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

Prostatic atrophy may be histologically and at ultrasound similar to adenocarcinoma causing diagnostic confusion, its frequency increases with age but the etiopathogenesis is unknown. Based on a systematic study in autopsies previously done by one of us, ischemia due to local intense arteriosclerosis seems to be a potential factor for its pathogenesis. Absent blood flow in areas of prostatic atrophy might be a further evidence for a possible role of ischemia. From a total of 298 patients biopsied and studied by gray-scale and color Doppler transrectal ultrasound in the period 1998 to 2001, 33 patients had suspicious lesions (37 hypoechoic nodules and 3 heterogeneous lesions) showing prostatic atrophy as the only diagnosis on all these biopsied lesions. Adenocarcinoma, high-grade intraepithelial neoplasia or other atypical lesions were absent in all patients. On color Doppler the suspicious areas showed absent flow in 24/40 (60%), present flow in 12/40 (30%), and increased flow in 4/40 (10%) of the lesions. Absent flow in the majority of the lesions studied may be a further evidence for a possible role of local ischemia in the etiopathogenesis of prostatic atrophy.
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PMID:Prostatic atrophy: evidence for a possible role of local ischemia in its pathogenesis. 1289 25

Necrosis of the digits is a rare complication of warfarin therapy of obscure pathogenesis. We report a 61-year-old woman with a 12-month history of Raynaud's phenomenon who developed multiple digital necrosis following aortic valve replacement with mechanical prosthesis for aortic insufficiency caused by nonbacterial thrombotic endocarditis. Exacerbation of Raynaud's phenomenon occurred during the postoperative period, with daily episodes of ischemia of the fingers and toes that improved with local warming. However, coincident with the occurrence of immune heparin-induced thrombocytopenia, and while undergoing routine warfarin anticoagulation because of the mechanical valve prosthesis, the patient abruptly developed progression of digital ischemia to multiple digital necrosis on postoperative day 8, at the time the international normalized ratio reached its peak value of 4.3. All limb pulses were readily palpable, and vascular imaging studies showed thrombosis only in the superficial femoral and popliteal veins of the right leg. Coagulation studies showed greatly elevated levels of thrombin-antithrombin complexes and prothrombin fragment F1.2 levels, consistent with uncontrolled thrombin generation. After vitamin K administration, no abnormalities of the protein C anticoagulant pathway were identified, consistent with previous studies of other patients with warfarin-induced necrosis complicating heparin-induced thrombocytopenia. Subsequently, the patient was shown to have metastatic breast adenocarcinoma, which explained the patient's initial presentation with nonbacterial thrombotic endocarditis. This patient case suggests that multiple digital gangrene can result from the interaction of various localizing and systemic factors, including compromised microvascular blood flow (Raynaud's phenomenon), increased thrombin generation (heparin-induced thrombocytopenia, adenocarcinoma), and warfarin-induced failure of the protein C natural anticoagulant pathway.
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PMID:Warfarin-associated multiple digital necrosis complicating heparin-induced thrombocytopenia and Raynaud's phenomenon after aortic valve replacement for adenocarcinoma-associated thrombotic endocarditis. 1469 34

Cephalic pancreaticoduodenectomy is the best treatment for cephalic pancreas cancers. A rare complication is the liver ischemia after the divison of gastroduodenal artery. This complication can occur when a celiac trunk stenosed by the median arcuate ligamentous is not recognised. We report the case of a 40 old woman who underwent cephalic pancreaticoduodenectomy for an adenocarcinoma of pancreas head. There was no complication immediatly. Two weeks later, she presented two episodes of angiocholitis. An abdominal tomodensitometry showed a liver arterial ischemia associated with a celiac trunk stenosis. There was a left hepatic artery wich came from the left gastric artery. Medical treatment of the angiocholitis was successful. Surgical revascularization was not necessary. Nine months after, arterial revascularization by the left hepatic artery and biological hepatic tests were restored. This case report talks about the importance of angioscanner before pancreatic surgery when celiac and mesenteric angiography is not available. Also, it underlines the importance of the gastroduodenal artery occlusion test before his ligation during pancreaticoduodenectomy.
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PMID:[Liver arterial ischemia after cephalic pancreatico-duodenectomy. A case report]. 1629 63

