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)

Twenty-three patients with stage III germinal neoplasia of the testis were treated with a variation of our original vinblastine-bleomycin program. This modification consisted of 0.4 mg/kg of vinblastine given in two fractions on Days 1 and 2 followed by continuous intravenous administration of 30 units of bleomycin in 1000 cc of 5% glucose and distilled water over a 24-hour period for 5 successive days beginning on Day 2. Therapy was repeated every 28-35 days as toxicity permitted. There were 17 responses, nine of which were complete (39%). Eight of the complete responses were in patients with massive disease in whom a low complete response rate was expected. Toxic effects consisted of severe leukopenia in 90% thrombopenia in 50%, and unexplained transient hyperbilirubinemia in about 30% of the patients. Bleomycin pneumonitis occurred in one patient and resulted in death. Hypertension was a new and unexpected side reaction experienced by four patients. Further trials are indicated since the complete response rate in patients with advanced massive disease appears to be improved.
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PMID:Continuous intravenous bleomycin (NSC-125066) therapy with vinblastine (NSC-49842) in stage III testicular neoplasia. 5 12

It is suggested that patients with the haemolytic-uraemic syndrome and related disorders (such as thrombotic thrombocytopenic purpura) lack a plasma factor which stimulates prostacyclin (P.G.I2) activity. Normal plasma would supply the missing factor and is a rational treatment for some life-threatening symptoms (thrombocytopenia, haemolytic anaemia, hypertension) of this syndrome.
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PMID:Haemolytic-uraemic syndrome: deficiency of plasma factor(s) regulating prostacyclin activity? 8 15

Neocarzinostatin (NCZ), an acidic polypeptide antibiotic, was given to 47 patients with cancer and leukemia, and tolerance to two schedules, a single dose given as a 2 hour infusion and a continuous infusion over 5 days was investigated. Immediate reactions, including fever, chills, rigor, hypertension and mental confusion, were dose-limiting for the 2 hour infusion schedule, occurring at 3000 U/m2 and higher. Continuous administration for 5 days eliminated the immediate reactions and then hematological toxicity--often prolonged leukopenia and thrombocytopenia--became dose-limiting. Other toxicities of NCZ at both dose schedules included anemia, fever and chills, anorexia, nausea and vomiting, hepatic dysfunction, azotemia, hypophosphatemia, aminoaciduria, stomatitis, phlebitis and/or cellulitis at the venous infusion site and pruritus. Patients with solid tumors who had received little or no prior chemotherapy and had good bone marrow reserve tolerated up to 6000 U/m2/24 hours X 5 days. One patient with previously treated acute myelocytic leukemia was induced into a good partial remission lasting 10 weeks.
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PMID:Phase I study with neocarzinostatin: tolerance to two hour infusion and continuous infusion. 15 43

To sum up, some hematological side effects are seen after antihypertensive drugs. They are, however, few, usually not severe and furthermore reversible. And so, from the viewpoint of the hematologist, there are no contraindications against antihypertensive treatment. The prevalence of side effects on blood and blood-forming organs from antihypertensive drugs is low. Of certain interest are 1) the tendency of modern diuretics (thiazides) to cause a moderate and reversible thrombocytopenia and 2) the positive antiglobulin reaction (Coomb's test) sometimes seen after alpha-methyldopa therapy and in a few cases causing autoimmune hemolytic anemia. Even though case reports have appeared on leukopenia/agranulocytosis related to almost all drugs used in the treatment of hypertension, none of these drugs seem to be especially prone to cause any damage to leukocytes and/or leukocyte production.
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PMID:Hematological side effects from antihypertensive drugs. 28 2

Three cases of postpartum hemolytic uremic syndrome (HUS) are presented. Symptoms of acute renal failure, hypertension and microangiopathic hemolytic anemia with thrombocytopenia occurred 10, 17 and 24 days after delivery. Despite early heparin therapy in all cases, one patient went into terminal renal failure needing chronic hemodialysis, with persistent hypertension which became uncontrollable requiring bilateral nephrectomy 6 months later. The second patient had diuresis one month after starting hemodialysis, but 3 months later developed malignant hypertension. Slight improvement in renal function with persistent hypertension occurred after hemodialysis for 20 months. The third patient showed complete clinical recovery after 2 months. Pathological examination of renal tissue showed the typical lesions of thrombotic microangiopathy (TMA). However, striking differences were observed in the lesion seen in early and late specimens. Early lesions could be differenciated from infancy TMA because the medium-dize arteries were more severely involved. Late lesions were variable, ranging from minor changes in glomeruli and blood vessels, via ischemic and sclerotic lesions in glomeruli with arteriolosclerosis, to the vascular and glomerular lesions seen in malignant nephrosclerosis. There was a good correlation between the renal pathology and the clinical outcome of the patients. HUS with renal TMA as a cuase of postpartum renal failure has been reported in 49 patients with a fatal outcome in 61%. The pathogenesis of the syndrome probably involves a primary endothelial damage. This causes local renal intravascular coagulation in the presence of the usual postpartum hypercoagulable state. This is shown by the presence of fibrin-fibrinogen in glomeruli and vessels, increased plasma fibrin degradation products, thrombocytopenia and lowered levels of coagulation factors. There is little hematological or pathological evidence fo disseminated intravascular coagulation or an immune-complex disease. Hypocomplementemia seen frequently is probably due to local C3 activation via the alternative pathway.
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PMID:Postpartum hemolytic uremic syndrome: a study of three cases with a review of the literature. 38 9

