Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied the activity of blood serum amine oxidase in patients with atherosclerosis obliterans and endarteritis obliterans. It was found that amine oxidase activity exceeded the normal value. 2.6 times in patients with stage 1-2 atherosclerosis obliterans and was reduced by more than 12 times in patients with stage 3-4 of the disease. The activity of the enzyme was absent in patients with endarteritis obliterans, whatever the stage of limb ischemia. On the basis of the obtained facts, the authors voice a new opinion on the nature of hypercatecholaminemia in obliterative diseases and suggest a new trend in the treatment of chronic ischemia of the limbs-activation of the processes of catabolism of vasoconstrictive biogenic amines.
...
PMID:[Effectiveness of pathogenetic treatment of arterial obliterative diseases of the extremities]. 808 43

Postoperative adhesions occur in 60% to 90% of patients undergoing major gynecologic surgery and represent one of the most common causes of intestinal obstruction in the industrialized world. The incidence of adhesion-related intestinal obstruction after gynecologic surgery for benign conditions without hysterectomy is approximately 0.3%, increasing to 2% to 3% among patients who undergo hysterectomy, and is as high as 5% if a radical hysterectomy is performed. Other adhesion-related complications include chronic pelvic pain, ureteral obstruction, and voiding dysfunction. Intraperitoneal adhesions also can limit the effectiveness of intraperitoneal therapeutic agents used in cancer treatment. Postoperative adhesions are sequelae of impaired fibrinolysis of the fibrin and cellular exudate after peritoneal injury. Adequate blood supply is essential for normal fibrinolysis. Therefore factors that increase ischemia and potentiate adhesion formation include thermal injury, infection, presence of a foreign body, and radiation-induced endarteritis. Only recently, appropriate animal models have been developed to study the process of adhesion formation and prevention. Until clinical confirmation of findings from these investigations exists, only a meticulous surgical technique can be advocated to minimize these untoward effects of surgery.
...
PMID:Adhesions after extensive gynecologic surgery: clinical significance, etiology, and prevention. 817 80

Radiation therapy of cancers in the pelvic region may lead to radiation proctitis. Radiation injury to the rectal wall eventually causes connective tissue fibrosis and obliterative endarteritis with subsequent local tissue ischemia. Patients with radiation proctitis may be minimally ill and heal spontaneously. However, symptoms of proctitis may persist, and the disease progresses to chronic bleeding and/or stricture and fistula formation. Medical therapy is often unsuccessful, and surgery is eventually required. Because of numerous postoperative complications and no guarantee of success, surgery should only be done as a last resort.
...
PMID:Radiation proctitis: a review. 867 84

The results of treatment of 17 patients with endarteritis obliteran and 44 patients with atherosclerosis obliteran of the lower limbs were analysed. The complex of therapeutic measures included direct and indirect stimulation of lymphatic drainage in the tissues. The effect of lymphostimulation on regional hemodynamics, microcirculation, and metabolism in the tissues of the ischemic lower limb are appraised. Changes in the lymphatic system resorption capacity, in microcirculation, in the composition and properties of the peripheral lymph in the limb in stimulation of lymphatic drainage of tissues are analysed. Indirect lymphostimulation contributed to the improvement of the indices under study in patients with IIb and IIIa stages of ischemia. Direct stimulation of lymphatic drainage caused a more pronounced effect in cases of stage IIIa ischemia of the limb and may be applied in preoperative and postoperative management of patients with stage IIIb ischemia.
...
PMID:[Stimulation of tissue lymphatic drainage in the treatment of patients with arterial diseases]. 868 20