Endoscopic mucosal resection (EMR) offers curative treatment for patients with node-negative early gastric carcinoma of less than 2 cm without ulceration or ulceration scar. Follow-up biopsies are frequently performed to ensure the absence of residual neoplasia. We performed a retrospective analysis of post-EMR biopsies from 33 patients who underwent gastric EMR. Histologic changes included inflammation (100%), stromal edema (97.0%), foveolar hyperplasia (78.8%), ectatic vessels (66.7%), epithelial atypia (60.6%), increased glandular mitoses (57.6%), epithelial anisonucleosis (54.5%), fibrinopurulent materials (51.5%), ischemia (48.5%), stromal hemorrhage (33.3%), mucin depletion (12.1%), clear cell degeneration (15.2%), and signet-ring cell-like change (6.1%). Especially, clear cell degeneration and signet-ring cell-like change were conspicuous in the area of ischemia. Residual adenocarcinomas were noted in 4 of 33 cases, and consistently showed high nuclear-to-cytoplasmic ratio with high glandular density. Glandular clear cell degeneration and/or signet-ring cell-like change were worrisome and sometimes difficult to be distinguished from residual neoplastic glands. However, these degenerative glands were usually embedded in a nondesmoplastic stroma and showed anisonucleosis of glandular epithelia. Mimics of residual adenocarcinoma, namely clear cell degeneration and signet-ring cell-like change should be judiciously assessed to avoid unnecessary surgery.
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PMID:Post-gastric endoscopic mucosal resection surveillance biopsies: evaluation of mucosal changes and recognition of potential mimics of residual adenocarcinoma. 1669 21

Pneumatosis intestinalis is an uncommon finding that may indicate the presence of several alarming pathological conditions, including bowel ischemia, that require urgent surgical intervention. We report the case of a 51-year-old man with celiac disease who underwent resection of a large duodenal adenocarcinoma. Although he initially recovered rapidly from his procedure, he subsequently developed abdominal distention and leukocytosis. Abdominal imaging revealed extensive small bowel pneumatosis and pneumoperitoneum. Emergent surgical exploration revealed only bowel wall air cysts and dilated bowel but failed to demonstrate any intra-abdominal pathology. The patient recovered uneventfully and was discharged without any further complications or recurrence of symptoms. We review the current literature on the rare finding of pneumatosis intestinalis in the setting of celiac disease. In all reported cases, even when pneumatosis is accompanied by pneumoperitoneum, these alarming findings have proved to be of "benign" origin, that is with no evidence of bowel ischemia, perforation, or peritonitis. The available evidence suggests that pneumatosis in the setting of celiac disease may reflect the dissection of intraluminal gas into the inflamed bowel wall without accompanying intra-abdominal pathology. We conclude that pneumatosis intestinalis, even with accompanying pneumoperitoneum, does not uniformly mandate surgical exploration in patients with celiac disease.
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PMID:Benign pneumatosis intestinalis in the setting of celiac disease. 1676 47

In patients with celiac axis occlusion, performance of pancreaticoduodenectomy involves sacrifice of the gastroduodenal artery which results in a risk of hepato-pancreato-biliary and other organic ischemia. Celiac axis occlusion does not recently seem an uncommon finding in cases of pancreaticoduodenectomy but diagnosis of celiac axis occlusion may be difficult in patients with former abdominal surgery. The present case report shows a patient with pancreatic head adenocarcinoma, in whom a preoperative diagnosis of celiac axis occlusion was not proved because of displacement of the celiomesenteric arterial branches based on former distal gastrectomy with Kocher's maneuver. A 56-year-old man with malignant obstruction of the lower bile duct was referred to our hospital for undergoing pancreaticoduodenectomy. In his past history, the patient had undergone distal gastrectomy reconstructed with Billroth I method due to gastric ulcer. In preoperative abdominal angiography, the celiac axis was not detected at the normal position and was incorrectly recognized to be anomalously originated from the superior mesenteric artery. During surgery, hepatic arterial flow was markedly diminished by clamping of the gastroduodenal artery. Celiac axis occlusion was then proved and the thick and tight median arcuate ligament was detected. Hepatic arterial blood flow was recovered by a complete division of the median arcuate ligament. Postoperative course of the patient was uneventful. In cases of pancreaticoduodenectomy, careful preoperative angiographic diagnosis is needed for patients with celiac axis occlusion who have undergone former gastric surgery because the celio-mesenteric arterial branches have been displaced by Kocher's maneuver. The present report also demonstrates another patient with a typical celiac axis stenosis.
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PMID:Celiac axis occlusion of a patient undergoing pancreaticoduodenectomy after distal gastrectomy. 1752 29

