Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242429 (sore throat)
2,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of Sweet syndrome (SS) associated with acute megakaryoblastic leukemia (AMKL) is reported. A 66-year-old male was admitted to Ashikaga Red Cross Hospital because of skin eruption and sore throat. His eruption was tender and erythema-like nature. He developed a spiking fever after admission. CBC revealed pancytopenia, and a bone marrow specimen showed increased megakaryoblasts and fibrosis. These blasts were shown to be CD41-positive by flow cytometric analysis. A diagnosis of AMKL was then made. Skin biopsy revealed infiltration of neutrophils without vasculitis, compatible with SS. Oral administration of prednisolone was begun which improved his skin lesions considerably. He was then treated with low dose Ara-C, which was however ineffective. The blasts increased in the peripheral blood and he died on the 72nd hospital day. There are 37 reported cases of SS associated with acute nonlymphocytic leukemia, and this is the first case report of SS associated with AMKL.
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PMID:[Acute megakaryoblastic leukemia associated with Sweet's syndrome, including review of the literature]. 847 86

We experienced 4 cases of agranulocytosis due to anti-tuberculosis drugs (rifampicin [RFP], isoniazid [INH], ethambutol [EB], streptomycin [SM] or pyrazinamide [PZA]) among some 6,400 tuberculosis patients who underwent chemotherapy over the past 20 years from 1981 to 2002 in our hospital, and the incidence rate of agranulocytosis was estimated at 0.06%. The 4 cases of agranulocytosis were as follows. CASE 1: A 51-year-old woman with right chest pain and fever was admitted to our hospital on Jan 4, 2001. The white blood cell (WBC) count was 5,200/microliter. The tubercle bacilli were cultured in her sputum. The treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, allopurinol and teprenone was started on Jan 13. Pyrazinamide and allopurinol were stopped because of hyper-uric acidemia on Feb 7. Agranulocytosis and eosinophilia (WBC 1,300 [Neut 1%, Ly 57%, Eos 35%]) developed on Feb 13. All drugs were withdrawn and G-CSF drug nartograstim 100 micrograms was injected subcutaneously for 3 days. The WBC recovered to normal level and she was thereafter treated with INH, EB and Levofloxacin (LVFX) without any further trouble. Agranulocytosis in this case was supposed to be due to RFP. CASE 2: A 66-year-old man who had had nephrotic syndrome and hypothyroidism and has been treated with prednisolone 10 mg/day was admitted to our hospital on Aug 9, 2000 because of miliary tuberculosis. The tubercle bacilli were cultured in his sputum and the treatment with INH 0.3, RFP 0.45, and EB 0.75 g/day were started on Aug 10, but it was withdrawn on Aug 17 because of general skin eruption. After re-starting treatment with EB and INH on Aug 24, RFP was added in small dosage (0.05 g) on Oct 12, but agranulomatosis (WBC 2,300/microliter [Neut 2%]) developed on Nov 21, and all drugs were withdrawn again. The G-CSF drug filgrastim was used once subcutaneously, and WBC recovered immediately. He was thereafter treated with INH, EB, LVFX successfully. Agranulocytosis was supposed to be due to RFP. CASE 3: A 60-year-old woman without symptoms had abnormal chest roentgenograph, and consulted with our hospital on Aug 26, 2002. The broncho-alveolar lavage fluid was smear and culture-negative, but PCR-TB positive, and the case was diagnosed as pulmonary tuberculosis. Treatment with INH 0.3, RFP 0.45, EB 0.75, PZA 1.2 g/day, alloprinol 300 mg and rebamipide 300 mg/day was started on Sept. 5, 2002. Late in September, she complained of appetite loss. The laboratory data on Oct 3 revealed WBC 900/microliter (Neut 1%, Ly 94%), aspartate aminotransferase (AST) 199 IU/l, and alanine aminotransferase (ALT) 253 IU/l, showing agranulocytosis and drug-induced hepatitis. The chemotherapy was immediately withdrawn and she was admitted to our hospital on the next day. Glycyrrhizin derivative (SNMC) 40 ml was injected for 5 days, and WBC recovered, and AST and ALT also became normal. CASE 4: A 60-year-old man was admitted to our hospital on March 11, 1981 because pulmonary tuberculosis had recurred. He had been treated with SM, PAS and INH in 1973 for pulmonary tuberculosis. On admission examination of blood count and blood chemistry were normal. Treatment with RFP, INH and SM was started on March 11. He stopped out from the hospital on April 17, but in a few days he returned back with sore throat, lower lip swelling and gingival bleeding. Blood cell count on April 24 showed pancytopenia with RBC 226, Hb 7.5, WBC 800 (Ly 96%, Eos 4%) and Plt 10,000/microliter. The bone-marrow showed NCC (nuceated cell count) of 5,500, and megakaryocyte 0. Thereafter ground glass appearance shadows were seen on the whole lung field, and he died May 26. Autopsy showed generalized aspergillosis. It was strongly suspected that either of RFP, INH or SM was responsible for his pancytopenia. We collected another 10 cases of agranulocytosis due to anti-tuberculosis drugs in the world wide literature, and found men/women ratio 5/8 (in one case gender was not known), the duration of chemotherapy before appearance of agranulocytosis 1-3 months, no change in the lymphocyte count of the peripheral blood, and the accompanying of another allergic signs such as skin eruption, blood eosinophilia or drug-induced hepatitis in some cases, and these findings suggest that the mechanism of agranulocytosis due to anti-tuberculosis drugs was allergic in nature.
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PMID:[Agranulocytosis due to anti-tuberculosis drugs including isoniazid (INH) and rifampicin (RFP)--a report of four cases and review of the literature]. 1467 45

