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)

Captopril has not yet been included in the list of drugs causing hypersensitivity lung disease. We report a patient with hypertension, congestive heart failure, and chronic renal failure who, when rechallenged with captopril, developed upper lung field infiltrates associated with productive cough and striking peripheral eosinophilia. Gallium scan, transbronchial biopsy histologic findings, and direct immunofluorescent study were consistent with an immune-complex-mediated hypersensitivity reaction. There was no other etiology discovered for the patient's eosinophilia, nor was there evidence for an infectious etiology to explain his presentation.
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PMID:Captopril-induced hypersensitivity lung disease. An immune-complex-mediated phenomenon. 252 35

Following a renal PTA a 63-year-old man developed a multisystem illness caused by disseminated cholesterol embolism. The clinical manifestations were changing myalgia, peripheral ischaemia, livedo reticularis, episodic hypertension, eosinophilia and rapidly progressive renal insufficiency. The diagnosis was made on the clinical picture and confirmed by skin biopsy. Ultimately, chronic intermittent haemodialysis was necessary. There is no specific treatment available for this disease. It is possible that this complication occurs more frequently, but often remains subclinical.
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PMID:[Terminal kidney insufficiency caused by disseminated cholesterol emboli as a complication of intra-arterial manipulation]. 252 70

The case of a 17 year old patient with severe course of toxocariasis is reported. Over a period of 6 months the patient developed signs of serious systemic condition with fever, respiratory infections, diarrhea, urticaria, weight loss, and muscular atrophies. The most remarkable organ derangements involved bilateral exudative neuroretinitis, severe degree of peripheral motoneuron derangement, and grave kidney damage with developing polyuria, hypokalemia, metabolic alkalosis and therapeutically hardly tractable hypertension. The most important laboratory findings were high erythrocyte sedimentation, absolute and relative eosinophilia, and hypergammaglobulinemia. Serological examination exhibited weak larval toxocariasis positivity. Treatment with Mintezol and subsequent administration of prednisone resulted in complete restoration of the clinical state, including organ and laboratory manifestations. The reported case documents the occurrence of larval toxocariasis in our population as well as the possibility of a very severe course of this parasitic infection in man. The therapeutic effect is remarkable since literary data have so far reported mostly unsatisfactory results of toxocariasis treatment.
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PMID:[Larval toxocariasis--a severe course of the manifest infection]. 259 Aug 55

A case of atheroembolic renal failure diagnosed by renal biopsy was presented. A 69-year-old man was referred because of progressive renal failure two months after major angiography for occlusive arterial disease of lower limbs. The physical examination on admission revealed an uncontrollable hypertension. The laboratory findings showed elevated serum creatinine (7.5 mg/dl) and eosinophilia (1022/mm3) with normal urinalysis findings. Renal biopsy disclosed a occlusive lesion of the arcuate artery which contained cholesterol clefts and foam cells, and showed ischemic renal parenchymal changes. These findings were compatible with cholesterol atheroembolic renal disease. In spite of the aggressive medical treatment, renal function had deteriorated progressively and the patient has been on regular hemodialysis. Atheroembolic renal failure after arteriography have been reported recently, but the case diagnosed by renal biopsy has been rare. Since there is no therapeutic way to reverse this type of renal failure, strict selection of patients for the angiographic examination and use of flexible catheter might be mandatory. Subacute course of renal failure after angiography and eosinophilia seem to be the important diagnostic clues for this disorder.
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PMID:[Cholesterol atheroembolic renal failure after arteriography. Report of a case diagnosed by renal biopsy]. 262 43

Cholesterol embolization is a puzzling event that may be increasingly iatrogenic in origin. Diagnosis is difficult and requires a high index of suspicion, an appropriate clinical picture, and usually, confirmation by biopsy. Certain laboratory abnormalities may be helpful; the elevated sedimentation rate and relative eosinophilia found in our patients concurs with other cases reported in the literature. Prognosis is related to the extent of systemic involvement, but renal disease is particularly threatening and gangrene and infection can be lethal. Multiple therapeutic regimens have been generally unsuccessful in altering the course of the disease process. The most significant impact on the disease can be made by its prevention. Cholesterol emboli occur spontaneously, but also after invasive aortic procedures such as diagnostic angiography or cardiovascular surgery. In addition, cardiac catheterization and percutaneous transluminal coronary angioplasty have the potential for arterial trauma and consequent cholesterol embolization. Although the apparent increasing numbers of cholesterol emboli may be a reflection of the increased use of arterial invasive procedures, they are being performed on an older, more severely ill population, with other risk factors for the development of embolic phenomena, i.e., age, smoking history, diabetes mellitus, hypertension, and peripheral vascular disease. Our observed cases and review of the literature do not furnish information concerning the comparative incidences of embolization as related to the suggested etiologies. Careful documentation of the clinical situation preceding the event, the type of procedure, the site of arterial entry, and the duration, difficulty, and extent of the intravascular invasion (i.e., above or below the left subclavian artery) are necessary for this purpose. Such data should help to develop guidelines for patient and procedure selection in order to minimize the possibility of cholesterol embolization.
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PMID:Cholesterol emboli after cardiac catheterization. Eight cases and a review of the literature. 305 19

