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)

The degree of participation and regional specificity of virus infection in relation to atraumatic acute peripheral facial palsy was studied, placing particular emphasis on change in the CF titre of varicella zoster virus (VZV), herpes simplex virus (HSV) and adenovirus (adeno). The subjects of the study were 91 patients with Hunt's syndrome and 396 patients with Bell's palsy treated at 17 institutions all over Japan in the period between April 1985 and November 1986. Among the cases of Hunt's syndrome, the positive conversion rate of CF antibody titre of VZV was 81%. In Bell's palsy cases, virus participation was detectable in 8% with VZV, 4% with HSV and 4% with adeno. With regard to the age distribution, Bell's palsy cases with possible virus involvement tended to be observed in younger patients than those without that possibility. As to regional specificity, the incidence of Bell's palsy with possible virus involvement tended to be higher in densely populated areas. With regard to the main cause of acute peripheral facial palsy, virus infection has been implicated, as well as insufficient blood circulation (ischemia). Even in cases of acute peripheral facial palsy, in which herpes zoster oticus is not observed, the participation of varicella zoster virus (VZV) as a cause of paralysis has been pointed out in some cases (zoster sine herpete). Furthermore, it is known that the serum antibody titres of various viruses such as herpes simplex virus (HSV) change significantly in some cases of Bell's palsy (2, 5-13).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Viral infections in acute peripheral facial paralysis. Nationwide analysis centering on CF. 284 57

Multicystic encephalomalacia (MCE) is a rare lesion that arises during the perinatal period. Although hypoxic-ischemic insults may be responsible for this lesion, recent evidence suggests that herpesviruses may represent another etiologic agent. To elucidate the pathogenesis of MCE, eight cases collected over a 34-year period were evaluated for destructive lesions in gray and white matter. Immunocytochemical methods, in situ hybridization and polymerase chain reaction (PCR) methodology were employed to search for herpes simplex viruses types 1 and 2 (HSV1 and HSV2), cytomegalovirus (CMV), varicella zoster virus (VZV), Epstein-Barr virus (EBV) and JC variant of papovavirus (JCV). Review of the clinical histories revealed that there had been a complicated labor and delivery in 6/7 cases. Neuropathological lesions consisted of extensive tissue destruction, neuronal loss and gliosis in hemispheric white matter, cerebral cortex, basal ganglia, thalamus, cerebellum and brainstem tegmentum. Only one case showed evidence of latent HSV infection by PCR. CMV, VZV, JCV and EBV were not detected. Arteriopathy was noted in one case. The widespread nature of the lesions and their association with perinatal ischemia suggest that severe hypoxia may be the more common etiology of MCE. Term infants appear especially susceptible to this type of cerebral damage.
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PMID:Multicystic encephalopathy: review of eight cases with etiologic considerations. 787 94

The case of a 67-year-old woman with terminal renal insufficiency, who developed extensive encephalopathy with predominant involvement of the white matter is reported. The encephalopathy was the consequence of preexisting hypertensive alterations, acidosis, hypoxia, ischemia, bacteremia and varicella-zoster meningoencephalitis. The vasculitic alterations associated with meningoencephalitis had a major influence on the development and the extent of the leukoencephalopathy.
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PMID:Vasculitic, hypoxic-ischemic leukoencephalopathy. 792 81

We have observed in our department a subacute left inferior limb ischemia by a forty one years old man in the following of a chicken pox while big arteries (arteria profunda femoris, lateral plantar artery, arteria dorsalis pedis) were attacked. We have not noticed in the medical literature such a case described. We have treated this ischemia by an in situ fibrinolysis which lead to a total clinical recovery, a complete patency of the lateral plantar artery and the arteria dorsalis pedis, and an incomplete patency of the arteria profunda femoris. We expose a few physiopathological hypothesis. But, in any case, we have not the proof of a connection between ischemia and the viral infection.
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PMID:[Chickenpox and limb ischemia. Report of a case]. 854 6

Eleven patients with rapidly progressive herpetic retinal necrosis (RPHRN) complicating AIDS were investigated retrospectively to study the disease spectrum, systemic involvement, and therapy. The mean CD4 cell count was 24/microL. There was a characteristic disease pattern with rapid progression, 82% bilaterality, relative resistance to intravenous antiviral therapy, and 70% retinal detachment. Varicella-zoster virus was the probable cause in 10 patients (detected by polymerase chain reaction in two eyes investigated), and herpes simplex virus was the probable cause in one. Cutaneous zoster occurred previously in 73% but was not concurrent. Seventy-three percent had central nervous system disease, possibly virus-related. RPHRN may be a local herpetic recrudescence in an immune-privileged site with transneural spread. Only four of 20 affected eyes retained useful vision. Poor ocular bioavailability, retinal ischemia, acquired drug resistance, and strain pathogenicity may underlie treatment failure. Acyclovir therapy appears relatively ineffective. Combined intravenous and intravitreal therapy with foscarnet and ganciclovir may be the best current management. Research advances are needed urgently.
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PMID:Rapidly progressive herpetic retinal necrosis: a blinding disease characteristic of advanced AIDS. 945 7

