significantly from an average of 72 +/- 3 to 52 +/- 9 mm Hg after 1 min. The effect that ketanserin had on platelets was also evaluated. Neither adverse nor salutary effects were seen in the platelet count, though a significant inhibition of serotonin-induced platelet aggregation was observed. Ketanserin proved effective for controlling hypertension during cardiopulmonary bypass but, despite inhibition of serotonin-induced platelet aggregation, it did not prevent thrombocytopenia.
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PMID:The effect of ketanserin on blood pressure and platelets during cardiopulmonary bypass. 366 60

Some pregnant patients with toxemia, especially those with thrombocytopenia, liver or renal dysfunction have elevated serum DLF (digoxin like factor). Since antidigoxin serum reduces the hypertension of DOCA hypertensive rats, it is proposed that antidigoxin antibodies be tried in the treatment of these select patients with toxemia of pregnancy.
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PMID:Will treatment with digoxin antibody benefit pregnant patients with toxemia and elevated digoxin like factor? 367 Jan 28

Patients with portal hypertension of varying etiology may develop pulmonary artery hypertension. In the present autopsy study, pulmonary and hepatic tissue was studied in 12 patients in whom pulmonary and portal hypertension coexisted. Plexogenic pulmonary arteriopathy was present in 10 patients, 7 of whom had coexistent thromboembolic lesions. One patient had isolated medial hypertrophy, which may be an early stage in the plexogenic category, whereas isolated thromboembolic pulmonary vascular disease was observed in one subject. Hepatic disease was consistent with alcoholic cirrhosis in seven patients, cryptogenic cirrhosis in four and extrahepatic portal hypertension without cirrhosis in one. Thrombocytopenia was present in all 10 patients whose platelet count was determined. This study suggests that pulmonary hypertension associated with portal hypertension commonly has a plexogenic appearance on histologic examination. However, thrombosis (whether embolic or in situ) may also contribute to vascular obstruction.
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PMID:Coexistent pulmonary and portal hypertension: morphologic and clinical features. 368 Jul 90

The diagnosis of preeclampsia near term is seldom difficult, even when complicated by altered liver function, hemolysis and thrombocytopenia. Three patients recently presented before term with thrombocytopenia, abnormal liver function tests and hemolytic anemia (two cases), with development of hypertension and proteinuria after days to weeks. Numerous disease processes during pregnancy are characterized by a similar presentation. Many of these cases may represent severe preeclampsia, previously unrecognized.
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PMID:Hepatic dysfunction, thrombocytopenia and late-onset preeclampsia. A report of three cases. 368 63

A 28-year-old female, who suffered from thrombotic thrombocytopenic purpura (TTP) in the 14th week of her first pregnancy, recovered after a plasma exchange followed by an induced abortion. From six months after the abortion, she no longer required plasma infusions every 3-4 weeks to prevent a relapse of TTP manifested as thrombocytopenia, and complete remission continued until her next pregnancy. In her second pregnancy, she had an immediate relapse of TTP and responded to plasma infusion until the 24th week. However, the TTP gradually became resistant to plasma infusion, and developed into toxemia with edema, hypertension and proteinuria in the 27th week. Although the TTP was alleviated by the infusion of large amounts of plasma, the placenta failed as the result of numerous white infarcts. She delivered a 948 g live baby by cesarean section in the 33rd week. The baby had transient thrombocytopenia but did not suffer from TTP. The mother required plasma infusions every 3-4 weeks for about five months, and she has continued in remission.
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PMID:Successful delivery in a female with thrombotic thrombocytopenic purpura. 369 21

The pathology of malignant hypertension in dogs induced either purposely or inadvertently by the Goldblatt procedure has not been previously reported. Malignant hypertension was experimentally produced in beagle dogs by a modified Goldblatt procedure; in a single surgical procedure, one kidney was removed and the blood flow to the remaining kidney was reduced by 50%. A sudden onset of severe clinical signs developed within one to three weeks after surgery. The dogs were markedly depressed or in shock, were vomiting, and had either bloody feces or bloody diarrhea. Hematologic changes compatible with a diagnosis of microangiopathic hemolytic anemia consisted of hemolysis, thrombocytopenia, and the presence of burr cells and schistocytes. Some dogs had neutrophilia and slight to moderate increases in blood urea nitrogen and creatinine. At necropsy, there were gross hemorrhages in the heart, brain, urinary bladder, and gastrointestinal tract. Histologic findings consisted of multifocal parenchymal hemorrhage, fibrinoid necrosis of arterioles, medial smooth muscle hyperplasia, adventitial fibroplasia and mononuclear cell infiltrates, and microthrombi. The vascular clamp most likely protected the kidney from the systemic hypertension since the remaining kidney was largely not remarkable by light or electron microscopy. The dog appears to be a good model to study the pathology of malignant hypertension and microangiopathic hemolytic anemia.
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PMID:Experimentally induced malignant hypertension in beagle dogs. 376 16


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