Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A former civilian employee of the U.S. Army brought suit against the Army and his former supervisor, alleging that he was forced to resign his position after testing positive for the human immunodeficiency virus (HIV). The plaintiff asserted that the Army had breached his employment contract. Additionally, his supervisor had violated his right to privacy and his Fourth Amendment right to be secure in his person from unreasonable searches and seizures, and had intentionally inflicted emotional distress. In granting the defendants' motion to dismiss the suit, the District Court held that: (1) the employee served by appointment and therefore the Army could not be held liable for breach of contract; and (2) his former supervisor was not liable for breach of the plaintiff's privacy or Fourth Amendment rights.
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PMID:Plowman v. U.S. Department of the Army. 1164 81

A 33-year-old Hispanic woman with newly diagnosed human immunodeficiency virus (HIV) infection, a CD4 T-lymphocyte count of 2, viral load of 730,000 copies/mL, candidal esophagitis, seizure disorder, a history of bacterial pneumonia, and recent weight loss was admitted with tonic clonic seizure. On admission, her vital signs were: pulse of 88, respiration rate of 18, temperature of 37.7 degrees C, and blood pressure of 126/76. Her only medication was phenytoin. On examination, the patient was found to have multiple umbilicated papules on her face, as well as painful, erythematous, large, punched-out ulcers on the nose, face, trunk, and extremities of 3 months' duration (Fig. 1). The borders of the ulcers were irregular, raised, boggy, and undermined, while the base contained hemorrhagic exudate partially covered with necrotic eschar. The largest ulcer on the left mandible was 4 cm in diameter. The oral cavity was clear. Because of her subtherapeutic phenytoin level, the medication dose was adjusted, and she was empirically treated with Unasyn for presumptive bacterial infection. Chest radiograph and head computed tomography (CT) scan were within normal limits. Sputum for acid-fast bacilli (AFB) smear was negative. Serologic studies, including Histoplasma antibodies, toxoplasmosis immunoglobulin M (IgM), rapid plasma reagin (RPR), hepatitis C virus (HCV), and hepatitis B virus (HBV) antibodies were all negative. Examination of the cerebrospinal fluid was within normal limits without the presence of cryptococcal antigen. Blood and cerebrospinal cultures for bacteria, mycobacteria, and fungi were all negative. Viral culture from one of the lesions was also negative. The analysis of her complete blood count showed: white blood count, 2300/microl; hemoglobin, 8.5 g/dL; hematocrit, 25.7%; and platelets, 114,000/microl. Two days after admission, the dermatology service was asked to evaluate the patient. Although the umbilicated papules on the patient's face resembled lesions of molluscum contagiosum, other infectious processes considered in the differential diagnosis included histoplasmosis, cryptococcosis, and Penicillium marnefei. In addition, the morphology of the ulcers, particularly that on the left mandible, resembled lesions of pyoderma gangrenosum. A skin biopsy was performed on an ulcer on the chest. Histopathologic examination revealed granulomatous dermatitis with multiple budding yeast forms, predominantly within histiocytes, with few organisms residing extracellularly. Methenamine silver stain confirmed the presence of 2-4 microm fungal spores suggestive of Histoplasma capsulatum (Fig. 2). Because of the patient's deteriorating condition, intravenous amphotericin B was initiated after tissue culture was obtained. Within the first week of treatment, the skin lesions started to resolve. Histoplasma capsulatum was later isolated by culture, confirming the diagnosis. The patient was continued on amphotericin B for a total of 10 weeks, and was started on lamivudine, stavudine, and nelfinavir for her HIV infection during hospitalization. After amphotericin B therapy, the patient was placed on life-long suppressive therapy with itraconazole. Follow-up at 9 months after the initial presentation revealed no evidence of relapse of histoplasmosis.
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PMID:Disseminated histoplasmosis presenting as pyoderma gangrenosum-like lesions in a patient with acquired immunodeficiency syndrome. 1170 24

