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)

Erythromelalgia is an acrocyanotic rheumatic disease presenting with erythema, and pain and a burning sensation in the hands and feet; it is rarely encountered during childhood. Hot or warm conditions may precipitate pain and erythema in the extremities and the symptoms may regress upon the application of cold water. The disease is usually secondary to other systemic diseases in adults. On the other hand, it is idiopathic in children. This article describes a case of erythromelalgia presenting with leukocytoclastic vasculitis and hypertension in a 7-year-old child who responded to therapy with prednisolone and phenoxybenzamine.
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PMID:Erythromelalgia associated with hypertension and leukocytoclastic vasculitis in a child. 953 98

We recently reported that norepinephrine and angiotensin II activate the Ras/mitogen-activated protein (MAP) kinase pathway through generation of a cytochrome P450 (CYP450) and lipoxygenase metabolites. The purpose of this study was to determine the contribution of Ras/MAP kinase to deoxycorticosterone acetate (DOCA)-salt-induced hypertension in rats. Administration of DOCA and 1% saline drinking water to uninephrectomized rats for 6 weeks significantly elevated mean arterial blood pressure (MABP) (166+/-5 mm Hg, n=19) compared with that of normotensive controls (95+/-5 mm Hg, n=7) (P<0.05). The activity of Ras and MAP kinase measured in the heart was increased in DOCA-salt hypertensive rats. Infusion of the Ras farnesyl transferase inhibitors FPT III (138 ng/min) and BMS-191563 (694 ng/min) significantly (P<0.05) attenuated MABP to 139+/-4 mm Hg (n=14) and 126+/-1 mm Hg (n=4), respectively. Moreover, infusion of MAP kinase kinase inhibitor PD-98059 (694 ng/min) also reduced MABP in hypertensive rats. Morphological studies of the kidney showed that treatment of rats with FPT III, which reduced Ras activity, minimized the hyperplastic occlusive arteriosclerosis and fibrinoid vasculitis observed in untreated hypertensive rats. In addition, the rise in CYP450 activity and MABP in hypertensive rats was prevented by the CYP450 inhibitor aminobenzotriazole (50 mg/kg) and was associated with a decrease in Ras and MAP kinase activity in the heart. These data suggest that the Ras/MAP kinase pathway contributes to DOCA-salt-induced hypertension and associated vascular pathology consequent to activation of CYP450.
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PMID:Contribution of Ras GTPase/MAP kinase and cytochrome P450 metabolites to deoxycorticosterone-salt-induced hypertension. 1064 41

HIV infection has reached endemic proportions in many African countries. In addition, HIV infection is a significant cause of renal dysfunction in the United States. HIV patients are at higher risk of developing hypertension at a younger age than the general population. Predisposing factors for developing hypertension include vasculitis in small, medium, and large vessels in the form of leukocytoclastic vasculitis, and aneurysms of the large vessels such as the carotid, femoral, and abdominal aorta with impairment of flow to the renal arteries. A syndrome of acquired glucocorticoid resistance has been described in patients with HIV with hypercortisolism and a lower affinity of the glucocorticoid receptors. The syndrome is characterized clinically by weakness, hypertension or hypotension, and skin pigmentation changes. Acute and chronic renal failure is often associated with HIV infection. The associated dysfunction in water and salt handling often induces hypertension. Finally, atherosclerosis has been described in young adults with HIV infection secondary to receiving highly active antiretroviral therapy.
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PMID:Hypertension in the HIV-infected patient. 1099 24

