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)

This review focuses on the prevalence, causes, evaluation, and treatment of headache in individuals infected with human immunodeficiency virus type 1 (HIV-1). Headaches, one of the commonest medical complaints in the general population, occur frequently in patients infected with the HIV-1. HIV-related headaches can occur at any time during the infection: at seroconversion, during the incubation period, in patients with symptomatic HIV-1 infection, or after an AIDS-defining illness. Causes of HIV-related headaches include HIV-1 itself, opportunistic conditions, or HIV-specific medications. Migraines, tension-type headaches, depression, and substance abuse enter into the differential diagnosis, particularly in the early stages of disease. The headaches seen in this population reflect a complex web of interactions imposed by immune competency, multiple etiologies, treatments, and premorbid conditions. Prompt recognition and early treatment of headache is essential since it may improve quality of life and, depending on the diagnosis, prolong survival. Physicians need to be alert and adaptable when assessing HIV-infected individuals with headache since multiple causes can exist in the same patient and new syndromes, complications, and investigational drugs are continually being identified.
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PMID:Headache and the human immunodeficiency virus type 1 infection. 777 85

Headache is one of the most important factors influencing the quality of life in patients infected with the human immunodeficiency virus type 1 (HIV). However, only symptomatic headache but not changes or primary headache types during HIV infection have been studied to date. Therefore, we aimed to determine the impact of an HIV infection on frequency and semiology of different primary headache types. Patients with confirmed HIV type 1 infection underwent a neurological examination, neuroimaging or EEG, and a standardized interview. Time pattern and symptoms of headaches (cross-sectional analysis), changes of headaches preexisting to their infection (longitudinal retrospective analysis), and changes of primary headaches during a 2-year follow-up (longitudinal prospective analysis) were evaluated as were the correlations between these headache patterns and different markers of HIV infection. One hundred thirty-one consecutive HIV-infected patients without evidence of a cerebral manifestation except mild encephalopathy were enrolled. The point prevalence of migraine was 16.0% (confidence interval (CI) 10.1-25.4%), of headache with a semiology of tension-type headache 45.8% (CI 33.7-62.2%), and of other headache types 6.1% (CI 3.0-12.5%). During the natural course of infection, the migraine frequency significantly decreased in the retrospective and in the prospective analyses, whereas the frequency of the headache with a semiology of tension-type headache significantly increased in all three analyses. In 20% of all patients, the tension-type headache could be considered as symptomatic due to the infection but not due to focal or general cerebral lesions. Changes of primary headache were significantly associated with different stages of the infection and with the presence of mild encephalopathy but not with antiretroviral treatment or CD4 cell count. HIV infection seems to be associated with a progressive decrease in migraine frequency and intensity which probably is related to the immunological state of the patients. Tension-type headache becomes more frequent during HIV infection. However, this can in part be related to secondary headache caused by the HIV in less than 50% of patients with tension-type headache. The progressing immunological deficiency of HIV-infected patients seems to influence pain processing of primary headache types in different ways.
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PMID:The impact of HIV infection on primary headache. Unexpected findings from retrospective, cross-sectional, and prospective analyses. 1069 18

This article addresses syndromes that clinically and/or radiologically resemble acute stroke. These syndromes generally fall into four categories. (1) Patients with acute neurological deficits with nonischemic lesions and no acute abnormality on diffusion-weighted images. These patients may have peripheral vertigo, migraines, seizures, dementia, functional disorders, amyloid angiopathy, or metabolic disorders. When these patients present, we can confidently predict that they are not undergoing infarction. (2) Patients with ischemic lesions with reversible clinical deficits. Nearly 50% of patients with transient ischemic attacks have lesions with restricted diffusion. Patients with transient global amnesia may have punctate lesions with restricted diffusion in the medial hippocampus, parahippocampal gyms, and corpus callosum. (3) Vasogenic edema syndromes that may mimic acute infarction clinically and on conventional imaging. These include eclampsia/hypertensive encephalopathy, other posterior leukoencephalopathies, human immunodeficiency virus encephalopathy, hyperperfusion syndrome following carotid endarterectomy, venous sinus thrombosis, acute demyelination, and neoplasm. These syndromes demonstrate elevated diffusion rather than the restricted diffusion associated with acute ischemic stroke. (4) Entities in which restricted diffusion may resemble acute infarction. These include pyogenic infections, herpes virus encephalitis, Creutzfeldt-Jakob disease, diffuse axonal injury, tumors with dense cell packing, and rare acute demyelinative lesions.
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PMID:Diffusion-weighted imaging as a problem-solving tool in the evaluation of patients with acute strokelike syndromes. 1114 28