We present four cases of cerebral amebae infection treated at our neurosurgical department. Patient 1 was a 12-year-old male with skin lesions of 2 years' progression involving the midface. He received a corticosteroid course, and, after that, he presented a right body hemiparesis. Patient 2 was a 5-year-old male, with a past surgical history of fibula fracture and osteomyelitis of 1-year evolution, associated with lesions of the surrounding skin that presented with partial seizures. Patient 3 was a 3-year-old female who presented with a stroke-like episode and with partial seizures. Patient 4 was a 6-year-old male who had ulcerative lesions in the face of 1-year evolution. After a corticosteroid course, he presented with right-body hemiparesis. All patients were human immunodeficiency virus-negative and died 1 month or less after surgery because of progressive evolution of the disease. Histopathology revealed granulomatous amebic encephalitis. All patients revealed infection from Balamuthia mandrillaris (Leptomyxiidae). Treatment consisting of pentamidine, clarithromycin, fluconazole, and 5-fluorocytosine was ineffective. Although extremely uncommon, granulomatous amebic encephalitis should be considered in the differential diagnosis of cerebral lesions while nonspecific, associated granulomatous skin lesions support the diagnosis of amebiasis.
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PMID:Pediatric granulomatous cerebral amebiasis: a delayed diagnosis. 1189 83

HIV infection or complications of HIV-induced immunodeficiency may affect the central nervous system (CNS). However, vascular cerebral pathologies are very rare, in particular intracerebral arteriovenous malformations (AVM). We report the case of an HIV-infected patient who had a cerebral AVM leading to symptoms such as recurring focal seizures. Only after initiation of potent antiretroviral combination therapy, but not antiretroviral monotherapy or bitherapy, could the viral load be suppressed and immunodeficiency resolved. Two years after the start of highly active antiretroviraL therapy (HAART) total occlusion of the AVM could be demonstrated. Taken together, this case report may demonstrate the potent angiogenic activity of HIV for AVM. Also, this case report might show that inhibition of such a cofactor may lead to resolution of an AVM.
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PMID:Disappearance of an intracerebral arteriovenous malformation in an HIV-infected patient after initiation of HAART. 1283 35

We present a case of thrombotic thrombocytopenic purpura (TTP) in a human immunodeficiency virus (HIV)-positive woman with altered mental status. Altered mental status with thrombocytopenia may be due to many causes, including consumptive coagulopathy, systemic lupus erythematosis, infection, and as side effects of commonly used anti-seizure medications. Of these, platelet transfusion is ineffective or specifically contraindicated in the consumptive coagulopathies, including TTP. TTP should be considered in all patients with altered mental status or neurologic dysfunction, thrombocytopenia, and hemolytic anemia to prevent morbidity and mortality.
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PMID:Thrombocytopenia and altered mental status in an HIV-positive woman. 1211 46

Stroke is an uncommon complication in pediatric patients with acquired immunodeficiency syndrome (AIDS). However, with the increasing life span of this patient population, more cases of stroke are being reported. We report the case of a 13-year-old girl with a known history of AIDS who presented with new-onset seizures and right hemiparesis. Serial imaging studies revealed progressive occlusion of the left middle cerebral artery and both anterior cerebral arteries with development of collateral circulation. The workup for other etiologies of stroke was negative. This nonatherosclerotic occlusive disease is most likely secondary to vasculopathy caused by the human immunodeficiency virus (HIV). HIV infection should be included in the differential diagnosis of children who present with seizures, mental status change or focal neurological deficits. Treatment options are limited. The different prognoses associated with the etiologies of stroke in this patient population mandate a careful and thorough evaluation.
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PMID:Stroke and pediatric human immunodeficiency virus infection. Case report and review of the literature. 1218 61

