Gene/Protein Disease Symptom Drug Enzyme Compound
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 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dengue is the most important human viral disease transmitted by an arthropod vector. The steadily increasing numbers of tourists visiting endemic areas coupled with the present resurgence of dengue, raises the risk of exposure for large numbers of travelers and imported dengue cases are increasingly observed in non-endemic countries. We aimed to study the epidemiology, clinical manifestations and laboratory findings in imported dengue at a City of Vienna hospital. Medical records of 93 patients (age: 17-68 years, 43f, 50m) with imported dengue in Vienna between 1990 and April 2005 were analyzed retrospectively. Forty-eight (52%) were classified as confirmed and 45 (48%) as probable dengue, according to the CDC criteria. The patients acquired the infection in South East Asia (56%), the Indian subcontinent (18%), Africa (10%) and Oceania (3%). The most important symptoms were fever, headache, arthralgia and myalgia, nausea and vomiting, diarrhea, chills, extreme fatigue and dizziness. A rash was observed in 43%, and lymphadenopathy in 22%. Laboratory findings were thrombocytopenia, leukopenia and elevated hepatic enzymes. Eighteen patients showed hemorrhagic manifestations, and 7 fulfilled the criteria of dengue hemorrhagic fever; 1 of them had dengue shock syndrome. Case fatality rate was nil. Dengue has to be considered in all febrile travelers returning from endemic areas. Prompt diagnosis and symptomatic treatment is warranted and should prevent patients from unnecessary and potentially harmful diagnostic and therapeutic procedures.
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PMID:Imported dengue fever in Austria 1990-2005. 1709 27

A 72-year-old male with liver cirrhosis and hepatocellular carcinoma experienced general fatigue. Four days later he was admitted to our hospital because of dizziness, dysbasia and left facial palsy (day 1). On day 6, a neurological examination revealed left trigeminal neuralgia, left medial longitudinal fasciculus (MLF) syndrome, skew deviation, hypacusia, tongue deviation and left limb ataxia. Magnetic resonance imaging of the brain including diffusion-weighted imaging showed previous lacunar infarctions at the left thalamus and pons. The immunological investigation for viral infection in his serum samples showed high titers of IgM antibody against cytomegalovirus (CMV). Cerebrospinal fluid (CSF) investigation revealed mononuclear pleocytosis, elevated protein levels and high titers of IgG antibody against the varicella-zoster virus (VZV). Anti-CMV antibody measurement and CMV-DNA detection by the polymerase chain reaction in CSF revealed that the central nervous system (CNS) was not infected by CMV. We diagnosed this case as brainstem encephalitis following multiple cranial neuropathy associated with CMV and VZV infections. The neurological symptoms gradually improved with aciclovir and prednisolone therapy. The titers of antibody for CMV in his serum samples normalized 4 months later after onset. Although there was no evidence of CMV infection in the CNS was obtained, parainfection or autoimmune mediated responses followed by viral infections might have led to brainstem encephalitis with multiple cranial nerve involvements in our patient.
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PMID:[A case of brainstem encephalitis following multiple cranial neuropathy in a hepatocellular carcinoma patient--association with cytomegalovirus and varicella-zoster virus infection]. 1804 5

The presence of IgM paraproteinemia in low-grade lymphomas is usually considered a clinical syndrome known as Waldenstrom's macroglobulinemia (WM). In the WHO classification, WM is associated to lymphoplasmacytic lymphoma (LPL); it is a clinicopathologic entity characterized by a monoclonal expansion of predominantly small B-lymphocytes with variable plasmacytoid differentiation. LPL constitutes less than 5% of all NHL and it is associated with hepatitis C virus infection in 26% of cases. Cells of LPL/WM are B cells positive for monocytic Ig light chains, IgM, pan-B-cell markers, and negative for CD3 and CD103. The t(9;14)(p13;q32) is present in 50% of LPL, and determines PAX-5 over-expression. 6q21 deletion is observed in 42% of cases. LPL occurs in older adults. Clinical presentation usually consists of disseminated disease, but extranodal involvement and leukemic phase are rare. Most WM patients have symptoms attributable to tumour infiltration and/or monoclonal protein. In fact, a monoclonal serum paraprotein of IgM type and hyperviscosity symptoms may occur in more than 20% of cases (WM). Hyperviscosity syndrome is usually manifested by bleeding, blurring or loss of vision, dizziness, headache, and neurologic symptoms. Malignant infiltration of the CNS (Bing-Neel syndrome) is uncommon. LPL/WM is an indolent malignancy that is not usually curable with conventional treatments. The median survival of patients with LPL or WM is 50-60 months, transformation to large cell lymphoma may occur. Stage definition is irrelevant in WM considering that initiation of therapy is decided on the bases of prognostic factors and the development of disease-related symptoms and signs. The main adverse prognostic factors are older age, B symptoms, anemia, low albumin serum levels, raised SGOT, and high beta 2-microglobulin values. Several therapeutic alternatives for newly diagnosed or relapsed LPL/WM are available; however, the best location for every strategy is a matter of investigation. Several new drugs are being assessed in prospective trials. As a significant progress in this field, response criteria and therapeutic recommendations were updated during the Third International Workshop on WM (7-10 October 2004, Paris, France).
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PMID:Lymphoplasmacytic lymphoma-Waldenstrom's macroglobulinemia. 1849 69

