Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathologic changes induced by high dose intermittent cyclophosphamide therapy are described in 39 patients with solid tumors, lymphohematopoietic malignant disease, and bone marrow transplants. Patients receiving 50 to 120 mg. per kg. daily for one to four days showed transmural bladder injury affecting all component tissue; toxic vasculitis involving small arteries, capillaries, and venules; and interstitial, myocardial, and vascular changes in the heart. Myocardial necrosis with heart failure was the dose limiting factor of very high dose therapy. Patients receiving 15 to 30 mg. per kg. for four days showed variable degrees of bladder injury limited to the mucosa and lamina propria and vascular changes consisting only of telangiectasia. Both groups showed atypia of transitional urinary and esophageal epithelia as well as of mesenchymal cells in the lamina propria of the bladder, persistent and total ablation of spermatogenesis, and long lasting absence of ovarian follicular maturation. Bone marrow hypoplasia and lymphoid depletion developing after cyclophosphamide therapy completely disappeared an average of 3.5 weeks after the last dose.
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PMID:Pathology of high dose intermittent cyclophosphamide therapy. 118 93

A 54 year-old man, who had a hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease; O-W-R) accompanied by pulmonary arteriovenous fistulas (PAVFs) and congestive heart failure, developed seizure, right hemiparesis and dysphasia. A brain CT scan revealed a cystic lesion with perifocal edema in left frontoparietal lobe. A contrast enhanced CT scan showed a ring-like enhancement. Dynamic CT scans disclosed that the ring in the cortical side was enhanced more thickly than that in the ventricular side. Considering the severity of the cardio-pulmonary condition, and the deep location of the abscess, we performed an echo-guided aspiration and drainage of the abscess under local anesthesia. No bacteria were demonstrated in the culture of the contents of the abscess. After the surgery, the right hemiparesis and dysphasia were much improved and a CT scan showed the marked reduction of the abscess. However, around eight days after the surgery, the patient showed severe pleural effusion due to progressive heart failure and died on the 11th postoperative day. Autopsy disclosed a shrunken brain abscess, multiple cerebral infarction, multiple PAVFs and severe constrictive pericarditis which was regarded as the cause of death in the patient. In this report, we presented the therapeutic advantage of echo-guided surgery for the treatment of brain abscess in a high-risk patient. We also discussed the mechanism of the formation of brain abscess in patients of O-W-R disease by reviewing published cases.
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PMID:[A case of Osler-Weber-Rendu disease with brain abscess; the mechanism of the formation of brain abscess and its treatment in Osler-Weber-Rendu disease]. 194 83

We present two cases of hemorrhagic hereditary telangiectasia (HHT) or Osler-Weber-Rendu disease which started as heart failure. Both had multiple arteriovenous fistulas, one of them in a rare localization in this disease, a lower extremity. We conclude stressing the importance of thinking of HHT in the presence of obscure heart failure or arteriovenous fistulas and of looking for internal fistulas when faced by a HHT.
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PMID:High out-put congestive heart failure as first manifestation of Osler-Weber-Rendu disease. 648 18

Symptomatic hepatic involvement is a rare complication of hereditary hemorrhagic telangiectasia and most commonly consists of fibrosis or cirrhosis. We describe a 33-year-old woman in whom multiple hepatic arteriovenous malformations led to high output cardiac failure and liver failure due to biliary necrosis with refractory biliary sepsis, requiring orthotopic liver transplantation. Hepatic arteriovenous malformations were the first manifestation of the disease and a similar asymptomatic hepatic tumour was subsequently detected in her 60-year-old father who also had the classical cutaneous stigmata of the syndrome. Unrecognised genetic factors may determine the clinical spectrum of hereditary haemorrhagic telangiectasia including the hepatic manifestations.
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PMID:Liver transplantation for hepatic arteriovenous malformation in hereditary haemorrhagic telangiectasia. 765 Mar 40

Radiation therapy is the elective treatment of inoperable non small cell lung cancer, but is potentially curative only for a few of them: failures result from distant metastases and/or from progressive local disease. During the last years, following the progress in chemotherapy, combining radiation and drugs is becoming a more common approach. Nevertheless, one of the main concerns remains the potential interference between both modalities leading to an increased toxicity, which may outweigh all potential benefit. Several organs can be a target for acute or late toxicity: lung (pneumonitis and fibrosis), esophagus (acute esophagitis, stenosis), heart (pericarditis, impaired ventricular functions, heart failure, coronary stenosis), spinal cord (transient myelopathy, radiation myelitis), skin (moist desquamation, fibrosis, telangiectasia). The current published trials combining drug and radiation appear to be a rather safe approach especially when avoiding concomitant treatment. However, several points remain unsolved: the optimal combination scheme, the real risk of late damage observation including the second cancer occurrence risk. This risk is uneasy to evaluate due to the long latency period. The way of describing the late damage is crucial, seeking for a more precise system of evaluating, recording and reporting late effects, taking into account objective damage as well as the patient's symptoms. Therefore, combining drug and radiation should preferentially be performed within prospective studies, with precise evaluation procedures.
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PMID:[Non small-cell bronchial cancers: toxicity of the association radiotherapy-chemotherapy. Review of the literature]. 794 85

