Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polymerase chain reaction (PCR) was prospectively performed with cerebrospinal fluid (CSF) from 51 patients whose CSF was available for analysis and was submitted for viral culture and/or herpes simplex virus (HSV) serology and 20 patients whose CSF was submitted exclusively to the Clinical Biochemistry Laboratory. Primers were used that flanked a 92 bp segment of the HSV DNA polymerase gene (35 cycles). Amplified products were electrophoresed on agarose gel, blotted onto nylon membrane, and probed with a 32P-labelled sequence internal to the primers. For nested PCR, 1 microliter of PCR product was amplified for an additional 35 cycles before electrophoresis and Southern blot analysis. Review of the clinical records revealed that 15 patients had central nervous system (CNS) infections. Specific HSV DNA sequences were detected in CSF specimens of three of the individuals [PCR(2), nested PCR(1)]. Two of these patients had disseminated HSV infection including encephalitis and one patient had aseptic meningitis. The diagnoses of the 12 patients with CNS infection who did not have HSV DNA detected in CSF included encephalitis [varicella-zoster virus (1), cytomegalovirus (1), Mycoplasma pneumoniae (1)], meningitis [Neisseria meningitidis (1), Coccidioides immitis (1), Enterovirus (1), aseptic meningitis (1)], varicella-zoster radiculitis (2), human immunodeficiency virus dementia (2), and transverse myelitis due to Epstein-Barr virus (1). Importantly, HSV DNA was also not detected in the CSF of the 36 patients who did not have CNS infection and 20 samples submitted exclusively to the Clinical Biochemistry Laboratory. Our findings demonstrate the utility of PCR as a rapid, non-invasive method for the routine laboratory diagnosis of CNS infection due to HSV.
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PMID:A prospective study of the polymerase chain reaction for detection of herpes simplex virus in cerebrospinal fluid submitted to the clinical virology laboratory. 133 47

Cerebrospinal fluid (CSF) cytology, white blood cell (WBC) count and protein were evaluated in 32 human immunodeficiency virus (HIV)-infected patients with the acquired immune deficiency syndrome (AIDS) or an AIDS-related complex who manifested a variety of neurologic symptoms. Of 17 patients with AIDS-related encephalitis (ARE), 13 had hypocellular CSFs; elevated WBCs and pleocytosis were noted in 4, multinucleated giant cells in 2 and elevated CSF protein was found in 4 of 8 specimens tested. Three patients with central nervous system (CNS) toxoplasmosis had unremarkable CSF cytology findings, but all had elevated CSF proteins. In five patients with cryptococcal meningitis, cytologic examinations demonstrated organisms in four and elevated proteins in three. Of five patients with primary CNS lymphomas, one had cytology positive for large cell lymphoma; two showed suspicious cells and two manifested "atypical lymphocytes." Elevated CSF protein was present in four. Other conditions observed included progressive multifocal leukoencephalopathy, tubercular meningitis and cytomegaloviral (CMV) meningitis or encephalitis. Twenty-five percent of patients with ARE manifested pleocytosis with multinucleated giant cells; pleocytosis with CMV inclusions was noted in a CMV viral radiculitis. The CSF cytologic examination in HIV-infected patients with neurologic complications seems helpful in diagnosing cryptococcal meningitis and lymphoma, but less so for diagnosing toxoplasmosis.
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PMID:Cerebrospinal fluid manifestations of the neurologic complications of human immunodeficiency virus infection. 253 86

To determine if there is a relationship between neurological abnormalities and human immunodeficiency virus (HIV) infection in patients with lymphadenopathy syndrome (LAS), we studied 39 homosexual/bisexual men with LAS (mean duration of LAS, 4.1 years) and 38 homosexual/bisexual men who were seronegative for HIV (controls). Six LAS patients had histories of symptoms suggesting mononeuropathy, 9 had symptoms suggesting distal symmetrical polyneuropathy, and 9 had histories of herpes zoster radiculitis. Overall, significantly more LAS patients (18) than controls (3) had histories of symptoms or signs of neurological abnormality (odds ratio, 10.0; p = 0.0003). By neuropsychological assessment, 9 of 18 LAS patients and 2 of 26 controls were abnormal (odds ratio, 12.0; p = 0.004). Of those abnormal on the neuropsychological assessment, the majority scored in the mildly impaired range. Magnetic resonance imaging was abnormal in 1 LAS patient and in 1 control. Neither neurological nor neuropsychological abnormalities correlated with duration of LAS, absolute T-helper lymphocyte count, or T-helper/T-suppressor lymphocyte ratio. These results indicate an association of neurological and neuropsychological abnormalities with HIV in patients with LAS. They suggest that mild neurological abnormalities in LAS are common and that HIV may directly or indirectly be the cause.
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PMID:Neurological complications of human immunodeficiency virus infection in patients with lymphadenopathy syndrome. 334 67