Acute hemorrhagic leukoencephalopathy (AHLE) is a rare, acute disorder characterized by perivenular demyelination and diffuse hemorrhagic necrosis of the central nervous system. AHLE is thought to represent a hyperacute form of acute disseminated encephalomyelitis. AHLE is associated with a greater morbidity and mortality and, fortunately, is much less common than acute disseminated encephalomyelitis. Since most cases of AHLE result in patient demise, forensic pathologists should be cognizant of this entity and consider it in their differential diagnosis.Here we describe an interesting case of a previously healthy 11-year-old boy who initially complained of vague gastroenteritis-like symptoms while visiting a mountain lake. The boy's symptoms evolved to include severe headache and dizziness, necessitating a visit to a rural emergency department. He presented with focal neurologic findings, and head computed tomography (CT) scan confirmed thalamic edema. Cerebrospinal fluid analysis was suggestive of infectious etiology, and multiple empiric therapies were initiated. He was transferred to our institution, and his clinical status continued to worsen. Given the poor prognosis, the family requested withdrawal of supportive care. On day 14 of symptoms the boy succumbed to his illness. An autopsy was requested to further characterize the proximate cause of death.AHLE often presents with abrupt onset of fever, neck stiffness, seizure, and/or focal neurologic signs several days following a viral illness or vaccination. Thus, AHLE can clinically mimic a direct central nervous system infection or a toxic ingestion. AHLE has a very poor prognosis, with rapid deterioration and death usually occurring within days to one week after onset of symptoms. The cause for AHLE is unclear. An autoimmune pathophysiology is likely, with immune cross-reactivity between myelin basic protein moieties and various infectious agent antigens. Treatment for AHLE is not well-established; some authors describe in recent literature that a combination of immunosuppressant medications and/or therapeutic plasma exchange may be of benefit in treating AHLE.
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PMID:Acute hemorrhagic leukoencephalitis: a critical entity for forensic pathologists to recognize. 2001 Feb 89

Seasonal flu is caused by influenza viruses A and B. These enveloped viruses have a genome made up of seven or eight RNA fragments. The different subtypes are determined by the nature of the two surface glycoproteins HA and NA. Seasonal flu is an epidemic wintertime illness occurring in temperate climate zones. Its epidemiology is linked to the great variability of the virus in time, necessitating an alert system that detects dominating circulating variants each year and that determines the vaccination composition. Clinical flu symptoms are not sufficiently specific to allow for diagnosis with virological tests. This is especially true during non-epidemic periods as well as in subjects older than 65 and younger than five. Children are especially vulnerable to influenza virus infections. Hospitalization occurs more frequently, the younger the child. In children younger than two years, the infection can be pauci-symptomatic and is sometimes detected from non-respiratory symptoms such as lethargy, convulsions, and dizziness. In all cases of respiratory syndrome compatible with influenza virus infection in hospitalized subjects, virological flu diagnosis is of utmost interest. Several tools are available to allow for direct viral detection in respiratory specimens: cell culture isolation, antigenic detection, RNA molecular detection. Choice of method is based on the characteristics of the test: sensibility, specificity, speed and ease of realization, and cost.
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PMID:[Seasonal flu]. 2030 76