A phase I and pharmacokinetic study of recombinant tumor necrosis factor (rH-TNF Asahi) was carried out in 29 patients, who received a total of 72 courses with doses ranging from 1 to 48 X 10(4) units/m2. Drug was given as 1-h i.v. infusions. Acute toxicities, taking the form of fever, chills, tachycardia, hypertension, peripheral cyanosis, nausea and vomiting, headache, chest tightness, low back pain, diarrhea and shortness of breath were seen, but were not dose-limiting or dose-related. Some early rise in SGOT, without any change in serum bilirubin, was noted at the highest doses. Eosinophilia, monocytosis, mild hypocalcemia and an increase in fibrin degradation products were seen in a few patients. The dose-limiting toxicity was hypotension, which occurred after the end of the drug infusion and was seen in all 5 patients treated at the highest dose. There was no mortality or long-term morbidity. There were no responses. Pharmacokinetic studies indicated a rapid plasma clearance and a short plasma half-life, generally less than 0.5 h.
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PMID:Phase I clinical trial of recombinant human tumor necrosis factor. 366 33

We report a case of diffuse interstitial pulmonary disease in a 73 year old woman treated for moderate hypertension for one year with the combination of hydrochlorothiazide (50 mg/day) and Amiloride (5 mg/day). The bronchoalveolar lavage showed a neutrophilia of 23% and a 5.5% eosinophilia. The absence of any other aetiological factor and the favourable outcome on cessation of the sole medication incriminate the latter as an aetiological agent in this interstitial pneumonitis.
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PMID:[Subacute pneumopathy caused by hydrochlorothiazide. Cytologic study of the broncho-alveolar lavage]. 378 31

During an outbreak of trichinosis, two young men--one with established trichinosis and the other with suspected infection--were found to have clinical, radiologic and histologic stigmata of a systemic necrotizing vasculopathy equivalent to classic polyarteritis nodosa. The parasitosis manifested as a pentad of fever, myalgias, facial edema, eosinophilia and hyperimmunoglobulinemia E. Features of the arteritis included mononeuritis multiplex, pain in the abdomen and joints, weight loss, hypertension, leukocytosis, thrombocytosis, microhematuria and raised alkaline phosphatase levels. A sustained remission was achieved by the administration of thiabendazole, prednisone and cyclophosphamide. Pathogenetic links between the two diseases are presented: (1) deposition of circulating immune complexes in the vessel wall; (2) adjuvant activity with cross reaction between parasitic antigen and human vessel wall; (3) immunoglobulin E (IgE) aggregates and soluble antigen IgE complexes precipitation in vessel wall; and (4) hypereosinophilia-induced tissue damage. A causal relationship of trichinosis to polyarteritis nodosa is persuasive, and we suggest that cases of hepatitis B surface antigen (HBsAg) negative polyarteritis nodosa, especially those in which myalgias and eosinophilia are prominent, may be related to trichinosis and that, conversely, patients with trichinosis and multiorgan disease should be studied for polyarteritis nodosa.
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PMID:Trichinosis-related polyarteritis nodosa. 611 36

The initial symptoms of a new multisystem disease probably caused by ingestion of denatured rapeseed oil were acute pleuropneumopathy, fever, headache, exanthems, myalgia, and eosinophilia. Later features were severe myalgia and thromboembolic accidents. The present phase of the illness is typified by scleroderma-like involvement, pulmonary arterial hypertension, and a neuromuscular syndrome. Nearly all the patients with these late changes are women. The pathological lesion is a peculiar form of non-necrotising vasculitis which primarily affects the intima.
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PMID:Toxic epidemic syndrome, Spain, 1981. Toxic Epidemic Syndrome Study Group. 612 35

We report the findings in 26 cases of occlusive aortopathy (Takayasu's disease) encountered during eight years. The mean age was 25.3 years and female to male ratio was 2.7:1. Chest and local pain, fever, hypertension (70%) and absent pulses were accompanied by high erythrocyte sedimentation rate (ESR) 38 to 126 mm, eosinophilia 4 to 26%. All immunological tests were negative except tuberculin-test (PPD) with 65% positive. EKG was normal in three cases, 23 showed left ventricular hypertrophy, ST-T changes in two and acute myocardial infarction in two cases. The classification: Type I cervico-brachial or arch type with five cases, type II thoraco-abdominal type with six cases, type III peripheral type with four cases and generalized types combination of two or more of three types and/or pulmonary artery involvement, showed good correlation with clinical findings and prognosis. The occlusive aortopathy is an inflammatory disease of unknown origin, an auto-immune or genetic etiology may be involved.
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PMID:Occlusive thromboaortopathy (Takayasu's disease): clinical findings and angiographic classification. 613 36


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