Classical late-infantile neuronal ceroid lipofuscinosis (LINCL) is caused by mutations in tripeptidyl peptidase I (TPP-I), a pepstatin-insensitive lysosomal protease, resulting in neurodegeneration, acute seizures, visual and motor dysfunction. In vitro studies suggest that TPP-I is secreted from cells and subsequently taken up by neighboring cells, similar to other lysosomal enzymes. As such, TPP-I is an attractive candidate for enzyme replacement or gene therapy. In the present studies, we examined the feasibility of gene transfer into mouse brain using recombinant adenovirus (Ad), feline immunodeficiency virus (FIV) and adeno-associated virus (AAV) vectors expressing TPP-I, after single injections into the striatum or cerebellum. A dual TPP-I- and beta-galactosidase-expressing adenovirus vector (AdTTP-I/nlsbetagal) was used to distinguish transduced (beta-galactosidase positive) cells from cells that endocytosed secreted TTP-I. Ten days after striatal injection of AdTTP-I/nlsbetagal, beta-galactosidase-positive cells were concentrated around the injection site, corpus callosum, ependyma and choroid plexus. In cerebellar injections, beta-galactosidase expression was confined to the region of injection and in isolated neurons of the brainstem. Immunohistochemistry for TPP-I expression showed that TPP-I extended beyond areas of beta-galactosidase activity. Immunohistochemistry for TTP-I after FIVTTP-I and AAV5TTP-I injections demonstrated TPP-I in neurons of the striatum, hippocampus and Purkinje cells. For all three vectors, TPP-I activity in brain homogenates was 3-7-fold higher than endogenous levels in the injected hemispheres. Our results indicate the feasibility of vector-mediated gene transfer of TPP-I to the CNS as a potential therapy for LINCL.
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PMID:Viral-mediated delivery of the late-infantile neuronal ceroid lipofuscinosis gene, TPP-I to the mouse central nervous system. 1252 35

Anticonvulsant hypersensitivity syndrome (AHS) is a rare, potentially life-threatening allergic disorder, which is well described in relation to many aromatic anticonvulsants. Lamotrigine is a relatively new aromatic anticonvulsant agent that is thought to act on voltage-dependent sodium channels. Initially, it was licensed as add-on therapy for seizures inadequately controlled by other medications. However, its use has been broadened to other indications, including stand-alone therapy for seizures as well as for bipolar disorder. There is extensive experience with hypersensitivity syndromes related to phenytoin, carbomazepine, primidone, and phenobarbital, but fewer reactions have been reported to lamotrigine because of its relatively recent release. Patients with human immunodeficiency virus (HIV) have a higher rate of adverse reactions to many medications. It is unknown if they react more commonly to anticonvulsants such as lamotrigine. It is also unknown if the syndrome lias a tendency to be more severe or prolonged in such patients. The diagnosis of AHS may be particularly elusive in patients with HIV because its common features can easily be confused with an infectious etiology. We report the occurrence of a prolonged hypersensitivity syndrome likely related to lamotrigine in a 32-year-old female with HIV and review the literature regarding this condition.
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PMID:Prolonged anticonvulsant hypersensitivity syndrome related to lamotrigine in a patient with human immunodeficiency virus. 1252 8