The short bowel syndrome (SBS) can result from a variety of conditions, including postoperative complications and malignancy. Continence-preserving operations are generally performed for either ulcerative colitis (UC) or familial polyposis (FAP). These procedures can be associated with high morbidity and the potential for future malignancy. Our aim was to determine the causes and consequences of SBS in patients undergoing these procedures. Twenty-four patients (12 men and 12 women) 18 to 64 years of age were identified with SBS after continence-preserving procedures. Eighteen had pelvic procedures, and six had continent ileostomies. All SBS patients had a proximal ostomy. Remnant length measured <60 cm in five patients, 60-120 cm in ten patients, and >120 cm in nine patients. Overall 13 patients required long-term PN. Four FAP patients with desmoid tumors died. One patient with UC underwent intestinal transplant and expired. Follow-up ranges from 6 to 192 months. Overall 14 patients had UC, nine had FAP, and one had functional disease. Eight patients with an initial diagnosis of UC had subsequent Crohn's disease necessitating further resection and pouch excision. Eight patients (five with UC, two FAP, and one with functional disease) had postoperative complications, including obstruction or mesenteric ischemia requiring resections. One UC patient developed adenocarcinoma in a continent ileostomy. Seven of the nine FAP patients required resection for desmoid tumors. Six of these underwent resection alone. Three died at 10, 11, and 13 months after SBS from liver failure and sepsis while awaiting transplant. One patient has recurrent desmoid at 30 months, another is alive and well at 48 months, and the other patient, who was not a transplant candidate, died from an unrelated cardiac operation at 23 months. A single patient underwent resection with simultaneous multivisceral transplantation. SBS can develop after continence-preserving procedures. This occurs with inflammatory bowel disease when unsuspected Crohn's disease is present or complications occur. SBS related to desmoid tumors has a poor prognosis in patients undergoing resection alone. A more aggressive approach to intestinal transplantation in these patients may be warranted.
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PMID:Short bowel syndrome after continence-preserving procedures. 1796 30

A patient with sigmoid colon adenocarcinoma and hypercoagulable state developed acute visceral ischemia secondary to thrombus involving the suprarenal aorta, celiac axis and superior mesenteric artery. A large, laminated fibrin thrombus was removed via supraceliac aortotomy. Attempts to clear thrombus from branches of the celiac axis and superior mesenteric artery by open and catheter-based techniques were of limited success. Extensive visceral infarction ensued and the patient died.
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PMID:Aortic, celiac axis, and superior mesenteric artery thrombosis associated with sigmoid colon adenocarcinoma and hypercoagulable state. 1916 64

This report describes a patient who presented with acute critical right leg ischemia leading to the diagnosis of esophageal adenocarcinoma with widespread metastases. His limb was salvaged with urgent thromboembolectomy. However, he died 3 weeks after presentation due to progressive cancer. Pathogenesis of arterial thromboembolism in the setting of malignancy remains uncertain but multiple factors probably contribute to this phenomenon. Management is challenging and conservative approach is generally advocated especially when the prognosis related to the malignancy is poor. When arterial thromboembolism develops in patients with malignancy, the prognosis is usually very poor. Therefore, acute arterial thromboembolism has been suggested as an agonal event. Where possible in such setting, revascularisation can be attempted to provide pain relief and improve quality of life but major vascular reconstructive surgery is not recommended in most cases.
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PMID:Acute critical leg ischemia: an uncommon initial manifestation of esophageal adenocarcinoma. 1971 77

Prostatic atrophy is a benign lesion that may mimic adenocarcinoma histologically and on imaging. It is more frequent in the peripheral zone and has gained importance with the increasing use of needle biopsies. Diffuse atrophy occurs secondarily to radiotherapy and/or endocrine therapy. Inflammation and/or chronic local ischemia may cause focal atrophy with an increasing frequency in age. Atrophy may be classified morphologically into diffuse and focal. The latter may be partial, complete or combined. Partial focal atrophy is the most frequent mimicker of adenocarcinoma on needle biopsies. Complete focal atrophy may be subtyped into simple, sclerotic and hyperplastic (or postatrophic hyperplasia). Combined lesions are frequent and partial atrophy may precede complete atrophy. The several morphologic types of focal atrophy may represent a morphologic continuum and the hyperplastic (or postatrophic hyperplasia) subtype seems to be at the extreme end of this continuum. Chronic inflammation associated to focal atrophy (proliferative inflammatory atrophy) has been linked to high-grade prostatic intraepithelial neoplasia and/or carcinoma. This link, however, remains controversial in the literature. The question whether inflammation directly produces tissue damage and atrophy or some other insult induces atrophy directly, with inflammation occurring secondarily, is still unresolved. An intriguing finding that needs further studies is a possible association of extent of atrophy to serum PSA elevation.
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PMID:Prostatic atrophy. Clinicopathological significance. 2081 46


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