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)

A 28-year-old hemophilia A patient was admitted to our hospital in July, 1991 because of high fever, chronic diarrhea and anemia. The patient had been recognized as a asymptomatic carrier of human immunodeficiency virus (HIV) in 1985 and had developed Pneumocystis carinii pneumonia and had been diagnosed as acquired immunodeficiency syndrome (AIDS) in 1990. Hematologic laboratory examinations on admission revealed pancytopenia and a CD4+ cell count of 3/mm3. X-ray findings of chest and abdomen were normal and bacterial cultures of sputum, urine, blood, stool, cerebrospinal fluid and bone marrow yielded no pathogenic microorganisms. Microscopical examination of the stained specimens showed no acid-fast bacilli. On his fifth hospital day, his liver and spleen enlarged markedly and an abdominal CT scan obtained on the 13th day revealed high-grade hepatosplenomegaly. Administration of several kinds of antibiotics, antifungal agents, antiviral agents, antituberculous agents and gamma-globulin medicines did not relieve the symptoms. On the 28th day the patient had developed a subarachnoid hemorrhage and died five days later. Retrospectively all cultures for acid-fast bacilli of the specimens on his admission yielded nontuberculous mycobacteria. The bacteria were identified as Mycobacterium avium by polymerase chain reaction and his disease was eventually diagnosed as disseminated Mycobacterium avium complex (MAC) infection. The liver and spleen weighed 2,660 g and 1,840 g respectively at autopsy. Although hepatosplenomegaly is commonly recognized in AIDS patients with disseminated MAC infection, such massive and rapid enlargement has been rarely observed. This case study emphasize the importance of diagnosis and rapid treatment at the early stage of MAC infection.
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PMID:[Massive and progressive hepatosplenomegaly caused by disseminated nontuberculous mycobacteriosis in a patient with acquired immunodeficiency syndrome]. 756 51

Replication of human immunodeficiency virus type 1 (HIV-1) is regulated by a host transcription factor, nuclear factor kappaB (NF-kappaB). NF-kappaB belongs to a group of inducible transcription factors and its activity is regulated by multiple cellular signal transduction pathways, including kinases. These kinases are known to be involved in signal-induced NF-kappaB activation and in the induction of HIV-1 gene expression from latently infected cells. In this study we have examined the effect of a newly developed serine/threonine kinase inhibitor, fasudil hydrochloride (FH), on the replication of HIV-1. Although FH was initially developed as a compound that inhibited a myosin light chain kinase (MLCK) and had been approved for clinical use in the treatment of vasospasm after subarachnoid hemorrhage, this study shows its efficacy in blocking HIV-1 replication in latently infected patients. When FH was added to monocytic cell lines latently infected with HIV-1, U1 and OM10.1, the induction of HIV-1 replication by TNF-alpha was blocked at noncytotoxic doses. The IC50 values of HIV-1 induction by FH were 9.3 and 24 microM for U1 and OM10.1, respectively. Because FH could block TNF-alpha-induced, NF-kappaB-dependent gene expression, as examined by the transient luciferase expression assay, the effect of FH was considered to be due to the blocking of the signal transduction pathway of NF-kappaB activation. Although the in vivo effect of FH in blocking HIV-1 induction is not yet known, these findings indicate the feasibility of clinical use of FH and its derivatives in decreasing viral load to prevent clinical development of acquired immunodeficiency syndrome (AIDS) among HIV-1-infected individuals.
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PMID:Inhibition of human immunodeficiency virus type 1 replication by a bioavailable serine/threonine kinase inhibitor, fasudil hydrochloride. 951 89

Two cases of fusiform cerebral aneurysms in human immunodeficiency virus (HIV) positive children are presented. To our knowledge, only 9 patients with this association have been reported. One of our patients represents the first report of a patient with an aneurysm associated with varicella-zoster vasculitis. One patient presented with a subarachnoid hemorrhage, Hunt-Hess grade IV, and posed difficult surgical management. The other patient suffered a cerebral infarct with a resulting hemiparesis. The first patient had a ventriculostomy placed, initially improved, and subsequently died from rebleeding. The second patient improved with medical management. AIDS arteriopathy, and specifically fusiform aneurysms, are being increasingly reported. The various presentations of this surgically challenging entity in light of other AIDS-related syndromes pose difficult management decisions. On occasion, the intracranial aneurysm may be the initial form of presentation as was present in our first patient.
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PMID:Two cases of cerebral aneurysms in HIV+ children. 969 27