The guidance in this report is for evaluation and treatment of patients with complications from smallpox vaccination in the preoutbreak setting. Information is also included related to reporting adverse events and seeking specialized consultation and therapies for these events. The frequencies of smallpox vaccine-associated adverse events were identified in studies of the 1960s. Because of the unknown prevalence of risk factors among today's population, precise predictions of adverse reaction rates after smallpox vaccination are unavailable. The majority of adverse events are minor, but the less-frequent serious adverse reactions require immediate evaluation for diagnosis and treatment. Agents for treatment of certain vaccine-associated severe adverse reactions are vaccinia immune globulin (VIG), the first-line therapy, and cidofovir, the second-line therapy. These agents will be available under Investigational New Drug (IND) protocols from CDC and the U.S. Department of Defense (DoD). Smallpox vaccination in the preoutbreak setting is contraindicated for persons who have the following conditions or have a close contact with the following conditions: 1) a history of atopic dermatitis (commonly referred to as eczema), irrespective of disease severity or activity; 2) active acute, chronic, or exfoliative skin conditions that disrupt the epidermis; 3) pregnant women or women who desire to become pregnant in the 28 days after vaccination; and 4) persons who are immunocompromised as a result of human immunodeficiency virus or acquired immunodeficiency syndrome, autoimmune conditions, cancer, radiation treatment, immunosuppressive medications, or other immunodeficiencies. Additional contraindications that apply only to vaccination candidates but do not include their close contacts are persons with smallpox vaccine-component allergies, women who are breastfeeding, those taking topical ocular steroid medications, those with moderate-to-severe intercurrent illness, and persons aged < 18 years. In addition, history of Darier disease is a contraindication in a potential vaccinee and a contraindication if a household contact has active disease. In the event of a smallpox outbreak, outbreak-specific guidance will be disseminated by CDC regarding populations to be vaccinated and specific contraindications to vaccination. Vaccinia can be transmitted from a vaccinee's unhealed vaccination site to other persons by close contact and can lead to the same adverse events as in the vaccinee. To avoid transmission of vaccinia virus (found in the smallpox vaccine) from vaccinees to their close contacts, vaccinees should wash their hands with warm soapy water or hand rubs containing > or = 60% alcohol immediately after they touch their vaccination site or change their vaccination site bandages. Used bandages should be placed in sealed plastic bags and can be disposed of in household trash. Smallpox vaccine adverse reactions are diagnosed on the basis of clinical examination and history, and certain reactions can be managed by observation and supportive care. Adverse reactions that are usually self-limited include fever, headache, fatigue, myalgia, chills, local skin reactions, nonspecific rashes, erythema multiforme, lymphadenopathy, and pain at the vaccination site. Other reactions are most often diagnosed through a complete history and physical and might require additional therapies (e.g., VIG, a first-line therapy and cidofovir, a second-line therapy). Adverse reactions that might require further evaluation or therapy include inadvertent inoculation, generalized vaccinia (GV), eczema vaccinatum (EV), progressive vaccinia (PV), postvaccinial central nervous system disease, and fetal vaccinia. Inadvertent inoculation occurs when vaccinia virus is transferred from a vaccination site to a second location on the vaccinee or to a close contact. Usually, this condition is self-limited and no additional care is needed. Inoculations of the eye and eyelid require evaluation by an ophthalmologist and might require therapy with topical antiviral or antibacterial medications, VIG, or topical steroids. GV is characterized by a disseminated maculopapular or vesicular rash, frequently on an erythematous base, which usually occurs 6-9 days after first-time vaccination. This condition is usually self-limited and benign, although treatment with VIG might be required when the patient is systemically ill or found to have an underlying immunocompromising condition. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. EV occurs among persons with a history of atopic dermatitis (eczema), irrespective of disease severity or activity, and is a localized or generalized papular, vesicular, or pustular rash, which can occur anywhere on the body, with a predilection for areas of previous atopic dermatitis lesions. Patients with EV are often systemically ill and usually require VIG. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. PV is a rare, severe, and often fatal complication among persons with immunodeficiencies, characterized by painless progressive necrosis at the vaccination site with or without metastases to distant sites (e.g., skin, bones, and other viscera). This disease carries a high mortality rate, and management of PV should include aggressive therapy with VIG, intensive monitoring, and tertiary-level supportive care. Anecdotal experience suggests that, despite treatment with VIG, persons with cell-mediated immune deficits have a poorer prognosis than those with humoral deficits. Infection-control precautions should be used to prevent secondary transmission and nosocomial infection. Central nervous system disease, which includes postvaccinial encephalopathy (PVE) and postvaccinial encephalomyelitis (or encephalitis) (PVEM), occur after smallpox vaccination. PVE is most common among infants aged < 12 months. Clinical symptoms of central nervous system disease indicate cerebral or cerebellar dysfunction with headache, fever, vomiting, altered mental status, lethargy, seizures, and coma. PVE and PVEM are not believed to be a result of replicating vaccinia virus and are diagnoses of exclusion. Although no specific therapy exists for PVE or PVEM, supportive care, anticonvulsants, and intensive care might be required. Fetal vaccinia, resulting from vaccinial transmission from mother to fetus, is a rare, but serious, complication of smallpox vaccination during pregnancy or shortly before conception. It is manifested by skin lesions and organ involvement, and often results in fetal or neonatal death. No known reliable intrauterine diagnostic test is available to confirm fetal infection. Given the rarity of congenital vaccinia among live-born infants, vaccination during pregnancy should not ordinarily be a reason to consider termination of pregnancy. No known indication exists for routine, prophylactic use of VIG in an unintentionally vaccinated pregnant woman; however, VIG should not be withheld if a pregnant woman develops a condition where VIG is needed. Other less-common adverse events after smallpox vaccination have been reported to occur in temporal association with smallpox vaccination, but causality has not been established. Prophylactic treatment with VIG is not recommended for persons or close contacts with contraindications to smallpox vaccination who are inadvertently inoculated or exposed. These persons should be followed closely for early recognition of adverse reactions that might develop, and clinicians are encouraged to enroll these persons in the CDC registry by calling the Clinician Information Line at 877-554-4625. To request clinical consultation and IND therapies for vaccinia-related adverse reactions for civilians, contact your state health department or CDC's Clinician Information Line (877-554-4625). Clinical evaluation tools are available at http.//www.bt.cdc.gov/agent/smallpox/vaccination/clineval. Clinical specimen-collection guidance is available at http://www.bt.cdc.gov/agent/smallpox/vaccination/vaccinia-specimen-collection.asp. Physicians at military medical facilities can request VIG or cidofovir by calling the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) at 301-619-2257 or 888-USA-RIID.
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PMID:Smallpox vaccination and adverse reactions. Guidance for clinicians. 1261 10