Ergotism is a rare condition of acute vasospasm found classically in young and middle-aged women taking ergot alkaloid agents to treat migraine headache. We report the case of a young man with human immunodeficiency virus (HIV) positivity and describe the drug interaction between protease inhibitors and ergot alkaloid agents, which most likely predisposed to development of ergot toxicity. The HIV-positive population receiving antiviral therapy may be an under-recognized group at risk for ergotism through decreased hepatic metabolism of ergot preparations.
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PMID:Ergotism associated with HIV antiviral protease inhibitor therapy. 1261 10

Headache in patients with human immunodeficiency virus (HIV) infection may indicate life-threatening illnesses such as opportunistic infections or neoplasms. Alternatively, such patients may develop benign self-limiting headaches. Hence, defining the various types of headache in these patients is essential for proper management. This study describes the clinical characteristics of primary headaches occurring in a group of HIV-infected patients. Of 115 patients seen from 1990 to 1996, 44 (38%) had headaches. Primary headaches were present in 29 (66%) patients and secondary causes were identified in 15 (34%). Among those with primary headaches, migraine occurred in 22 (76%), tension-type headache in 4 (14%), and cluster headache in 3 (10%) patients. Half of those with migraine (n=ll), 1 patient with tension-type headache, and 1 patient with cluster headache developed chronic daily headaches which were severe and refractory to conventional headache or antiretroviral therapy. We conclude that primary headaches in patients with HIV infection are: (1) the commonest type of headache; (2) may present for the first time in individuals with severe immunosuppression; (3) usually bear no relationship to antiretroviral drug therapy; (4) polypharmacy, depression, anxiety, and insomnia are commonly associated comorbidities; (5) frequently do not respond to conventional management and carry a poor prognosis; and (6) do not require neuroradiological and/or cerebrospinal fluid evaluations.
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PMID:Primary headaches in HIV-infected patients. 1561 88

Adolescent perception of physical and social impact of chronic illness was assessed to determine (1) if there is greater prejudice toward epilepsy than other chronic disease and (2) if adolescents with chronic disease have less prejudice toward similarly affected peers with all types of chronic disease or just their specific chronic disease. Cognitively normal teens aged 13 to 18 years without chronic disease (n = 41) and with epilepsy (n = 32), asthma (n = 38), diabetes (n = 21), and migraine (n = 17) were interviewed in the outpatient clinics of a tertiary care pediatric center regarding their perceptions of the physical and social impact of eight chronic diseases (epilepsy, asthma, diabetes, Down syndrome, arthritis, migraine, leukemia, human immunodeficiency virus [HIV] infection). Epilepsy was perceived to have a more adverse physical impact than all chronic illnesses except Down syndrome. The perception was that it more frequently caused mental handicap, injured the afflicted individual and bystanders, and led to death. Epilepsy was also perceived to have a more negative social impact, particularly on behavior, honesty, popularity, adeptness at sports, and fun. Significantly more adolescents expressed reluctance to befriend peers with epilepsy, both from their own and their perceived parental perspectives. Having a chronic disease did not generally alter the adolescents' perceptions of peers with chronic disease. However, cases with epilepsy ranked this disease to have less social impact than teens with other chronic diseases. In conclusion, adolescents consider epilepsy to have a greater physical and social impact than most chronic diseases. Educational efforts should focus on the "normality" of most persons with epilepsy and emphasize the low risk of injury when proper first aid is followed.
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PMID:Adolescents' perception of epilepsy compared with other chronic diseases: "through a teenager's eyes". 1690 23

