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)

We report a 49-year-old man who was an HTLV-I carrier with an immunodeficiency state and intracranial pyramidal tract lesion revealed by MRI. He was born in Hokkaido and was admitted to our hospital because of fluminant hepatitis. On admission, neurologic examination revealed exaggerated deep tendon reflexes including the jaw jerk; the plantar response was flexor. Laboratory examination revealed decrease in the number of lymphocytes and CD4-positive lymphocytes in the peripheral blood and CD4/CD8 ratio was consistently low, indicating the presence of cellular immunodeficiency state. Serum anti-HTLV-I antibody was markedly increased but he did not have HTLV-I associated myelopathy (HAM). He had no underlying disease which would cause immunodeficiency state such as adult T-cell leukemia (ATL) or HIV infection. We concluded that the HTLV-I carrier state induced his immunodeficiency. During the course, he developed retrobulbar neuritis. T2 weighted cranial MRI revealed high signal lesions in the bilateral corona radiata, posterior limb of the internal capsule, and the pontine base, corresponding to the location of the pyramidal tracts. His hospital course was complicated by opportunistic infections such as Pneumocystis carinii pneumonia, cytomegalovirus infections, and meningitis, and died of multiple organ failure 7 months after the admission. Cellular immunodeficiencies in ATL patients are well known. Intracranial central nervous system (CNS) lesions in HAM patients are also mentioned. Recently coincidence of ATL and HAM in the same patients has also been reported. Asymptomatic HTLV-I carriers may have a latent immunodeficiency state and/or CNS lesions. We shall have to be alert about the presence of such carriers.
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PMID:[A patient with marked immunodeficiency in an HTLV-I carrier: a case report]. 1083 33

Tuberculous radiculomyelitis (TBRM) is a complication of tuberculous meningitis (TBM), which has been reported rarely in the modern medical literature. We describe a case of TBRM that developed in an human immunodeficiency virus (HIV)-infected patient, despite prompt antituberculous treatment. To our knowledge, this is the second case of TBRM reported in an HIV-infected patient. We also review 74 previously reported cases of TBRM. TBRM develops at various periods after TBM, even in adequately treated patients after sterilization of the cerebrospinal fluid (CSF). The most common symptoms are subacute paraparesis, radicular pain, bladder disturbance, and subsequent paralysis. CSF evaluation usually shows an active inflammatory response with a very high protein level. MRI and CT scan are critical for diagnosis, revealing loculation and obliteration of the subarachnoid space along with linear intradural enhancement. As in other forms of paradoxical reactions to antituberculous treatment, there is evidence that steroid treatment might have a beneficial effect.
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PMID:Tuberculous radiculomyelitis complicating tuberculous meningitis: case report and review. 1085 62

Our purpose was to determine whether triple-dose delayed contrast-enhanced images would improve lesion detection in patients with symptomatic human immunodeficiency virus (HIV) infection. We reviewed 33 MRI studies on 29 patients. Single-dose immediate T1-weighted spin-echo (1x-T1) images were compared with delayed triple-dose images (D3x-T1). Two neuroradiologists decided which technique showed more lesions, increased lesion conspicuity and/or altered the radiologic diagnosis. The D3x-T1 technique improved lesion detection in 14 of 29 patients (48%). In two patients (7%), the improvement changed the radiologic diagnosis by showing new meningeal lesions.
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PMID:Triple-dose contrast-enhanced images in neurologically symptomatic HIV-positive patients. 1087 68

Cerebral ischaemia caused by inflammatory vasculopathies has been described as complication of human immunodeficiency virus (HIV) infection. Imaging studies have shown ischaemic lesions and changes of the vascular lumen, but did not allow demonstration of abnormalities within the vessel wall itself. Two HIV-infected men presented with symptoms of a transient ischaemic attack. Initial MRI of the first showed no infarct; in the second two small lacunar lesions were detected. In both cases, multiplanar 3-mm slice contrast-enhanced T1-weighted images showed aneurysmal dilatation, with thickening and contrast enhancement of the wall of the internal carotid and middle cerebral (MCA) arteries. These findings were interpreted as indicating cerebral vasculitis. In the first patient the vasculopathy progressed to carotid artery occlusion, and he developed an infarct in the MCA territory, but then remained neurologically stable. In the second patient varicella zoster virus (VZV) infection was the probable cause of vasculitis. The clinical deficits and vasculitic MRI changes regressed with antiviral and immunosuppressive therapy.
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PMID:MRI in human immunodeficiency virus-associated cerebral vasculitis. 1095 87