Pneumonia is the most common serious complication of varicella infection in adults. A variety of thrombotic complications including purpura fulminans and disseminated intravascular coagulation have been reported in children with varicella but not in adults. Two men with varicella pneumonia who had profound lower extremity ischemia caused by thrombosis of the profunda femoris and tibial arteries are reported. Both patients had free protein S deficiency and vascular thrombosis in association with varicella pneumonia without overt evidence of disseminated intravascular coagulation or purpura fulminans. Antiphospholipid immunoglobulin G and immunoglobulin M antibodies were present in one, whereas the other had evidence of the lupus anticoagulant. The proposed pathogenesis and management options including intraarterial thrombolytic therapy with urokinase and the need for long-term anticoagulation are discussed.
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PMID:Spontaneous tibial artery thrombosis associated with varicella pneumonia and free protein S deficiency. 954 47

Varicella-associated purpura fulminans (PF) is a rare complication to varicella infection. The condition is due to autoantibodies directed against protein S which forms part of the anticoagulation system. Lack of protein S leads to disseminated intravascular coagulation in the small vessels, which causes thrombosis and ischemia. Despite early treatment, amputation and skin-grafting is often necessary. In this case story, we give a brief review of the pathogenesis and possible modes of treatment. Knowledge of PF is necessary since early treatment may be life-saving.
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PMID:[Purpura fulminans]. 2061 77

Varicella (chickenpox), a common childhood infection caused by the varicella-zoster virus, is self-limiting and usually benign. Although atypical manifestations of the virus are occasionally seen, it rarely presents with cardiovascular sequelae. Cardiovascular complications of varicella can include pericarditis, myocarditis, or endocarditis. Herein, we report the case of a 17-year-old boy who had varicella infection and severe chest pain. Examination revealed atypical electrocardiographic findings of pericarditis and remarkably elevated cardiac biomarker levels: peak cardiac troponin I, 37.2 ng/mL; total creatine kinase, 1,209 U/L; and creatine kinase-MB fraction, 133.6 ng/mL. After results of coronary angiography reliably excluded ischemia and myocardial infarction, the diagnosis was varicella myopericarditis. The patient was placed on a medical regimen during and after 5 days of hospitalization. In 2 weeks, he was asymptomatic, and at 6 months, he was doing well and had normal electrocardiographic and echocardiographic results.To our knowledge, cardiac enzyme elevations to these levels have not been reported in cases of cardiovascular sequelae of varicella. We discuss the diagnostic challenges of this atypical case and suggest that clinicians be aware that varicella disease is most often, but not always, benign.
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PMID:Varicella myopericarditis mimicking myocardial infarction in a 17-year-old boy. 2172 Apr 75

A 72-year-old man with varicella zoster virus (VZV) encephalitis complicated by an ischemic stroke in the right internal capsule, possibly due to secondary small-vessel vasculopathy, is described in this case report. The focus of this article is on the electroencephalogram (EEG) description of varicella zoster encephalitis and secondary vasculopathy because EEG descriptions are scarce in the literature and detailed descriptions are lacking. In this patient's EEG, right temporal theta waves were found in combination with a mild slowing of the background rhythm to 7.5 to 8 Hz in the acute stage with an amplitude asymmetry (right temporal lobe amplitudes were significantly higher compared with the left side). The theta waves were thought to originate from the ischemic lacunar stroke, the slowing of the background rhythm from early encephalitis, and the amplitude asymmetry was presumed to be of physiologic origin. A follow-up EEG 6 days after initiation of treatment with acyclovir showed a normal symmetrical background rhythm of 8 to 8.5 Hz, wherein the theta waves were significantly reduced in abundance, and the amplitude asymmetry was unchanged. In conclusion, the EEG may localize focal abnormalities possibly due to cortical or lacunar ischemia, which could be explained by early small and/or large vessel vasculopathy in patients with suspected VZV encephalitis.
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PMID:Ischemic Stroke as a Complication of Varicella Zoster Encephalitis: A Case Report With Detailed EEG Discussion. 2429 59

Ocular involvement after primary infection with varicella zoster virus is very rare. We report a case of a healthy 18-year-old man who presented with unilateral ischemic retinal vasculitis 10 days after the onset of chickenpox. He developed acute severe visual loss and a relative afferent pupillary defect in his right eye. Fundus imaging, optical coherence tomography, fundus fluorescence angiography, and electrophysiologic studies confirmed the diagnosis of retinal vasculitis, which led to generalized retinal ischemia. Although aggressive treatment with systemic steroids and antiviral drugs was administered, a poor visual outcome still resulted.
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PMID:Ischemic retinal vasculitis in an 18-year-old man with chickenpox infection. 2459 14


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