A clinical study in 946 human volunteers was done to compare Candid #1 vaccine manufactured in Argentina with the vaccine produced in USA that had been previously used. The efficacy was evaluated using immunogenicity measured by the detection of neutralizing antibodies as a subrogate marker. Safety was evaluated comparing the rate of adverse events. Both vaccines showed a comparable rate of seroconversion, slightly higher than the efficacy estimated from previous studies (95.5%). There were no severe adverse events related to the vaccines. The general events considered related to the vaccines were not clinically relevant and disappeared either spontaneously or with symptomatic treatment. Similar rates of adverse events (29.9% for the Argentine vaccine and 35.0% for the USA vaccine) were found for both vaccines. These included: headache, weakness, myalgias, mild low blood cell (< 4,000/mm(3)) and platelet (< 150,000/mm(3)) counts, nausea and/or vomiting, fever, retroocular pain, dizziness, microhematuria, low backache and exantema. These results indicate that the vaccine Candid#1 manufactured in Argentina is equivalent to the manufactured in USA. These results allowed the National Institute of Human Viral Diseases (INEVH) to register the vaccine produced locally under the National Regulatory Authority (ANMAT).
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PMID:[Candid#1 vaccine against Argentine hemorrhagic fever produced in Argentina. Immunogenicity and safety]. 2052 69

Systemic lupus erythematosus (SLE) co-morbid with rheumatoid arthritis (RA) is known as 'Rhupus syndrome' and is estimated to be present in between 0.01 and 2% of SLE and RA patients. The occurrence of aplastic anaemia in a patient with rhupus is very rare and a treatment for this condition has not been reported. A 52-year-old woman presented complaining of nausea and dizziness during the preceding month. She had been treated for rheumatoid arthritis for 16 years. At the time of presentation, she had a malar rash, multiple arthritis, pancytopenia, pleural effusion, proteinuria, and positive anti-nuclear and anti-dsDNA antibodies. A kidney biopsy revealed ISN/RPS class IV-G (A) lupus nephritis. Bone marrow aspiration and biopsy showed aplastic anaemia with no evidence of viral infection. The patient was successfully treated using cyclosporine and prednisolone and she remained symptom-free at the one-and-a-half-year follow-up. To our knowledge, this is the first report of a successful treatment using cyclosporine in a patient with rhupus complicated by aplastic anaemia.
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PMID:Successful treatment using cyclosporine in a patient with rhupus complicated by aplastic anemia: a case report and review of the literature. 2181 67

The Ramsay-Hunt syndrome is the association of facial palsy and varicella-zoster virus infection with involvement of the ear canal and eardrum. It may be associated with deafness, tinnitus and dizziness. It can sometimes affect the lower cranial nerves. A case of an immunocompetent patient with affectation of the VII, VIII and X cranial nerves is presented.
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PMID:[Ramsay-Hunt syndrome presenting laryngeal paralysis]. 2200 Apr 84

Ramsay-Hunt syndrome is caused by varicella zoster virus infection in the geniculate ganglion of the facial nerve. It is characterized by facial palsy, otic pain, and herpetic vesicles around the auricle and external auditory canal. Additionally, symptoms may develop related to other cranial nerve involvement, such as dizziness or hearing loss by the vestibulocochlear nerve being invaded. We report a rare case of a Ramsay-Hunt syndrome patient who developed dysphagia due to multiple cranial nerve involvement including the glossopharyngeal nerve and vagus nerve.
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PMID:Dysphagia in Ramsay Hunt's Syndrome - A Case Report -. 2250

Codeine is widely prescribed in clinical settings for the relief of pain and non-productive coughs. Common adverse drug reactions to codeine include constipation, euphoria, nausea, and drowsiness. However, there have been few reports of serious adverse reactions after codeine ingestion in adults. Here, we present a case of severe anaphylaxis after oral ingestion of a therapeutic dose of codeine. A 30-year-old Korean woman complained of the sudden onset of dyspnea, urticaria, chest tightness, and dizziness 10 minutes after taking a 10-mg dose of codeine to treat a chronic cough following a viral infection. She had previously experienced episodes of asthma exacerbation following upper respiratory infections, and had non-atopic rhinitis and a food allergy to seafood. A skin prick test showed a positive response to 1-10 mg/mL of codeine extract, with a mean wheal size of 3.5 mm, while negative results were obtained in 3 healthy adult controls. A basophil histamine release test showed a notable dose-dependent increase in histamine following serial incubations with codeine phosphate, while there were minimal changes in the healthy controls. Following a CYP2D6 genotype analysis, the patient was found to have the CYP2D6*1/*10 allele, indicating she was an intermediate metabolizer. An open label oral challenge test was positive. To the best of our knowledge, this is the first report of a patient presenting with severe anaphylaxis after the ingestion of a therapeutic dose of codeine, which may be mediated by the direct release of histamine by basophils following exposure to codeine.
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PMID:A Case of Codeine Induced Anaphylaxis via Oral Route. 2440


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