Since the onset of the acquired immune deficiency syndrome (AIDS) epidemic fifteen years ago, much has been learned about the effects of the human immunodeficiency virus (HIV) in the nervous system. This review summarizes the pathology findings in the central nervous system (CNS). There is now abundant evidence that HIV can infect the CNS directly, leading to a characteristic HIV encephalitis (HIVE) which occurs in 10-50 p. 100 of AIDS autopsy series. Multinucleated giant cells are the pathognomonic feature of HIVE and are found predominantly in the central white matter and deep grey matter. Evidence of productive HIV infection in the CNS is confined to cells of the microglial/macrophage lineage, from which the giant cells are almost certainly derived. These cells are known to express both CD4 and beta-chemokine receptors, which act in conjunction to permit HIV entry. Restricted infection of astrocytes has also been identified by a variety of methods. HIVE is frequently associated with white matter damage ranging from inflammatory (microglia, macrophages and sparse lymphocytes) to degenerative (myelin loss and axonal damage) pathology. Although giant cells are seen less frequently in neocortical grey matter, significant neuronal loss has been established in a number of studies. Recent investigations using markers of apoptosis, (including TUNEL, Bcl-2 and BAX), have established the presence of DNA damage in some neurons and in other cell types. Axonal damage has also been confirmed by evidence of amyloid precursor protein expression. The CNS is also vulnerable to opportunistic infections and high grade B-cell lymphomas as a result of the immune suppression of advanced HIV infection. Cytomegalovirus (CMV) infection is reported in 10-30 p. 100 of AIDS cases at autopsy, toxoplasma in 10-25 p. 100, progressive multifocal leucoencephalopathy in about 5 p. 100 and lymphomas, usually primary, in up to 10 p. 100. A wide variety of other infections has also been reported. These may coexist with HIVE and may be difficult to diagnose in life. CMV gives rise to microglial nodular encephalitis, ventriculitis, necrotising encephalitis and myelo-radiculitis. Presymptomatic HIV positive patients do not show HIVE or opportunistic infections or lymphomas in the CNS. They frequently display a low-grade T-cell infiltrate in the leptomeninges and parenchyma, particularly around vessels. This lymphocytic infiltrate has been attributed to presumed early invasion of the CNS by HIV although the exact timing of entry is uncertain. It is possible that reported abnormalities in presymptomatic cases such as gliosis, microglial activation and rising proviral load may anticipate the onset of HIVE but most studies show that significant CNS damage and HIV-related pathology is confined to patients with AIDS. HIV-related pathology in the spinal cord includes not only HIV myelitis, opportunistic infections and lymphomas, but also vacuolar myelopathy (VM) which affects predominantly the dorsolateral white matter tracts. The cause of VM is not understood and has not been unequivocally linked with HIV infection. It is noted that none of these neuropathological features (including HIVE) correlates exactly with the clinical expression of AIDS-related dementia (ARD). The exact contribution of macrophage activation and cytokine release, astrocytic infection, neuronal loss and axonal damage to the neuropsychiatric syndromes of advanced HIV infection remain to be determined. While the current understanding of the pathogenesis of HIVE and ARD is beyond the scope of this review it is axiomatic that accurate documentation of neuropathology findings will help to resolve the outstanding dilemmas relating to HIV infection of the CNS. There is considerable optimism that progress in therapeutic regimes for HIV-infected patients will succeed in eliminating the virus from the blood and from lymphoid tissue. (ABSTRACT TRUNCATED)
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PMID:The neuropathology of adult HIV infection. 993 3