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

Despite more than 15 years of extensive investigative efforts, a complete understanding of the neurological consequences of HIV-1 CNS infection remains elusive. Although the resources of numerous investigators have been focused on studies of HIV-1-associated CNS disease, the complex nature of the disease processes that underlie the clinical, pathological, and cellular manifestations of HIV-1 CNS infection have required a larger volume of studies than was initially envisioned. Several major areas remain as the focus of current research efforts. One of the more pressing issues facing researchers and clinicians alike is the search for correlates to the development of HIV-1-associated CNS neuropathology and the onset of HIVD. Although numerous parameters have been studied, none have been shown to be absolute predictors or markers of HIV-1-related CNS dysfunction. The identification of solid correlates of HIVD is an important goal that would permit clinical identification of individuals at risk for developing potentially crippling, life-threatening CNS abnormalities and would facilitate early treatment of nascent neurological problems. A more complete comprehension of the cellular foundations of CNS dysfunction and HIVD is also a fundamental part of strategies designed to treat or prevent HIV-1-associated CNS disease. Future investigations will strive to expand the body of knowledge concerning the complex interactions between infected and uninfected neuroglial cells and the roles of numerous cytokines, chemokines, and other soluble agents that are deregulated during HIV-1 CNS infection. In particular, a thorough understanding of the mechanisms of neurotoxicity may facilitate the development of new therapies that alleviate or eliminate the clinical consequences of CNS infection. Finally, investigators will continue to study HIVD within the context of single and combination drug therapies used in the treatment of HIV-1 infection and AIDS. As newer and more effective systemic treatments for HIV-1 infection and AIDS are introduced, the effects of these treatments on the onset, incidence, and severity of HIVD will also require intensive study. The impact of drug therapies on the ability of the CNS to act as an HIV-1 reservoir will also need to be addressed. Introduction of each new drug or drug combination will necessitate studies of drug penetration into the CNS and efficacy against the development of CNS abnormalities. Furthermore, as more effective treatments prolong the lifespan of individuals infected with HIV-1, the impact of extended survival on the occurrence and severity of HIVD will also require further investigations. The quest for answers to these and other questions will be complicated by the diversity of experimental systems used to study different aspects of HIV-1 CNS infection and HIVD. Each system has its own unique strengths and weaknesses. Clinical observations provide a continuous spectrum of symptomatic findings but reveal little about the underlying mechanisms of disease. In vivo imaging techniques, such as CT and MRI, also provide a continuum of observations, but the images are limited in their resolution. Neuropathological examinations of postmortem HIV-1-infected brains offer gross, cellular, and molecular views (including phenotypic and genotypic analyses of CNS viral isolates) of the diseased brain, but only provide a snapshot of the end-stage neurologic dysfunction. Studies that rely on animal surrogates for HIV-1, including SIV, simian-HIV (SHIV), feline immunodeficiency virus (FIV), visna virus, and HIV-1 SCID-hu models, permit experimental protocols that cannot be carried out in humans, but are limited by the fidelity with which each virus and animal model emulates the conditions and events observed in the human host. Finally, in vitro techniques, which include the use of primary cells and cell lines, adult or fetal human cell cultures, and BBB barrier model systems, are also convenient means by which aspe
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PMID:HIV-1-associated central nervous system dysfunction. 1101 68