A case of pediatric progressive systemic sclerosis is reported and a literature review concerning medical and dental aspects of this condition is provided. Systemic features include sclerodactyly, Raynaud's phenomenon, telangiectasia, calcinosis, myositis, arthritis, tenosynovitis, renal failure, esophageal hypomotility, pulmonary fibrosis and heart failure. Oral manifestations include reduced interincisal distance, xerostomia, telangiectasia, increased periodontal ligament width, osseous resorption of the mandible, periodontal disease, and increased decayed, missing, and filled teeth (DMFT). The prognosis is difficult to predict because spontaneous remission has been documented, but death may result from extensive visceral involvement (heart, kidney, and lung).
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PMID:Progressive systemic sclerosis in a child: case report. 824 4

Heart failure occurred in a 50-year-old woman as a result of calcified haemangiomatosis of the liver with a high shunt volume. In the subsequent years there were several bleedings from peptic ulcers. Ultrasonography revealed an increase in liver size and the previously diagnosed calcification. 14 years later the patient was again hospitalized because of increasing weakness and stress dyspnoea; the haemoglobin level was 5.5 g/dl. In addition to the florid gastric and duodenal ulcers, angiodysplasias were for the first time demonstrated in the stomach, duodenum and sigmoid colon, as were telangiectasias in the face and echo-dense round foci in the spleen. After transfusion of red cell concentrates and healing of the peptic ulcers under a 14-day treatment with omeprazole (20 mg two times daily by mouth) and amoxycillin (750 mg three times daily by mouth) the haemoglobin level increased at first (10 g/dl), then tarry stools were once again noted. The condition stabilized after laser coagulation of all accessible gastrointestinal angiodysplasias. The isolated calcified hepatic haemangiomatosis, diagnosed 14 years previously, is most likely a rare variant of hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu disease).
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PMID:[Liver hemangiomatosis in Osler's disease]. 833 48

Hepatic involvement in hereditary hemorrhagic telangiectasia (HHT) is rare. Among local pathologic alterations like fibrosis and cirrhosis, arteriovenous shunts lead to hypercirculatory heart failure and require efficient therapy. Present therapeutic strategies consist of percutaneous selective embolization or complete ligation of the hepatic artery. We describe a 53-year-old woman with HHT in whom percutaneous selective embolization of the left hepatic artery failed because of unfavorable anatomy. Instead of ligation a new method of adjustable banding of the hepatic artery was tested. After small-incision laparotomy an expander prosthesis was put on the proper hepatic artery. By filling the prosthesis via the implanted port system the hepatic perfusion could be reduced under control. This method led to effective reduction of the liver perfusion and heart time volume and to successful treatment of heart failure. The method described is an alternative treatment to ligation of the hepatic artery in cases in which percutaneous embolization failed or is not possible.
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PMID:[Adjustable "banding" of the hepatic artery in treatment of shunt-induced heart failure in Osler-Rendu-Weber disease]. 967 67

We report a case of hereditary hemorrhagic telangiectasia complicated by high output heart failure caused by intrahepatic arteriovenous malformations. This patient was treated using transcatheter embolization of the intrahepatic arteriovenous malformations with concurrent measurement of cardiac output to monitor progress of the embolization.
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PMID:Hereditary hemorrhagic telangiectasia causing high output cardiac failure: treatment with transcatheter embolization. 973 49

Hereditary hemorrhagic telangiectasia, commonly known as Osler-Weber-Rendu disease, is a systemic autosomal dominant inherited disorder, that occurs in Caucasian populations. We report the case of a 56-year-old housewife who was admitted to the gastrointestinal and cardiovascular ward because she had suffered from recurrent gastrointestinal bleeding and heart failure from 1994 to 1997. Panendoscopy showed vascular ectasia scattered over the tongue, larynx, esophagus, and posterior wall of the gastric body. Colonoscopy showed clusters of telangiectasia over the cecum and ascending colon. Arteriovenous malformations (AVMs) were found in the liver and lungs on computerized tomography. Recurrent gastrointestinal bleeding was controlled by estrogen treatment during the follow-up period. In July 1997, the patient was readmitted to our cardiovascular section due to aggravated dyspnea, orthopnea and bilateral lower leg edema. Cardiac catheterization showed a large fistula from the left pulmonary artery to the left atrium and left ventricle, pulmonary arterial pressure of 37/13 mmHg and cardiac output of 9.61/minute. Other studies excluded the possibility of sepsis, and high-output cardiac failure was suspected. The patient was discharged in a stable condition and scheduled for AVM embolization management. Unfortunately, she died of a suspected heart attack at home two weeks following discharge.
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PMID:Recurrent gastrointestinal bleeding and high output cardiac failure caused by hereditary hemorrhagic telangiectasia. 1082 Sep 15


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