This multicentre retrospective study describes the clinical features and prognostic significance of Varicella-zoster virus (VZV)-associated neurological complications. The study was performed in patients with human immunodeficiency virus (HIV) infection, hospitalized for VZV neurological complications, confirmed in every case by positive VZV polymerase chain reaction (PCR) in cerebrospinal fluid (CSF). Between 1990 and 1995, 34 HIV-infected patients were included in the study. At diagnosis, 59% had AIDS, with a median CD4 count of 11 x 10(9)/l. A past history of zoster was noted in 35% of cases. A concomitant herpes zoster rash and/or acute retinal necrosis were noted in 71% and 12% of patients, respectively. The predominant neurological manifestations were encephalitis (13), myelitis (8), radiculitis (7) and meningitis (6). The mean CSF white blood cell count was 126/mm3 and the mean CSF protein concentration was 2.3 g/l. Interferon-alpha level was increased in 36% of patients. VZV was isolated from CSF cultures in 2/6 cases. Magnetic resonance imaging was abnormal, demonstrating encephalitis lesions. After intravenous antiviral therapy, complete recovery was obtained in 18 cases (53%), serious sequelae were observed in 10 cases (29%) and 6 patients died (18%). Severe symptoms and a low CD4 cell count appeared to be associated with death or sequelae. In conclusion, VZV should be considered as a possible cause of encephalitis, myelitis, radiculitis or meningitis in HIV-infected patients, especially in patients with a history of or concomitant herpes zoster or acute retinal necrosis. VZV-PCR in the CSF may allow rapid diagnosis and early specific antiviral treatment.
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PMID:Neurological complications of varicella-zoster virus infection in adults with human immunodeficiency virus infection. 1144 Feb 37

Our purpose was to describe the range of MRI findings in infectious and neoplastic involvement of the spine and spinal cord in symptomatic patients with the acquired immunodeficiency syndrome (AIDS). MRI studies in 55 patients with AIDS and neurological signs and symptoms thought to be related to the spine or spinal cord were reviewed. We categorized the findings according to the spinal compartment involved. There were 29 patients with extradural, 11 with intradural-extramedullary and 9 with intramedullary disease. In 6 patients more than one compartment was involved simultaneously, and patients presented with multiple lesions in the same compartment. The most common causes of extradural disease were bone lesions (28); an epidural mass was seen in 14 and spondylodiscitis in 4 patients. Cytomegalovirus polyradiculitis was the most common cause of intradural-extramedullary disease (in 10 cases); herpes radiculitis was seen in two, and tuberculous infection in another two. In three cases leptomeningeal contrast enhancement was due to lymphoma. Human immunodeficiency virus (HIV) myelitis was seen in two patients, presumed vacuolar myelopathy in two, toxoplasma myelitis in four, intramedullary lymphoma in one, and herpes myelitis in one. Familiarity with the various potential pathological entities that can affect the spine and spinal cord in the AIDS population and their imaging characteristics is crucial for initiation of further diagnostic tests and appropriate medical or surgical treatment.
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PMID:MRI of infections and neoplasms of the spine and spinal cord in 55 patients with AIDS. 1099 60

Beside immunodepression induced by the human immunodeficiency virus, fungal infections of the central nervous system are extremely rare in heroin-addict patients. We report here a case of meningo-encephalitis with myelo-radicular lesions in a 25-year-old intravenous heroin addict but non-HIV patient, who was admitted for an acute confusion associated with gait disorders. The diagnosis of Candida albicans meningo-encephalo-myelo-radiculitis was established by magnetic resonance imagery and mycological and serological examinations of cerebrospinal fluid. The infection was cured with amphotericin B lipid complex and 5-fluorocytosine. Early diagnosis and antifungal therapy for 6 months resulted in a favorable outcome. The detection of circulating Candida mannan in cerebrospinal fluid with a more sensitive technique combined to MRI were particularly decisive to confirm Candida infection diagnosis, allowing an appropriate antifungal therapy.
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PMID:[Candida albicans meningo-encephalo-myelo-radiculitis at an addict]. 1623 Feb 95