The haemolytic uraemic syndrome is an acute illness characterised by the occurrence of renal injury, haemolytic anaemia with red cell fragmentation and thrombocytopenia. Haemorrhagic diathesis, arterial hypertension and neurological manifestations often complicate the acute phase of the disease. In this article, we shall discuss in more detail the aspects of this phase. Data obtained in 72 patients treated at the Wilhelmina Children's Hospital in Utrecht, from 1964 to 1977, are used to illustrate the characteristics of the disease.
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PMID:Haemolytic uraemic syndrome. 39 9

Two patients with the hemolytic uremic syndrome were treated with plasma exchange an infusion: in both cases, the reduced platelet count reverted to normal values and the microangiopathic anemia ceased within a few days. Systemic blood pressure and requirement for antihypertensive drug therapy were also markedly reduced following treatment with plasma. Venousprostacyclin (antiplatelet aggregating) activity was undetectable in both patients before but was restored after treatment with plasma. The plasma samples collected before, but not those collected at various intervals after replacement therapy, had decreased capacity to stimulate prostacyclin activity in rat aortic rings. It is suggested that in patients with the hemolytic uremic syndrome or with other clinical conditions which can be included under this rubric (such as thrombotic thrombocytopenic purpura) a plasma factor is lacking which stimulates prostacyclin activity. Plasma would supply such a missing factor, thus representing a rational treatment for some of the life-threatening manifestations (thrombocytopenia, hemolytic anemia, hypertension) of this severe syndrome.
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PMID:Treatment of the hemolytic uremic syndrome with plasma. 39 47

A urinary tract infection with possible septicemia and endocarditis developed in a 36-year-old man. The illness was complicated by pulmonary embolism, thrombocytopenia, hematemesis, hepatic dysfunction, paralytic ileus and accelerated hypertension. The latter finding suggested pheochromocytoma. Treatment with antibiotics and phenoxybenzamine hydrochloride was associated with notable clinical improvement. A chromaffin cell tumor was surgically removed above the lift kidney. Conclusively, a pheochromocytoma may mimic and be present in association with infection.
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PMID:Infection and pheochromocytoma. 57 92

A 4-year-old boy had hemolytic uremic syndrome (HUS) associated with depression of serum C3 level, a B-hemolytic streptococcal throat infection, and an elevated level of antistreptolysin O titer. In addition to the characteristic histologic changes associated with this syndrome, substantial infiltration of polymorphonuclear leukocytes and nodular deposits of C3 globulin were seen in the glomeruli of the first biopsy specimen. Two months after clinical remission, he had a recurrence of hemolytic anemia, thrombocytopenia, and acute renal failure. The serum C3 concentration had decreased again, and serum C3NeF was detected in the serum. The typical changes associated with HUS were still present on electron microscopy. Bilateral nephrectomy and renal transplantation were done because of the development of uncontrollable severe hypertension and increasing azotemia. This patient had three manifestations of HUS, but because of several differences, such as hypocomplementemia, serum C3NeF, a recurrence, and persistent glomerular deposits of C3 globulin, he appears to have had a different form of the syndrome.
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PMID:Hemolytic uremic syndrome with hypocomplementemia, serum C3NeF, and glomerular deposits of C3. 57 89

The hemolytic-uremic syndrome consists of microangiopathic hemolytic anemia, acute renal failure, and thrombocytopenia following a prodromal illness of gastroenteritis or upper respiratory infection. The syndrome can present in dramatic fashion with severe abdominal pain and signs of peritonitis suggesting an acute surgical crisis. In a series of 25 patients, 40% had abdominal pain, 25% had abdominal tenderness, and 20% had peritoneal signs. Clues to diagnosis in the early stages of the acute illness were mild to moderate hypertension, abnormal peripheral blood smear, anemia despite dehydration, and proteinuria. Significant abdominal pain and x-ray evidence of colitis may occur before development of typical laboratory findings, and these were evident in at least one case. Three patients underwent laparotomy for suspected bowel perforation. Colitis without perforation was found in all cases. In the absence of documented perforation, toxic megacolon, or intussusception, the decision to perform laparotomy in patients with hemolytic-uremic syndrome who have signs of peritonitis must be individualized. Failure to recognize the underlying renal problem can lead to serious errors in fluid and electrolyte management and delay of appropriate therapy.
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PMID:Hemolytic-uremic syndrome: a diagnostic and therapeutic dilemma for the surgeon. 73 58


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