Medical treatment of Buruli ulcer is mostly disappointing even if Mycobacterium ulcerans is susceptible to many antibacterial drugs. The inefficiency in vivo of the drugs may be due to the tissue vascularisation disorders caused by the toxin that Mycobacterium ulcerans produces. This toxin causes an endarteritis followed by a thrombosis of the dermal vessels responsible for an ischemia which prevents the antibacterial drugs from reaching the infected area. Removal or prevention of that thrombosis should allow the drugs to be more effective. To verify this assumption, we used a combined therapy with two gold standard medicines in an oedematous form of Buruli ulcer on the face which could not be surgically treated: heparin for its activity on thrombosis and rifampin for its bactericidal activity on Mycobacterium ulcerans. Rifampin was administered at 300 mg dose per day. Based on the management of envenomisation cases due to viper bites, we used standard heparin at 500 Ul dose per kg repeatedly administered by an electrical syringe releasing 1 cc per hour in the tubulure of isotonic glucose infusion. The results were encouraging. The dreadful oedema of the face started to reduce on the 15th day and disappeared on the 30th day. A small area at the temple dried. But we were obliged to stop the use of standard heparin due to an occurrence of Klebsiella oxytoca septicaemia from permanent vein route. Rifampin was still administered at the same dose. The face oedema reappeared quickly, followed by a full closure of the eyelids and an ulceration at the right temple level. The standard heparin was therefore substituted by low weight molecular heparin, enoxaparin, administered at 40 mg twice per day by subcutaneous route. 45 days later the oedema reduced and ulceration did not develop. After 90 days of treatment, usual signs of mycobacterial infection progression disappeared. We stopped therefore the use of enoxaparin but continued with rifampin until healing of the ulceration which occurred after 12 months of treatment. We observed no recurrence over a period of 16 months after complete healing. We can conclude that heparin combined with antimycobacterial drugs--which are active in vitro on Mycobacterium ulcerans--could provide an effective medical treatment for Buruli ulcer.
...
PMID:[Contribution of heparin therapy in the medical treatment of Buruli ulcer apropos of 1 case]. 1134 80

Buerger's disease (thromboangiitis obliterans or TAO) is a clinical syndrome characterized by the development of segmental thrombotic occlusions of the medium and small arteries of the extremities. It is clinically and pathologically distinguishable from arteriosclerosis and necrotizing arteritis. Afflicted patients are mostly young, male, inveterate tobacco smokers who present with distal extremity ischemia, ischemic ulcers, or frank gangrene of the toes or fingers. Large arteries are typically spared, as are the coronary, cerebral, and visceral circulations. While mortality is not increased, patients with Buerger's disease often suffer from severe ischemic pain and tissue loss culminating in minor and major limb amputation. Clinical diagnostic criteria generally include the following: (1) history of smoking or tobacco abuse; (2) age of onset less than 45 to 50 years; (3) infrapopliteal, segmental arterial occlusions with sparing of the proximal vasculature; (4) frequent distal upper extremity arterial involvement (Raynaud's syndrome or digital ulceration); (5) superficial phlebitis; and (6) exclusion of arteriosclerosis, diabetes, true arteritis, proximal embolic source, and hypercoagulable states. Typical arteriographic patterns have been described that are suggestive, but not pathognomonic. While the cause of Buerger's disease remains unknown, the disease onset and clinical course are inextricably linked to tobacco abuse. Acute Buerger's disease is characterized histopathologically by intensely cellular vessel wall inflammation, giant cell foci, and hypercellular thrombi, but with preservation of the elastic lamina and the overall vascular wall architecture. Most investigators feel that Buerger's disease is an immune-mediated endarteritis; recent immunocytochemical studies have identified the linear deposition of immunoglobulins and complement factors along the elastic lamina. The inciting antigen has not been discovered. Tobacco abstinence generally results in disease quiescence and remains the mainstay of treatment.
...
PMID:Buerger's disease in the 21st century: diagnosis, clinical features, and therapy. 1297 57

