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)

The authors conducted a study of tolerance to glucose with the aid of a prednisolone-glucose-tolerance test in 2 groups of patients with brain strokes. The first group consisted of 63 patients younger than 45 years, the second-of 5 cases-older than 55 years of age. In both groups a positive prednisolone-glucose-tolerance test was found in patients with atherosclerosis or hypertensive disease and was not ever seen in strokes of other etiology (rheumatism, nonspecific vasculitis, cerebral vascular aneurysms, blood diseases, etc.). Irrespective of the age, latent diabetus was somewhat more frequently depicted in severe, generalized forms of atherosclerosis. The authors are of the opinion that larvated abnormalities of the carbohydrate metabolism are one of the significant "risk" factors facilitating earlier onset of atherosclerosis and hypertensive disease, as well as their different complications, including cerebral stokes. The report contains facts according to which dysglycemia seen in older patients should be considered not as a physiological aging sysmptoms, but as a sign of latent diabetus.
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PMID:[Role of latent anomalies in carbohydrate metabolism in the pathogenesis of vascular lesions of the brain]. 84 23

The authors report the case of an AIDS patient with rare neurologic manifestations: primary vasculitis of the central nervous system and VIII cranial nerve dysfunction. The authors make a review on the subject, and call special attention for the differential diagnosis. In fact, the patient, a 36 year old woman, with promiscuous life, presented with dizziness, gait ataxia, nausea, headache and hypoacusia. Seven days after the admission, she noted blurred vision in both eyes and soon she became blind. The physical examination showed bilateral optic neuritis and vestibulocochlear dysfunction, stiff neck and fever. No abnormalities were detected on CT scan. CSF showed 40 mononuclear cells/mm3, 79 mg/dl of proteins and normal glucose content. Microbiological research was negative. Serum anti-HIV test was positive. The hypothesis of primary CNS vasculitis was made, and pulse methylprednisolone therapy was introduced with good recovery of neurological syndrome except for persistent amaurosis.
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PMID:[Isolated vasculitis of the central nervous system and involvement of the 8th cranial nerve: rare manifestations of acquired immunodeficiency syndrome]. 130 67

To determine the significance of various histopathologic features of pancreatic rejection, we reviewed the pathology of 53 biopsies taken to rule out rejection [32 bladder drained, (BD); 18 non-BD]. Twenty-six biopsies from 23 patients with allografts which ultimately failed (FLD) (7 BD, 16 non-BD) were compared with 27 biopsies from 27 patients with allografts which continue to function (FXN) (25 BD, 2 non-BD). The groups are similar in regard to age, sex, and time after transplant to biopsy. The mean follow-up is 13 months for FLD grafts versus 35 months for FXN grafts (p < 0.0001). In BD grafts, decreases in urine amylase usually led to biopsy, while in non-BD grafts, hyperglycemia usually prompted biopsy. More patients with ultimately FLD organs (17 of 26) presented with elevated blood glucose (BG) than patients with FXN grafts (2 of 27) (p < 0.0001). Multiple histologic features were examined related to the acinar tissue, pancreatic ducts, islets, vessels, and nerves. Features which strongly correlated with a negative outcome included moderate to severe inflammation of acinar tissue (p < 0.0001), acinar tissue loss and fibrosis (p < 0.0087) and vascular luminal narrowing due to chronic rejection (p < 0.003). Twenty-one pancreases showed chronic rejection and were treated with OKT3 or anti-lymphocytic globulin (ALG), six of these continue to function 1.6-9 years after biopsy, including two who presented with elevated BG levels. A normal biopsy was found in nine pancreases, all of which continue to function. Vasculitis was only seen in biopsies with moderate to severe inflammation, whereas endothelialitis was also seen in association with mild inflammation, suggesting that vasculitis is a more aggressive lesion. A rejection classification is proposed with endothelialitis partly defining mild rejection and vasculitis defining severe rejection. We conclude that several biopsy features and elevation of BG are strongly correlated with a high probability of failure; however, antirejection therapy is justified because recovery of function occurs in some cases. A normal biopsy obviates the need for therapy and predicts a good outcome, as do mild histological findings of rejection.
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PMID:Pancreas rejection. Significance of histopathologic findings with implications for classification of rejection. 147 30