Headache and/or migraine, a common problem in pediatrics and internal medicine, affect about 5% to 10% children and adolescents, and nearly 30% of middle-aged women. Headache is also one of the most common clinical manifestations of acquired Toxoplasma gondii infection of the central nervous system (CNS) in immunosuppressed subjects. We present 11 apparently nonhuman immunodeficiency virus-infected children aged 7 to 17 years (8 girls, 3 boys) and 1 adult woman with recurrent severe headaches in whom latent chronic CNS T. gondii infection not manifested by enlarged peripheral lymph nodes typical for toxoplasmosis, was found. In 7 patients, the mean serum IgG Toxoplasma antibodies concentration was 189 +/- 85 (SD) IU/mL (range 89 to 300 IU/mL), and in 5 other subjects, the indirect fluorescent antibody test titer ranged from 1:40 to 1:5120 IU/mL (n= <1:10 IU/mL). Some of the patients suffered also from atopic dermatitis (AD) and were exposed to cat and/or other pet allergens, associated with an increased IL-4 and decreased IFN-gamma production. These cytokine irregularities caused limited control of cerebral toxoplasmosis probably because IL-4 down-regulated both the production of IFN-gamma and its activity, and stimulated production of a low NO-producing population of monocytes, which allowed cysts rupture, increased parasite multiplication and finally reactivation of T. gondii infection. The immune studies performed in 4 subjects showed a decreased percentage of T lymphocytes, increased total number of lymphocytes B and serum IgM concentration, and impaired phagocytosis. In addition, few of them had also urinary tract diseases known to produce IL-6 that can mediate immunosuppressive functions, involving induction of the anti-inflammatory cytokine IL-10. These disturbances probably resulted from the host protective immune reactions associated with the chronic latent CNS T. gondii infection/inflammation. This is consistent with significantly lower enzyme indoleamine 2,3-dioxygenase (IDO) activity reported in atopic than in nonatopic individuals, and an important role that IDO and tryptophan degradation pathways plays in both, the host resistance to T. gondii infection and its reactivation. Analysis of literature information on the subjects with different types of headaches caused by foods, medications, and other substances, may suggest that their clinical symptoms and changes in laboratory data result at least in part from interference of these factors with dietary tryptophan biotransformation pathways. Several of these agents caused headache attacks through enhancing NO production via the conversion of arginine to citrulline and NO by the inducible nitric oxide synthase enzyme, which results in the high-output pathway of NO synthesis. This increased production of NO is, however, quickly down-regulated by NO itself because this biomolecule can directly inactivate NOS, may inhibit Ia expression on IFN-gamma-activated macrophages, which would limit antigen-presenting capability, and block T-cell proliferation, thus decreasing the antitoxoplasmatic activity. Moreover, NO inhibits IDO activity, thereby suppressing kynurenine formation, and at least one member of the kynurenine pathway, 3-hydroxyanthranilic acid, has been shown to inhibit NOS enzyme activity, the expression of NOS mRNA, and activation of the inflammatory transcription factor, nuclear factor-kB. In addition, the anti-inflammatory cytokines IL-4 and IL-10, TGF-beta, and a cytokine known as macrophage deactivating factor, have been shown to directly modulate NO production, sometimes expressing synergistic activity. On the other hand, IL-4 and TGF-beta can suppress IDO activity in some cells, for example human monocytes and fibroblasts, which is consistent with metabolic pathways controlled by IDO being a significant contributor to the proinflammatory system. Also, it seems that idiopathic intracranial hypertension, pseudotumor cerebri, and aseptic meningitis, induced by various factors, may result from their interference with IDO and inducible nitric oxide synthase activities, endogenous NO level, and cytokine irregularities which finally affect former T. gondii status 2mo in the brain. All these biochemical disturbances caused by the CNS T. gondii infection/inflammation may also be responsible for the relationship found between neurologic symptoms, such as headache, vertigo, and syncope observed in apparently immunocompetent children and adolescents, and physical and psychiatric symptoms in adulthood. We therefore believe that tests for T. gondii should be performed obligatorily in apparently immunocompetent patients with different types of headaches, even if they have no enlarged peripheral lymph nodes. This may help to avoid overlooking this treatable cause of the CNS disease, markedly reduce costs of hospitalization, diagnosis and treatment, and eventually prevent developing serious neurologic and psychiatric disorders.
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PMID:Recurrent headache as the main symptom of acquired cerebral toxoplasmosis in nonhuman immunodeficiency virus-infected subjects with no lymphadenopathy: the parasite may be responsible for the neurogenic inflammation postulated as a cause of different types of headaches. 1730 77