The human immunodeficiency virus type 1 (HIV-1) Tat protein is a key pathogenic factor in a variety of acquired immune deficiency syndrome (AIDS)-associated disorders. A number of studies have documented the neurotoxic property of Tat protein, and Tat has therefore been proposed to contribute to AIDS-associated neurological diseases. Nevertheless, the bulk of these studies are performed in in vitro neuronal cultures without taking into account the intricate cell-cell interaction in the brain, or by injection of recombinant Tat protein into the brain, which may cause secondary stress or damage to the brain. To gain a better understanding of the roles of Tat protein in HIV-1 neuropathogenesis, we attempted to establish a transgenic mouse model in which Tat expression was regulated by both the astrocyte-specific glial fibrillary acidic protein promoter and a doxycycline (Dox)-inducible promoter. In the present study, we characterized the phenotypic and neuropathogenic features of these mice. Both in vitro and in vivo assays confirmed that Tat expression occurred exclusively in astrocytes and was Dox-dependent. Tat expression in the brain caused failure to thrive, hunched gesture, tremor, ataxia, and slow cognitive and motor movement, seizures, and premature death. Neuropathologies of these mice were characterized by breakdown of cerebellum and cortex, brain edema, astrocytosis, degeneration of neuronal dendrites, neuronal apoptosis, and increased infiltration of activated monocytes and T lymphocytes. These results together demonstrate that Tat expression in the absence of HIV-1 infection is sufficient to cause neuropathologies similar to most of those noted in the brain of AIDS patients, and provide the first evidence in the context of a whole organism to support a critical role of Tat protein in HIV-1 neuropathogenesis. More importantly, our data suggest that the Dox inducible, brain-targeted Tat transgenic mice offer an in vivo model for delineating the molecular mechanisms of Tat neurotoxicity and for developing therapeutic strategies for treating HIV-associated neurological disorders.
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PMID:Neuropathologies in transgenic mice expressing human immunodeficiency virus type 1 Tat protein under the regulation of the astrocyte-specific glial fibrillary acidic protein promoter and doxycycline. 1270 54


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