Piscirickettsia salmonis, the etiologic agent of salmonid rickettsial septicemia (SRS), or piscirickettsiosis, causes substantial economic losses to the salmon industry. The pathogenesis of the disease has not been fully characterized. The aim of this study is to describe the hepatic lesions associated with experimental P. salmonis infection in Atlantic salmon juveniles. Fish were maintained in fresh water and inoculated intraperitoneally (IP), orally, or on the gill surface with P. salmonis. A group of uninfected fish was kept as control. Liver samples from 5 fish in each inoculated group and 3 controls were collected weekly and processed for histological and immunohistochemical examination. Thickening of the liver capsule by inflammatory cells was a characteristic histologic feature of IP inoculated fish. Three weeks post-IP inoculation, 8 fish had died and 2 fish were sampled. Histological changes at this time consisted of vasculitis, presence of fibrin thrombi, vacuolated hepatocytes and focal areas of necrosis. Leukocytes containing intracytoplasmic basophilic microorganisms were seen within hepatic sinusoids. Vasculitis and intracytoplasmic vacuoles were prominent features in fish inoculated orally and on the gill surface. The presence of P. salmonis within hepatocellular vacuoles, endothelial cells, and leucocytes was confirmed by immunohistochemistry. The intracellular location of P. salmonis and the vascular damage seen in infected fish are characteristic of rickettsial infections. Histological lesions induced by experimental infection with P. salmonis using the oral and gill surface routes were similar to those observed in natural outbreaks of piscirickettsiosis. The tropism of P. salmonis for endothelial cells explains the vascular lesions observed in SRS, whereas hepatic lesions are due to ischemic necrosis and direct injury by intracytoplasmic organisms.
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PMID:Pathogenesis of liver lesions caused by experimental infection with Piscirickettsia salmonis in juvenile Atlantic salmon, Salmo salar L. 1110 56

Neurocysticercosis is the most common parasitic disease of the central nervous system. Praziquantel and albendazole, the two antiparasitic drugs, have been reported to be effective against cysticercosis. Both the drugs effectively destroy the cerebral parenchymal cystic lesions. However, albendazole is possibly more effective in subarachnoidal, ventricular and spinal forms of cysticercosis, and frequently obviates the need for surgery. Initially, longer courses of albendazole and praziquantel had been advocated. Now even shorter treatment regimens are found equally effective. Complete course of praziquantel therapy can be administered in a single day with comparable efficacy instead of conventional treatment of 15 days. Similarly, one week therapy of albendazole is as effective as 30 days' treatment regimen. Recently, there is an intense debate whether anticysticercal treatment is useful and safe. Opponents of anticysticercal therapy argue that effectiveness of therapy is possibly a reflection of natural course of the disease. It has been observed that even if cysticercal lesions are left untreated, they either disappear spontaneously or calcify. Anticysticercal therapy is potentially risky, it may aggravate cerebral oedema, and may produce vasculitis and stroke, and several deaths have also been reported. To minimise these risks, concomitant corticosteroids should be administered especially, if there is a massive parasitic load. It is better to avoid anticysticercal treatment in patients with cysticercotic encephalitis. Doubts have been expressed that anticysticercal therapy really affects ultimate long-term clinical outcomes (e.g. control of seizure and possibility of seizure free state after discontinuation of antiepileptic drugs). So far, definite evidences in this regard, based on finding of well planned placebo-controlled studies, are lacking and an opinion that, there is an urgent need for such a study, has been expressed. Measures for effective prevention like provision for safe drinking water and safe excreta disposal should be emphasisfxed.
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PMID:Medical management of neurocysticercosis. 1179 3

The purpose of the present study was to evaluate the effectiveness of fish oil in preventing tissue pathologies associated with monocrotaline (MCT) toxicity. Twenty-four weanling rats were randomly assigned to one of two groups: (1) 12 to a group fed a diet containing 15% (w/w) corn oil (control) and (2) 12 to a group fed a diet containing fish oil (13%) and corn oil (2%) as the source of fat. Rats were fed for 4 weeks prior to MCT treatment. Six rats in each group were subcutaneously injected with MCT and six injected with its vehicle (water) and all were continued on their respective diets. All rats were sacrificed 3 weeks after injection. In rats receiving MCT, we observed severe interstitial pneumonia, septal fibrosis, vasculitis with virtual obliteration of the lumen of the small arteries and arterioles, right ventricular hypertrophy (RVH), and hepatomegaly and hepatocyte vacuole formation. Dietary fish oil significantly reduced septal fibrosis and development of pneumonia. There was a slight, but statistically insignificant decrease in vasculitis and fish oil did not prevent RVH (pulmonary hypertension). In addition, fish oil effectively protected the MCT-treated rats from development of hepatocyte vacuoles (steatosis), hepatic inflammation and vasculitis, increased presence of fibroblasts and collagen deposition in the centrilobular and, to a lesser extent, in the periportal spaces. These results suggest that lung parenchymal inflammation can be attenuated without altering the course of development of pulmonary hypertension in the MCT model. These results also indicate that fish oil protects against inflammation and fibrosis in the lung and liver, and against hepatocyte vacuole formation in MCT-treated rats.
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PMID:Dietary fish oil protects against lung and liver inflammation and fibrosis in monocrotaline treated rats. 1204 31