Thrombocytopenia is a relatively frequent complication in patients infected by human immunodeficiency virus (HIV). Most frequent mechanisms of thrombopenia are destruction of half-filled platelets by immunocomplex and defects in production. We present two cases of severe thrombocytopenia associated to HIV infection. Case 1: A male patient, 45 years old with fever and diarrhea that lasted for 1 month that presented with thrombopenia of 3,000 platelets/mm3. After beginning zidovudine and lamivudine therapy, he normalized the platelet count in 5 days. Case 2: A male patient of 30 years old, who suffered during one day migraine, nausea, vomits and then seizures. A criptococccal meningitis was confirmed. Concomitantly he had a platelet count of 59,000/mm3. He started antiretroviral therapy with zidovudina and lamivudina, then was changed to didanosine plus stavudine plus nevirapine. After 6 months of severe thrombocytopenia, platelets count was restored to normal values. A literature review is presented.
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PMID:[Severe thrombocytopenia and human immunodeficiency virus infection. Report of two cases and review]. 1736 74

The aim of this article is to describe the roles of water channel proteins (WCPs) in brain functionality. The fluid compartments of the brain, which include the brain parenchyma (with intracellular and extracellular spaces), the intravascular and the cerebrospinal fluid compartments are presented. Then the localization and functional roles of WCPs found in the brain are described: AQP1, AQP2, AQP3, AQP4, AQP5, AQP7, AQP8, AQP9 and AQP11. In subsequent chapters the involvement of brain WCPs in pathologies are discussed: brain edema, brain trauma, brain tumors, stroke, dementia (Alzheimer's disease, human immunodeficiency virus--HIV-dementia), autism, pain signal transduction and migraine, hydrocephalus and other pathologies with neurological implications: eclampsia, uremia. New WCP ligands for brain imaging are also discussed.
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PMID:Brain water channel proteins in health and disease. 2250 60

Astrocyte-elevated gene-1 (AEG-1/MTDH/LYRIC) is a potent oncogene that regulates key cellular processes underlying disease of the central nervous system (CNS). From its involvement in human immunodeficiency virus (HIV)-1 infection to its role in neurodegenerative disease and malignant brain tumors, AEG-1/MTDH/LYRIC facilitates cellular survival and proliferation through the control of a multitude of molecular signaling cascades. AEG-1/MTDH/LYRIC induction by HIV-1 and TNF highlights its importance in viral infection, and its incorporation into viral vesicles supports its potential role in active viral replication. Overexpression of AEG-1/MTDH/LYRIC in the brains of Huntington's disease patients suggests its function in neurodegenerative disease, and its association with genetic polymorphisms in large genome-wide association studies of migraine patients suggests a possible role in the pathogenesis of migraine headaches. In the field of cancer, AEG-1/MTDH/LYRIC promotes angiogenesis, migration, invasion, and enhanced tumor metabolism through key oncogenic signaling cascades. In response to external stress cues and cellular mechanisms to inhibit further growth, AEG-1/MTDH/LYRIC activates pathways that bypass cell checkpoints and potentiates signals to enhance survival and tumorigenesis. As an oncogene that promotes aberrant cellular processes within the CNS, AEG-1/MTDH/LYRIC represents an important therapeutic target for the treatment of neurological disease.
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PMID:The role of AEG-1/MTDH/LYRIC in the pathogenesis of central nervous system disease. 2388 91


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