We examined whether experimental pneumococcal meningitis induced the 72-kd heat shock protein (HSP72), a sensitive marker of neuronal stress in other models of central nervous system (CNS) injury. Brain injury was characterized by vasculitis, cerebritis, and abscess formation in the cortex of infected animals. The extent of these changes correlated with the size of the inoculum (P less than 0.003) and with pathophysiologic parameters of disease severity, i.e., cerebrospinal fluid (CSF) lactate (r = 0.61, P less than 0.0001) and CSF glucose concentrations (r = -0.55, P less than 0.0001). Despite the presence of numerous cortical regions having morphologic evidence of injury, HSP72 was not detected in most animals. When present, only rare neurons were HSP72 positive. Western blot analysis of brain samples confirmed the paucity of HSP72 induction. The lack of neuronal HSP72 expression in this model suggests that at least some of the events leading to neuronal injury in meningitis are unique, when compared with CNS diseases associated with HSP72 induction.
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PMID:Experimental pneumococcal meningitis causes central nervous system pathology without inducing the 72-kd heat shock protein. 163 71

The central nervous system (CNS) is clinically involved in approximately 40% of all systemic lupus erythematosis (SLE) patients. Minor psychiatric symptoms and abnormalities on neuropsychological testing are being detected with increasing frequency. This review summarizes current thinking concerning the diagnosis and pathogenesis of CNS lupus. The main symptoms of CNS lupus can be diffuse (generalized seizures, psychosis) or focal (stroke, peripheral neuropathies). Neuropsychiatric symptoms often occur in the first year of SLE, but are rarely the presenting symptoms of the disease. In studies on the pathology of CNS lupus, vasculopathy, infarcts and haemorrhages are often observed, whereas vasculitis is rare. Endocardial lesions and mural thrombi have also been reported in 33-50% of CNS lupus patients. In diagnostic imaging of the CNS, magnetic resonance imaging (MRI) scans often provide evidence for edema or small infarcts, both in focal and diffuse CNS lupus, whereas computerized tomography (CT) scans only show gross abnormalities. The first reports on position emission tomography (PET) scans in CNS lupus patients show decreased glucose uptake in the brain. The cerebral blood flow decreases during active diffuse and focal CNS lupus. The blood-brain barrier is somewhat more frequently impaired in diffuse CNS lupus. Intrathecal IgG and IgM production is observed in 25-66% of all CNS lupus patient. Various specificities of autoantibodies have been observed in CNS lupus. Of these, anticardiolipin (ACA) antibodies show a well-documented association with focal involvement of the CNS in SLE. These antibodies could cause thrombosis by interfering with the protein C pathway of fibrinolysis. In addition, they are associated with endocardial and valvular heart disease, which is often observed in SLE and which could cause embolism. The relation between ACA and diffuse CNS lupus is not yet clear. Low-avidity anti-DNA antibodies are also found in CNS lupus, possibly because of their cross-reaction with cardiolipin. Antineuronal antibodies and lymphocytotoxic antibodies have been associated with diffuse CNS lupus and abnormalities on neuropsychological testing. However, the population of these antibodies is rather heterogeneous and it has not been possible to assess a common target antigen. Therefore, it is still obscure whether there is also a second immune-mediated mechanism responsible for the development of the diffuse form of CNS lupus.
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PMID:Diagnosis and pathogenesis of CNS lupus. 186 69

In an effort to establish diagnostic criteria for rejection and recurrent disease in transplanted pancreas, a comparative study was performed based on clinical diagnosis. Clinical rejection was diagnosed in patients who had decreased urinary amylase or increased blood glucose; they were treated for rejection and improved. A clinical diagnosis of recurrent diabetes was made in syngeneic transplant recipients with islet dysfunction. In addition, two control groups were used--nontransplant, nondiabetic pancreatitis patients and pretransplant normal biopsies from patients in the study. Morphologically, tissues were assessed for acinar inflammation, ductal changes, islet and nerve inflammation, and vascular changes. Immunohistochemical staining for insulin and glucagon was also performed to quantitate differences between the groups. Vascular changes (endothelialitis, vasculitis, obliterative endarteritis) were specific for rejection. Also, rejection was characterized by a lymphocytic or mixed infiltrate that involved the ducts. Recurrent diabetes was characterized by selective loss of beta cells with isletitis. Leukocyte common antigen and UCHL1 staining was helpful in identifying islet inflammation. An insulin/glucagon ratio of less than 1.0 appears to be specific for recurrent disease and in the absence of isletitis is a reasonable method for detecting recurrent disease at an early stage.
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PMID:Pancreas transplant pathology. A morphologic, immunohistochemical, and electron microscopic comparison of allogeneic grafts with rejection, syngeneic grafts, and chronic pancreatitis. 199 30