Over the past few years, the cercarial dermatitis has become a new problem of public health, obviously linked to the prolonged stay of migrant birds on our territory. This is a skin affection characterized by pruriginous and papulous eruptions caused by penetration of avian bilharzian larvae under the skin. These larvae are emitted by molluscs, mostly limneids. In aquatic birds, especially in migrating Anatidae, these larvae reach the visceral vessels, become adults in a few weeks, lay eggs, then degenerate. Corresponding miracidia contaminate new limneids. Since 1993, the total number of annual cases of cercarial dermatitis has increased from only ten to thousands in France and the affection rages in pools where limneids, migrating water birds and swimmers gather together. Fever, respiratory and/or digestive allergic symptoms appear in some cases. This clinical pattern has encouraged to undertake research on the future of these bilharzian larvae in mammals organism. A preliminary investigation on a rodent model showed that, once the skin barrier had been crossed, the schistosomulae migrated into the lungs of the host; there they survived a week and induced lesions. The goal of this study is to carry on the research, over a longer period, after exposure to cercariae, simultaneously in mammals and birds, with two species of bilharziae present in France. The selected models are the gerbil Meriones unguiculatus for mammals, and the ducks Anas platyrhynchos and Cairina moschata, for birds. 5 M. unguiculatus and 2 A. platyrhynchos were exposed to cercariae emitted by Radix auricularia; 2 gerbils and 5 A. platyryhnchos to larvae of R. peregra, 3 C. moschata to larvae emitted by two species of molluscs: 70-230 from R. auricularia and 330-585 from R. peregra. 5 gerbils died between 2 and 5 weeks after exposure, 2 gerbils sacrificed early, served as control animals for skin manifestations. Eight ducks were sacrificed between 2 and 4 weeks after; the 2 last ones, exposed several times, were sacrificed respectively 7 and 13 weeks after the first exposure. Visceral and skin samples were submitted to histological study. The control gerbils developed skin dermatitis. In ducks, R. auricularia was the vector of Trichobilharzia franki, whose selective dwelling site was the mesentery; R. peregra was the vector of an indeterminate species found in the lungs and nose. This species is called Bilharzia sp. in this study. The ducks, exposed to two kinds of larvae, displayed worms in these two main locations. In gerbils, T. franki induced lesions in the mesenteric veins and the peritoneum. Bilharzia sp. gave rise to lesions in lung arteries, pleura and liver veins. Vascular changes encompassed endothelitis and lymphocytic vasculitis, while serosa displayed mesothelial hyperplasia. The types of lesions observed in gerbils were noticed in ducks, and, according to the species of bilharzia, in the homologous viscera. Additional foreign body granulomas centred on worm's debris or their eggs, and vascular thromboses were present, too. In addition, ducks displayed lesions involving several other viscera including the intestine, the kidneys and the peripheral nerves. These changes were multiple and diffuse in C. moschata exposed to two species of bilharziae. They were observed mainly in mesenteric and intestinal vessels, pulmonary arteries and hepatic veins. In gerbils, the lesions persisted 2 to 5 weeks after exposure, but worms were not identified in the neighbouring tissues near the damaged vessels. In ducks, lesions were important between 2 and 7 weeks after exposure; they co-existed with live or dead worms, sometimes paired, with or without eggs. The hepatic lesions regressed 13 weeks, after exposure. In mammals and birds, young worms could migrate into the same visceral vessels, and stimulating formation of persistent lesions. In individuals exposed to the same cercariae, development of similar lesions would be probable.
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PMID:[Visceral lesions in mammals and birds exposed to agents of human cercarial dermatitis]. 1259 66

