Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Besides classical necrotizing enterocolitis (in neonates), which is seen in India as elsewhere in the world, we observe sporadic cases of tropical enterocolitis, i.e. segmental jejunitis, ileitis or colitis and rarely duodenitis. This is a distinct clinico-pathological entity presenting as "acute abdomen", with pain, bilious vomiting, constipation or bloody diarrhoea. The clinical course is not as fulminating as neonatal necrotizing enterocolitis. Most cases are salvaged by conservative treatment especially after the confidence brought by laparoscopic vision of the abdomen, thus excluding perforation or gangrene of the bowel involved. Without laparoscopy, most of the cases end up in laparotomy. The pathology appears to be a kind of local hyperimmune reaction in the segment of bowel involved, ranging from punctate haemorrhages in the seromuscular layer of the bowel to a generalized red fiery look or perforation due to mucosal ulceration. Whatever the causative agent, the pathogenesis is of local vasculitis leading to ischemia and various patterns of disease.
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PMID:Tropical enterocolitis in children. 808 96

We present the clinical, morphological and neuropathological findings in a 44-year-old male suffering from the acquired immunodeficiency syndrome (AIDS) (CDC stage IV C2) who presented with rapidly progressive right-side hemiparesis and developed hemianopia and aphasia. Scans showed multiple, not contrast-enhancing, not space-occupying echo-intensive lesions in T2-weighted MR-imaging. No hint for an opportunistic infection, necrotizing vasculitis or vascular disease was found. All therapeutic regimens failed and 8 weeks after onset of neurological symptoms the patient died because of cardiorespiratory arrest. Post-mortem examination excluded opportunistic infection, progressive multifocal leukoencephalopathy, lymphoma, vasculitis and ischemia of the brain. In the presence of an unusually high amount of HIV-infected macrophages at immunohistochemical examination, the overall pathological findings were atypical both for HIV encephalitis and HIV leukoencephalopathy. We describe a pathologically distinct new form of HIV associated encephalopathy.
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PMID:A pathologically distinct new form of HIV associated encephalopathy. 815 18

Besides distal symmetrical sensory polyneuropathy (DSSP), middle-aged diabetic patients may present with focal or multifocal neuropathies, including proximal neuropathy of the lower limbs, the pathophysiological features of which are uncertain. We studied 10 non-insulin-dependent diabetic patients, 45 to 72 years of age, who developed a painful proximal neuropathy of the lower limbs for which other causes of neuropathy were carefully excluded. The proximal neuropathy was asymmetrical in all patients, sensory in 4, motor and sensory in the others. Signs of DSSP were present in all. A sample of the intermediate cutaneous nerve of the thigh, a sensory branch of the femoral nerve, was taken by biopsy and examined by light and electron microscopy. Examination of the nerve specimens revealed ischemic nerve lesions in 3 patients. Nerve ischemia was associated with vasculitis and inflammatory infiltration in 2 of them. In the other patients the lesions of the cutaneous nerve of the thigh included a varying incidence of axonal and demyelinative lesions similar to those observed in DSSP, with mild inflammatory infiltration in 4 of them. The density of myelinated and of unmyelinated was variably decreased. This study shows that axonal and demyelinative lesions similar to those found in diabetic DSSP are present in proximal nerves in mild forms of proximal diabetic neuropathy; while nerve ischemia, inflammatory infiltration, and vasculitis are encountered in the most severe forms of proximal diabetic neuropathy.
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PMID:Nerve biopsy findings in different patterns of proximal diabetic neuropathy. 817 2

This case illustrates the difficulty of diagnosing a colonic stenosis of ischemic origin. A 70-year-old lady presents with abdominal pain, fever and melaena. Lc are 15.2, ESR 39 mm, CEA 2.7 ng/ml. A barium enema shows a stenosis of the transverse colon that is suspicious of neoplasia. At time of operation, an induration of the transverse colon is found with edema of the corresponding mesocolon but no tumour is palpated. A resection of this area is performed and an end to end anastomosis performed. Pathology shows an ischemic colitis secondary to a lymphocytic thrombotic venulitis. The patient is discharged home one month postoperatively. 4 weeks later she is readmitted with the same symptoms. A gastrograffin enema shows a similar stenosis in the transverse colon including the anastomosis. The diagnosis is made of a recurrent ischemic stenosis. The patient improves over a 10-day period of conservative treatment (anticoagulation, TPN, steroids). A control barium enema shows a near resolution of the stenosis. The majority of ischemic colitis are of arterial origin nevertheless ischemic colitis of venous origin exists. The factor causing venous ischemia are not known. It is though thought to be associated with hypersensitivity vasculitis of drug origin. Its initial diagnosis versus neoplasia is difficult but once made there is a good response to a conservative treatment.
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PMID:[Segmental ischemic colitis in lymphocytic thrombotic venulitis]. 822 85

Eleven adult patients with stable sickle cell disease (SCD) were investigated twice at a 15-day interval by nail fold capillaroscopy (NFC), bulbar conjunctival angioscopy (BCA), and laser Doppler flux metering (LDF). NFC and BCA are essentially descriptive. NFC revealed, in some patients, network patterns similar to those observed in vasculitis. BCA provides a reproducible method for the visual assessment of the microcirculation. When using a rating scale with five criteria it identified abnormalities related to both altered red blood cells and vascular morphology but failed to discriminate between patients. LDF, in contrast, is quantifiable and showed reproducible characteristic reactive alterations of vasomotion in response to ischemia after 3 min of occlusion. The SCD patients had a delayed response, best measured by the recovery half time, which was four to five times longer than that of normal subjects. In addition, the cold provocative test was always abnormal, as evidenced by a significant drop in the contralateral flux, and was often poorly tolerated. The observed trends suggest that BCA and LDF should be performed in a large cohort of patients, both in the steady state and during vasoocclusive crises. These methods seem to be useful complementary noninvasive procedures to cellular and clinical evaluation monitoring for therapeutic trials.
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PMID:Comparative evaluation of laser Doppler flux metering, bulbar conjunctival angioscopy, and nail fold capillaroscopy in sickle cell disease. 847 39

