Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Waterhouse-Friderichsen (WFS) syndrome, also known as purpura fulminans, is described as acute hemorrhagic necrosis of the adrenal glands and is most often caused by meningococcal infection. This clinical entity is more frequently seen in the pediatric than the adult population and is associated with a high morbidity and mortality. The initial presenting complaints for patients with the WFS usually include a diversity of nonspecific, vague symptoms such as cough, dizziness, headache, sore throat, chills, rigors, weakness, malaise, restlessness, apprehension, myalgias, arthralgias, and fever. These symptoms are usually abrupt in their onset. Petechiae are present in approximately 50-60% of patients. The clinical diagnosis of WFS may be relatively straightforward or extremely challenging. Patients who appear in the initial and nontoxic-appearing stage without any skin lesions may be difficult to distinguish from a benign viral illness. When a patient presents with fever and petechiae, WFS must be considered, even when the patient has a non-toxic appearance. Due to the rapid progression and often devastating consequences, therapy should be instituted as soon as the diagnosis is suspected.
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PMID:Rupert Waterhouse and Carl Friderichsen: adrenal apoplexy. 969 86

An 82-year-old woman was admitted to our hospital because of dizziness and petechiae. Peripheral blood examination showed severe anemia and thrombocytopenia. Bone marrow aspiration revealed 42% leukemic blasts positive for peroxidase with multilineage dysplasia, leading to a diagnosis of acute myeloid leukemia with multilineage dysplasia. The levels of the patient's marrow plasma cells increased to 12%, whereas serum levels of IgG, A, and M dropped. lambda type Bence Jones protein was detected on urine immunoelectrophoresis. The total urinary protein was 3, 960 mg/day. Bone scintigraphy detected multifocal uptake in the ribs. The diagnosis was multiple myeloma developing simultaneously with acute myeloid leukemia. Possible mechanisms for the occurrence of acute myeloid leukemia and multiple myeloma were discussed.
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PMID:[Simultaneous occurrence of acute myeloid leukemia with multilineage dysplasia and multiple myeloma]. 1264 33

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis. 1533 85

Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne disease caused by the arbovirus Crimean-Congo hemorrhagic fever virus (CCHFV), which is a member of the Nairovirus genus (family Bunyaviridae). CCHF was first recognized during a large outbreak among agricultural workers in the mid-1940s in the Crimean peninsula. The disease now occurs sporadically throughout much of Africa, Asia, and Europe and results in an approximately 30% fatality rate. After a short incubation period, CCHF is characterized by a sudden onset of high fever, chills, severe headache, dizziness, back, and abdominal pains. Additional symptoms can include nausea, vomiting, diarrhea, neuropsychiatric, and cardiovascular changes. In severe cases, hemorrhagic manifestations, ranging from petechiae to large areas of ecchymosis, develop. Numerous genera of ixodid ticks serve both as vector and reservoir for CCHFV; however, ticks in the genus Hyalomma are particularly important to the ecology of this virus. In fact, occurrence of CCHF closely approximates the known world distribution of Hyalomma spp. ticks. Therefore, exposure to these ticks represents a major risk factor for contracting disease; however, other important risk factors are known and are discussed in this review. In recent years, major advances in the molecular detection of CCHFV, particularly the use of real-time reverse transcription-polymerase chain reaction (RT-PCR), in clinical and tick samples have allowed for both rapid diagnosis of disease and molecular epidemiology studies. Treatment options for CCHF are limited. Immunotherapy and ribavirin have been tried with varying degrees of success during sporadic outbreaks of disease, but no case-controlled trials have been conducted. Consequently, there is currently no antiviral treatment for CCHF approved by the U.S. Food and Drug Administration (FDA). However, renewed interested in CCHFV, as well as increased knowledge of its basic biology, may lead to improved therapies in the future. This article reviews the history, epidemiology, ecology, clinical features, pathogenesis, diagnosis, and treatment of CCHF. In addition, recent advances in the molecular biology of CCHFV are presented, and issues related to its possible use as a bioterrorism agent are discussed.
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PMID:Crimean-Congo hemorrhagic fever. 1555 Feb 68