The CNS involvement is frequently found in human immunodeficiency virus (HIV) infection. The purpose of our study was to determine whether proton magnetic resonance spectroscopy (MRS) could detect early brain involvement in neurologically asymptomatic HIV-infected patients with normal MR imagings and to find the correlation between MRS and the immune status. We performed MRS in 30 HIV seropositive neurologically asymptomatic patients with normal MRI and compared the MRS findings with 13 controls. A statistically significant reduction in N-acetylaspartate (NAA)/creatine (Cr) and N-acetylaspartate (NAA)/choline (Cho) in both centrum semiovale (p < 0.005) and thalamic areas (p < 0.05) was found. There is no statistically significant difference as to choline (Cho)/creatine (Cr) and myoinositol (mI)/creatine (Cr) ratios in both regions. The difference of NAA/Cr was more pronounced in the white matter than in the gray matter. As for the immune status, there was a trend towards correlation between CD4 counts and NAA/Cr but devoid of statistical significance. Our results suggest that MRS is more sensitive than conventional MR imaging in detecting CNS involvement in neurologically asymptomatic HIV patients and may, therefore, be used for early detection of brain damage induced by HIV.
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PMID:Magnetic resonance spectroscopy of the brain in neurologically asymptomatic HIV-infected patients. 1102 80

Neuronal injury, dendritic loss and brain atrophy are frequent complications of infection with human immunodeficiency virus (HIV) type 1. Activated brain macrophages and microglia can release quinolinic acid, a neurotoxin and NMDA (N-methyl-D-aspartate) receptor agonist, which we hypothesize contributes to neuronal injury and cerebral volume loss. In the present cross-sectional study of 94 HIV-1-infected patients, elevated CSF quinolinic acid concentrations correlated with worsening brain atrophy, quantified by MRI, in regions vulnerable to excitotoxic injury (the striatum and limbic cortex) but not in regions relatively resistant to excitotoxicity (the non-limbic cortex, thalamus and white matter). Increased CSF quinolinic acid concentrations also correlated with higher CSF HIV-1 RNA levels. In support of the specificity of these associations, blood levels of quinolinic acid were unrelated to striatal and limbic volumes, and CSF levels of beta(2)-microglobulin, a non-specific and non-excitotoxic marker of immune activation, were unrelated to regional brain volume loss. These results are consistent with the hypothesis that quinolinic acid accumulation in brain tissue contributes to atrophy in vulnerable brain regions in HIV infection and that virus replication is a significant driver of local quinolinic acid biosynthesis.
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PMID:Elevated cerebrospinal fluid quinolinic acid levels are associated with region-specific cerebral volume loss in HIV infection. 1133 5

Toxoplasmosis represents a clinical problem which focuses attention of several specialists due to the multiorgan pathology it induces and difficulties in evaluating the activity of the morbid process. The infection creates a particularly difficult problem in cases when central nervous system is involved, which frequently leads to unfavorable sequelae. Contemporary data have been presented which pertain to the morphology and life cycle of Toxoplasma gondii, sources of the infection and ways through which the protozoon penetrates the host organism. The pathomechanism of disturbances in the course of toxoplasmosis with involvement of central nervous system is described, as related to the stage of invasion and immune responses of cell-mediated or humoral type. The clinical pathology of congenital and acquired toxoplasmosis is presented, including that developing in patients with immune deficiencies. Diagnostic criteria are given, indispensable in evaluating the activity of toxoplasmosis process, based on contemporary laboratory techniques (antigen detection, detection of antibodies to T. gondii antigen, molecular tests, like PCR, and radiological techniques, like CT and MRI studies. The studies are important not only in evaluation of the primary infection and also for appraisal of reactivation of T. gondii invasion in conditions of acquired immunodeficiency (AIDS), in the course of systemic diseases, during immunosuppressive treatment and in patients who without treatment for toxoplasmosis in the first year of life.
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PMID:[Neurotoxoplasmosis]. 1187 16

Significant eosinophilia and even eosinophilic tissue infiltration has been associated with a variety of clinical disorders including allergic and immunodeficiency states, drug reaction, infection, parasitic infestation and malignancy. Eosinophilia without an underlying aetiology and with multi-organ dysfunction has been designated idiopathic hypereosinophilic syndrome. We report a case of endomyocardial fibrosis with MRI findings.
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PMID:Idiopathic hypereosinophilic syndrome: magnetic resonance imaging findings in endomyocardial fibrosis. 1190 92


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