We describe a child with human immunodeficiency virus infection who presented with a large subarachnoid hemorrhage. She had multiple saccular and fusiform aneurysms in the proximal cerebral arterial circulation and no evidence of bacterial or fungal infection. The arteriopathy coincided with a high human immunodeficiency virus RNA load. Human immunodeficiency virus may cause cerebral arteriopathy with potentially life-threatening complications.
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PMID:Intracerebral aneurysms in human immunodeficiency virus infection: case report and literature review. 1103 89

The long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram. It is associated with precipitation of a polymorphic ventricular tachycardia, torsade de pointes, which may cause sudden death. The syndrome is a disorder of cardiac repolarization caused by the alterations in the transmembrane potassium and sodium currents. Six genetic loci for the congenital forms of the syndrome have been identified; sporadic cases occur because of spontaneous mutations. Acquired causes of the long QT syndrome include drugs, electrolyte imbalance, toxins, marked bradycardia, subarachnoid hemorrhage, stroke, myocardial ischemia, protein-sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease. Clinical symptoms are the result of the precipitation of torsade de pointes and range from such minor symptoms as dizziness to syncope and sudden death. Short-term treatment is aimed at preventing the recurrences of torsade de pointes and includes intravenous magnesium and potassium administration, temporary cardiac pacing, and correction of electrolyte imbalance; rarely, intravenous isoproterenol is indicated. Long-term management includes use of beta-blockers, permanent pacemaker placement, and cardioverter-defibrillator implantation. Asymptomatic patients are treated if under the age of 40 years at the time of diagnosis.
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PMID:Clinical and therapeutic aspects of congenital and acquired long QT syndrome. 1181 8

Patients infected with the human immunodeficiency virus (HIV) or suffering from acquired immunodeficiency syndrome (AIDS) are now surviving for longer periods of time secondary to improvements in medical management. As the classical causes of morbidity and mortality in this patient population have come under better control, new complications are becoming more prevalent. In our clinical practice, there appears to have been a rise in the number of patients with HIV infection and AIDS who have experienced aneurysmal subarachnoid hemorrhage (SAH). In this paper, we review the available literature regarding cerebral aneurysms in patients infected with HIV and/or suffering from AIDS.
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PMID:HIV and cerebral aneurysms. 1561 30

A 54-year-old human immunodeficiency virus type 1 (HIV-1)-infected homosexual Japanese male was found to have collapsed in his bathroom and was brought to our facility with diminished level of consciousness. Computed tomography showed subarachnoid hemorrhage (SAH). He was severely dehydrated with unstable general status that deterred us from performing emergent surgery. Cerebral angiography performed on the 18th hospital day revealed bilateral distal anterior cerebral artery aneurysms. Clipping of these aneurysms was performed on the 30th hospital day and no postoperative complications were experienced. The scalp wound showed no delayed healing, whereas the tracheostomy wound showed repeated wound dehiscence and delayed healing. Postoperative highly active antiretroviral therapy with antibiotic treatment gradually improved his general and immunological conditions. The patient was finally discharged as independent with mild muscle weakness in the bilateral lower extremities. HIV-1 infection should not be the guiding factor in the decision to aggressively treat concomitant aneurysmal disease. Clipping of cerebral aneurysms with full craniotomy or endovascular obliteration should be considered even in HIV-1-infected patients with SAH.
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PMID:Aneurysmal subarachnoid hemorrhage in a patient with human immunodeficiency virus type 1 infection. Case report. 1686 29

Human immunodeficiency virus (HIV)-associated cerebral aneurysmal arteriopathy is described in the pediatric medical literature and features diffuse fusiform aneurysms of the arteries of the circle of Willis. We present the first report (to our knowledge) of this disease entity in an adult, a 29-year-old woman with acquired immunodeficiency syndrome who presented with subarachnoid hemorrhage.
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PMID:Cerebral aneurysmal arteriopathy associated with HIV infection in an adult. 1688 42