Vasculitis, inflammation of the vessel wall, can result in mural destruction with hemorrhage, aneurysm formation, and infarction, or intimal-medial hyperplasia and subsequent stenosis leading to tissue ischemia. The skin, in part due to its large vascular bed, exposure to cold temperatures, and frequent presence of stasis, is involved in many distinct as well as un-named vasculitic syndromes that vary from localized and self-limited to generalized and life-threatening with multi-organ disease. To exclude mimics of vasculitis, diagnosis of cutaneous vasculitis requires biopsy confirmation where its acute signs (fibrinoid necrosis), chronic signs (endarteritis obliterans), or past signs (acellular scar of healed arteritis) must be recognized and presence of extravascular findings such as patterned fibrosis or collagenolytic granulomas noted. Although vasculitis can be classified by etiology, many cases have no identifiable cause, and a single etiologic agent can elicit several distinct clinicopathologic expressions of vasculitis. Therefore, the classification of cutaneous vasculitis is best approached morphologically by determining vessel size and principal inflammatory response. These histologic patterns roughly correlate with pathogenic mechanisms that, when coupled with direct immunofluorescent examination, anti-neutrophil cytoplasmic antibody (ANCA) status, and findings from work-up for systemic disease, allow for specific diagnosis, and ultimately, more effective therapy. Herein, we review cutaneous vasculitis focusing on diagnostic criteria, classification, epidemiology, etiology, pathogenesis, and evaluation of the cutaneous vasculitis patient.
...
PMID:Cutaneous vasculitis update: diagnostic criteria, classification, epidemiology, etiology, pathogenesis, evaluation and prognosis. 1631 7

The incidence of radiation-induced chronic hemorrhagic proctitis is less than 10 to 20%. The onset of this proctitis is delayed relative to the radiation therapy and generally develops from 6 to 24 months later. There are numerous predisposing factors, the most important of which is the radiation therapy dose: risk increases exponentially above 40-45 Gy. Its pathophysiology involves progressive obliterating endarteritis and transmural interstitial fibrosis, which induce chronic ischemia that is irreversible and progressive during the years after radiation therapy. Its diagnosis depends most often on the combination of clinical history and typical endoscopic appearance (congestive mucosa and/or telangiectases). Topical administrative of sucralfate or corticosteroids as well as argon plasma coagulation, with formalin treatment if necessary, provides relief for most patients.
...
PMID:[Nonsurgical treatment of chronic radiation-induced hemorrhagic proctitis]. 1807 30

Radiation colitis refers to the characteristic changes in the mucosa of the colon and rectum secondary to pelvic radiation. Based on the interval from radiation to mucosal changes or symptoms, there are two well-defined forms of radiation colitis: acute, manifested by mucosal sloughing causing diarrhea, mucus discharge, and tenesmus; and chronic, characterized by obstructed defecation or ischemia of the mucosa due to obliterative endarteritis and resulting in mucosal telangiectasias, mucosal pallor, and friability causing rectal bleeding. Up to 25% of all patients receiving pelvic radiation develop mild symptoms, and 2% to 3% develop moderate to severe symptoms. Radiation colitis can be difficult to treat in some patients. There are several options for treating its symptoms. Argon plasma coagulation is the most common method of treating telangiectasias. Topical formaldehyde has also been used for distal telangiectasias. Obstructed defecation caused by radiation strictures (which are very fibrotic) usually can be treated successfully with stool softeners, colonic dilation, or steroid injection. Surgery should be avoided if possible because of its technical difficulty and the high incidence of postoperative complications such as anastomotic leak and fistula formation. New advances in radiation delivery techniques (eg, intensity-modulated radiation therapy) using specialized computer algorithms and medications such as amifostine may decrease the incidence of radiation colitis.
...
PMID:Approaches to the prevention and management of radiation colitis. 1879 28

Thromboangiitis obliterans, or Buerger disease, is a chronic nonatherosclerotic endarteritis manifesting as inflammation and thrombosis of distal extremity small and medium-sized arteries resulting in relapsing episodes of distal extremity ischemia. Takayasu arteritis is a rare syndrome characterized by inflammation of the aortic arch, pulmonary, coronary, and cerebral vessels, presenting with cerebrovascular symptoms, myocardial ischemia, or upper extremity claudication in young, often female, patients. Kawasaki disease is a small- and medium-vessel acute systemic vasculitis of young children, with morbidity and mortality stemming from coronary artery aneurysms. Microscopic polyangiitis, Churg-Strauss syndrome, and Wegener granulomatosis are systemic small-vessel vasculitides, affecting arterioles, capillary beds and venules, and each presenting with variable effects on the pulmonary, renal and gastrointestinal systems.
...
PMID:Nonarteriosclerotic vascular disease. 2388 34


<< Previous 1 2 3 Next >>