Leptospires, world-wide distributed spirochetes, affect a great variety of mammalian hosts; several serovars belonging to the L. interrogans s.l. species can cause clinical manifestations in humans, becoming infected through the contact of skin cuts and mucous membranes with water and soil polluted by infected animals' urine; rodents serve as the main reservoirs but the epidemiological importance of pets and cattle, as leptospire shedder is increasing. While the infection remains endemic in tropical regions, there is a new epidemiological trend in developed countries where, with the typical seasonal pattern, sporadic cases and/or outbreaks occur related more to recreational activities and poor sanitation than to occupational activities. The sudden onset presents a "flu-like" syndrome; the course is usually characterised by two clearly defined stages. All of the variable clinical manifestations, often independent of the responsible serovar, arise from the effects of a general vasculitis. The prognostic factors associated with severe forms (renal failure, jaundice, haemorrhagies) are not defined. Within the first days of illness, the leptospires can be isolated from blood and cerebrospinal fluid; serological diagnosis relies on microagglutination, IFA and ELISA; PCR early in the course, before the appearance of specific antibodies, allows etiological diagnosis. Prompt treatment has an enormous impact on outcome.
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PMID:[Leptospirosis: epidemiology, diagnosis and clinical aspects] 1275 85

Multiple renal adverse effects have been anecdotally reported with the ingestion of 3,4-methylenedioxymethamphetamine (Ecstasy), a widely used recreational drug. These side effects include acute renal failure, necrotizing vasculitis, and hyponatremia, the mechanisms for which are unknown. We report a case of transient acute proximal tubular injury and hyponatremia associated with Ecstasy use. An 18-year-old woman presented with new onset seizures and polydipsia. Her initial laboratory evaluation revealed hyponatremia (Na 117 mEq/L), polyuria (urine output >400 mL/h for several hours), renal glycosuria (blood glucose 120 mg/dL, urine glucose >1,000 mg/dL), and solute diuresis (urine osmolality 552 mOsm/kg H2O). Urine electrolyte values reflected a low tubular reabsorption of phosphorus (TRP) of 68.1% (expected TRP >85% at serum P 2.3 mg/dL) with an appropriate transtubular potassium gradient of 3.0 (serum K 3.7 mEq/L). Her hyponatremia was slowly corrected. A repeat TRP after 48 h had normalized to 86.5%, and her glycosuria resolved. An extensive toxin screen was later reported positive for Ecstasy. To our knowledge, this is the first example of an acute and transient proximal tubular injury with Ecstasy ingestion. This complication may become more apparent with increasing use of this drug.
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PMID:Transient proximal tubular renal injury following Ecstasy ingestion. 1277 21

The effects of water-soluble beta-cyclodextrin derivatives (beta-CyDs), such as 2-hydroxypropyl-beta-cyclodextrin (HP-beta-CyD) and sulfobutyl ether beta-cyclodextrin (SBE7-beta-CyD) on cytotoxicity of DY-9760e (3-[2-[4-(3-chloro-2-methylphenyl)-1-piperazinyl]ethyl]-5,6-dimethoxy-1-(4-imidazolylmethyl)-1H-indazole dihydrochloride 3.5 hydrate) toward human umbilical vein endothelial cells (HUVECs) in vitro and vascular damage of the auricular vein of rabbits by DY-9760e in vivo were investigated. The spectroscopic study revealed that of the four beta-CyDs SBE7-beta-CyD forms the most stable inclusion complex in phosphate-buffered saline, probably because of a synergetic effect of hydrophobic and electrostatic interactions. beta-CyDs inhibited DY-9760e-induced cell death toward HUVECs in an order of G(2)-beta-CyD < beta-CyD < HP-beta-CyD < SBE7-beta-CyD, which was consistent with the order of the magnitude of stability constants. When the DY-9760e solution was infused into the auricular vein of rabbits for 24 h, SBE7-beta-CyD suppressed a DY-9760e-induced irritation such as thrombus, desquamation of the endothelium vasculitis, and perivasculitis. The present data indicated that SBE7-beta-CyD formed an inclusion complex with DY-9760e in a buffer solution and possessed the protective effect on DY-9760e-induced cytotoxicity toward HUVECs and vascular damage in rabbits. These results suggested potential use of SBE7-beta-CyD as a parenteral carrier for DY-9760e.
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PMID:Inhibitory effect of sulfobutyl ether beta-cyclodextrin on DY-9760e-induced cellular damage: In vitro and in vivo studies. 1460 92


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