On May 19, 2004, azacitidine (5-azacytidine; Vidaza(trade mark); Pharmion Corporation, Boulder, CO, http://www.pharmion.com) for injectable suspension received regular approval by the U.S. Food and Drug Administration (FDA) for the treatment of all subtypes of myelodysplastic syndrome (MDS). This report summarizes the basis for this approval. Effectiveness was demonstrated in one randomized, controlled trial comparing azacitidine administered s.c. with best supportive care (observation group) and in two single-arm studies, one in which azacitidine was administered s.c. and in the other in which it was administered i.v. The dose of azacitidine, 75 mg/m2/day for 7 days every 28 days, was the same in all three studies. In the randomized trial, study participants were well matched with respect to age, sex, race, performance status, MDS subtype, and use of transfusion during the 3 months before study entry. Patients in the observation arm were permitted by protocol to cross over to azacitidine treatment if their disease progressed according to prespecified criteria. During the course of the study, more than half of the patients in the observation arm did cross over to the azacitidine treatment arm. The primary efficacy end point was the overall response rate. Response consisted of complete or partial normalization of blood cell counts and of bone marrow morphology. The response rate in the azacitidine arm was about 16%; there were no responses in the observation arm. The response rates in the two single-arm studies were similar (13% and 19%). The responses were sustained, with median durations of 11 months and 17 months respectively. Responding patients who were transfusion dependent at study entry lost the need for transfusions. In addition, about 19% of patients had less than partial responses (termed improvement), and two-thirds of them became transfusion independent. Common adverse events associated with azacitidine treatment were gastrointestinal (nausea, vomiting, diarrhea, constipation, and anorexia), hematologic (neutropenia, thrombocytopenia), fevers, rigors, ecchymoses, petechiae, injection site events, arthralgia, headache, and dizziness. Liver function abnormalities occurred in 16% of patients with intercurrent hepatobiliary disorders and in two patients with previously diagnosed liver cirrhosis. Renal failure occurred in patients during sepsis and hypotension. There were no deaths attributed to azacitidine. Azacitidine, the first drug approved by the U.S. FDA for MDS, has a favorable safety profile and provides a clinical benefit of eliminating transfusion dependence and complete or partial normalization of blood counts and bone marrow blast percentages in responding patients.
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PMID:FDA drug approval summary: azacitidine (5-azacytidine, Vidaza) for injectable suspension. 1579 20

A 30 years-old man was administrated with dizziness and fatigue for half month, and the big toe on his left foot got the prolonged bleeding of wound complicated with fever 7 days before the admission. The physical examination (PE) discovered that the case suffered from the anemic appearance, lower part tenderness of sternum, petechiae and purpura on skin of lower extremities, and with remaining not to be remarkable. The examination of blood routine showed WBC 2.3 x 10(9)/L, Hb 60/L, BPC 34 x 10(9)/L and blasts 0. 85. The bone marrow smear indicated markedly the hypercellularity, promyelocytes 89% and strongly positive myeloperoxidase (MPO). The PT and APTT were prolonged, and the FDP and D-dimer were positive. The acute promyelocytic leukemia (APL) with DIC was diagnosed. The patient was administered with all-trans retinoic acid (ATRA) with dosage of 20 mg three times per day. After 14 week treatment, the patient did not get complete remission. Then the tanshinone II A was taken orally with 30mg twice each day. After 8 week treatment of tanshinone II A, the blood routine was restored to normal. Four weeks later, the bone marrow also became normally, and the patient got a complete remission (CR). After more than 3 months of consolidation therapy with tanshinone II A, the patient was relapsed. When the homoharringtonine and cytarabine (HA) were given, the patient was got CR again. Three years later, he was relapsed secondarily, and then died of intracranial hemorrhage. The tanshinone II A could induce CR of APL with ATRA resistance, no side effect was observed; there is a reoccurring possibility from consolidation therapy with tanshinone II A.
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PMID:[Complete remission of acute promyelocytic leukemia resisting all-trans retinoic acid of one case treated by tanshinone II A]. 1723 2

Introduction. The authors are presenting a case of Thrombotic Thrombocytopenic Purpura (TTP) that presented with complaints of altered mental status and found to have petechiae. Case Presentation. An 81-year-old female patient presented to the Emergency Department (ED) of a tertiary care hospital with chief complains of dizziness, slurred speech, and weakness. She was found to have lower extremity petechiae on physical examination. On blood exam, she had thrombocytopenia, and her peripheral blood smear showed schistocytes. Her renal function was also impaired. The CT scan of head was without any abnormality. She was finally diagnosed as having TTP and transferred to ICU but ultimately passed away. Conclusion. TTP is a rare syndrome with preventable mortality if diagnosed early and managed appropriately with plasmapheresis. The Emergency Department physicians should be aware of the presenting symptoms and signs of TTP.
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PMID:Altered mental status and a not-so-benign rash. 2332 97