A means to monitor intestinal allografts will be crucial for the future success of small bowel transplantation. We have previously demonstrated the ability of high-frequency ultrasound (US) to diagnose porcine intestinal ischemia in vitro. The aim of this study was to compare the histologic appearance of normal porcine small bowel versus bowel undergoing acute rejection, using 8.5-MHz US images. We allowed porcine heterotopic small bowel allograft transplants to reject and then removed, at scheduled intervals from postoperative day 0 to 12, specimens of both the transplanted bowel and the native bowel. We examined the tissues in vitro with an 8.5-MHz linear array US system then studied them histologically. Histologically, the earliest changes of rejection occurred at days 4 to 5, with mild submucosal edema, endotheliitis, and vasculitis affecting the small vessels; the mucosa remained normal. By days 7 to 8, the submucosal endotheliitis became more prominent, with focal thrombosed small vessels; the mucosa now appeared abnormal with flattened villi, erosions, and necrosis. By days 10 to 12, marked submucosal edema, vasculitis, endotheliitis, and necrotic mucosa were present. Ultrasonically, normal intestinal wall has five wall layers, corresponding to mucosa, submucosa, muscularis propria, and subserosal fat. The US criteria for abnormality were loss of folds, decreased numbers of echo layers, discontinuity of layers, and a homogeneous appearance. Using these US criteria, blinded observers differentiated normal from abnormal bowel wall after transplantation with a sensitivity of 84% and a specificity of 81%. Most of the errors occurred with the day 4 and 5 specimens, which appeared nearly normal on US.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental use of high-frequency ultrasound to image bowel wall after porcine intestinal transplantation. 848 74

The pathogenesis of vasculitis syndromes is via a diverse array of mechanisms that disrupt vessel integrity and produce clinical signs and symptoms of tissue ischemia. In many patients with vasculitis, it is not possible to directly classify the syndrome according to a particular schema, and attempts to define the pathogenic process mediating vessel damage by biopsy and laboratory tests may be useful to guide therapy. The continued use of new techniques to probe immune cell types and cytokines in vasculitis lesional tissues will further clarify molecular mechanisms of vascular damage, and it is hoped that they will lead to new and more effective therapeutic strategies targeted at the vasculitis syndromes.
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PMID:Pathogenic mechanisms of vessel damage in vasculitis syndromes. 859 41

The paper presents general therapeutic principles applied in systemic vasculitis. Several factors may help to contain the clinical activity, such as the location and extent of the inflammatory process affecting the vascular system, the ultimate narrowing of the vascular lumen with subsequent ischemia of the affected tissue and organ. Treatment of vasculitis involves besides glucocorticoids not only cytotoxic drugs (cyclophosphamide, chlorambucil, methotrexate), and immunomodulatory therapeutic agents with immunosuppressive action (cyclosporin A) but also other immunomodulatory drugs, as e.g. dialyzed homogenate of leukocytes (DHL), pentoxyphylline, hydrolytic enzymes, and monoclonal antibodies. The authors emphasize the importance of a complex approach in the management of systemic vasculitis. (Tab. 1, Ref. 36.).
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PMID:[General therapeutic approaches in systemic vasculitides]. 862 Mar 28

Complications associated with the use of cocaine are varied, and include cerebral hemorrhage and ischemia, with vasculitis and vasospasm as possible etiologies. We reviewed selected brain samples from 14 autopsy cases of cocaine-related cerebrovascular disease. Intracerebral or subarachnoid hemorrhage was present in 12 cases. Intracranial arterioles were either normal or showed nonspecific changes. From these observations, we suggest that intracranial hemorrhages occur in the absence of readily detectable vascular abnormalities.
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PMID:Cocaine-associated intracranial hemorrhage: absence of vasculitis in 14 cases. 864 82

The anticardiolipin or antiphospholipid antibody syndrome is characterized by an increased incidence of venous and arterial thromboses. This syndrome may occur in association with systemic lupus erythematosus or independently. Gastroenterological manifestations have included Budd-Chiari syndrome, hepatic infarction, esophageal necrosis with perforation, intestinal ischemia and infarction, pancreatitis, and colonic ulceration. We report a 39-yr-old man with antiphospholipid antibody syndrome complicated by adrenal insufficiency secondary to bilateral adrenal infarction who presented with severe epigastric pain. Endoscopic evaluation disclosed progressive gastric ulceration with necrosis in the distal body. Angiography revealed no vasculitis. Because of intractable pain despite intravenous anticoagulation and narcotic analgesia, the patient was taken to surgery, and an antrectomy with Billroth II gastrojejunostomy was performed. Histological examination revealed widespread vascular occlusive disease involving veins, small arteries, and arterioles present in all layers of the stomach and the perigastric fat consistent with the vasculopathy of the antiphospholipid antibody syndrome. Treatment with high intensity oral anticoagulation and corticosteroids resulted in clinical and endoscopic improvement. This case report extends the gastroenterological manifestations of the antiphospholipid antibody syndrome to include giant gastric ulceration and emphasizes the importance of anticoagulation in treatment.
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PMID:Giant gastric ulceration associated with antiphospholipid antibody syndrome. 912 46


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