A 33-year-old man with a two-year history of asthma and sinusitis presented with wheezing, pleuritis, bilateral pleural effusions, and patchy basilar infiltrates on chest roentgenogram. Laboratory studies revealed peripheral blood eosinophilia, and pulmonary function studies showed an obstructive pattern which was bronchodilator responsive. Thoracocentesis yielded an acidotic exudative effusion with low glucose, low C3, eosinophilia, and a markedly increased rheumatoid factor. Open lung biopsy revealed extensive eosinophilic interstitial pneumonitis with necrotizing eosinophilic vasculitis. Although pleural effusions are present in 29 percent of Churg-Strauss patients, these effusions have not been well described. This report describes the pleural fluid findings in a case of Churg-Strauss syndrome.
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PMID:Pleural effusion in Churg-Strauss syndrome. 272 Dec 80

Eight patients with giant cell arteritis (6 with Horton's disease and 2 with polymyalgia rheumatica) were investigated for abnormalities in glycoregulation, previously reported in Horton's disease, using oral glucose tolerance tests with measurement of insulinaemia and C-peptide response to glucagon to evaluate pancreatic function. The results were compared with those obtained in an age and weight matched population of patients with inflammatory syndromes of other origins. All patients with giant cell arteritis had abnormal glucose tolerance tests, with diabetes mellitus in 6 and impaired glucose tolerance in 2. Insulinaemias at all stages of the test, insulin response areas and basal C-peptide values were elevated; C-peptide response to glucagon was normal. Similar results were observed in patients with other inflammatory syndromes. It is concluded that glycoregulation disorders are not incidental in giant cell arteritis, that the normal pancreatic function seems to exclude immune pancreatic vasculitis, and that the abnormal glycoregulation is probably due to insulin-resistance. Since these abnormalities cannot be explained by the patients' advanced age alone, the part played by the inflammatory syndrome, which was common to both groups, is discussed. Its responsibility for inducing insulin-resistance may account for the fact that corticosteroids, which are rapidly effective against giant cell arteritis, normalise oral glucose tolerance tests.
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PMID:[Glycoregulation disorders in giant-cell arteritis]. 316 17

In a 56-year old woman progressive partial lipodystrophy began at the age of 6 years on the face, thereafter extending slowly down to mid-thigh level (fig. 1 and 2), with moderate hypertrophy of the subjacent fatty tissue and a fatty macroglossia (fig. 3). Histological examination of the lipodystrophic skin not only showed an absence of fatty tissue, but also abnormalities at the dermis-epidermis junction with hyaline bodies (fig. 4). At the age of 23 she developed purpura, predominantly on the legs, which rapidly became chronic (fig. 5); histological examination showed leucocytoclasic vasculitis of dermal vessels (fig. 6) with granular deposits of C3 on the vessels and of IgM at the dermis-epidermis junction. Episodes of polyarthralgia and headaches were frequent. Regressive neuritis of the external popliteal nerve occurred when she was 53-year old. Renal function tests proved normal, but renal biopsy was not performed. There was no diabetes mellitus, but an oral glucose tolerance test and a somatostatin insulin glucose test elicited definite resistance to insulin. A search for a serum factor inhibiting insulin receptors was negative. Permanent abnormalities in serum were a very deep fall in C3, a pronounced fall in CH50 and a low C4 level. Besides, a C3 nephritic factor (NeF) at a high level and circulating immune complexes were present (table I); a mixed IgM-IgG cryoglobulin was found intermittently (fig. 7). Clearance of the immune complexes by splenic macrophages was extremely slow. During a series of plasma exchanges, serum C3 increased transiently, whereas serum C4 remained unchanged (fig. 8).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Barraquer and Simons lipodystrophy. Complement anomalies and cutaneous leukocytoclasic vasculitis]. 343 45

A 49-year old man without relevant prior neurological disorder but with overweight, dyslipidaemia and mild glucose dysregulation, noticed on awakening a spontaneous, left-sided and painless numb chin, attributed to isolated mental neuropathy, which regressed entirely within a few weeks. The clinical condition was stable at 1-year follow-up. Ancillary investigations (including electromyography) did not disclose any cause to this episode, notably there was no underlying malignancy or systemic disease. A thorough literature review revealed another similar case which too remained unexplained. The hypothesis of a microvascular neuropathy in relation to vascular risk factors is cautiously raised; such a mechanism has been inferred previously in exceptional cases of regressive mental neuropathy in the context of sickle-cell crisis or systemic vasculitis. Thus, at variance with classical notions, the outlook of the numb chin syndrome is occasionally benign.
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PMID:[Benign neuropathy of the chin]. 748 83


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