In this study, the clinical and laboratory features of 26 infectious mononucleosis (IMN) cases who have been diagnosed between the years of 1984-2005 were evaluated retrospectively. The mean age of the patients was 26+/-11 years, the rate of being hospitalized was 65%, and mean hospitalization period was 9.2+/-6 days. Fever (81%), weakness (50%), sore throat (50%), headache (50%) and swollen neck (35%) were the most common symptoms, while in the physical examination cervical lymphadenopathy (81%), splenomegaly (69%), hyperemic pharynx (65%), hepatomegaly (54%) and tonsillitis (50%) were observed. Laboratory results yielded leukocytosis in 21%, leucopenia in 12%, anemia in 44%, thrombocytopenia in 5% and elevated transaminase levels in 84% of the patients. Of the patients 15 (57.7%) had the history of using antibiotics before the diagnosis. Serological diagnosis was performed by Paul-Bunnel test and/or IgM positivity against Epstein-Barr virus (EBV) viral capsid antigen (VCA). Tonsillo-pharyngitis secondary to edema and respiratory distress due to lymphadenopathy pressure were detected in four patients, whereas pancytopenia was established only in one patient, as complications. This study emphasized that, although IMN is a self-limited infection, the diagnostic difficulties may arise when the clinical course is atypical, and rarely seen life-threatening complications may also develop during IMN course.
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PMID:[Retrospective evaluation of patients who were diagnosed as infectious mononucleosis between 1984-2005]. 1742 57

A 47-year-old woman was admitted to our emergency room because of anemia and acute tonsillitis. She reported recurrent fever and a sore throat. Clinical examination and CT scans showed general lymph node swelling and liver enlargement. In the course of the disease she developed pancytopenia with neutropenic fever, pleuropneumonia, and deep vein thrombosis. The histological examination of a lymph node showed a reactive, EBV-associated lymphadenitis. The examination of the bone marrow showed an activated marrow. The diagnosis of an active EBV infection was established with 2 x 10(6)/ml EBV gene copies in the blood. In addition, systemic lupus erythematosus was diagnosed because of the typical autoantibody constellation and clinical findings. The immunohematological examination showed autoantibodies against the three blood cell compartments. Because of the severe pancytopenia as a result of the EBV- and SLE-associated autoantibodies and despite recurrent infections, we initiated immunosuppressive therapy with low-dose corticosteroids. This therapy resulted in normalization of the blood counts. Anitibody levels and the EBV genome levels became negative.
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PMID:[Pancytopenia and lymph node swelling. Cardinal symptoms of an unusual differential diagnosis]. 1921 64

A 66-year-old woman complained of fever, sore throat, and neck pain due to pharyngitis and painful lymph node swelling. CBC revealed severe pancytopenia and markedly hypocellular marrow. The administration of antibiotics and granulocyte-colony stimulating factor (G-CSF) successfully ameliorated the inflammatory lesions, and hematopoiesis recovered. Causes for pancytopnenia was unlikely to be virus infection or drugs, and aplastic anemia was also unlikely since only the plasma levels of tumor necrosis factor-alpha (TNF-alpha) was markedly elevated, erythropoietin (EPO) was slightly elevated, interferon-gamma (IFN-gamma) was normal, and flow cytometric analysis for paroxysmal nocturnal hemoglobinuria (PNH)-type cells was negative. These results suggested that the cause of impaired hematopoiesis in the present patient might have been due to elevated TNF-alpha in overwhelming infection, although the pathogen was not identified.
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PMID:Transient severe pancytopenia due to elevated tumor necrosis factor-alpha in overwhelming infection. 1929 48

A 21-year-old man admitted for idiopathic fever and sore throat was diagnosed with virus-associated hemophagocytic syndrome (VAHS) when bone marrow aspirate showed hemophagocytosis. ELISA for HIV antibodies was negative, although HIV RNA was positive. VAHS is extremely rare as an initial manifestation in HIV infection, being reported, to our knowledge, in only 4 subjects in Japan. Hemophagocytic syndrome (HPS) features fever and hepatosplenomegaly associated with pancytopenia, hypertriglyceridemia, and hypofibrinogemia, due to hypercytokinemia. Physicians should thus be aware that primary HWV infection may involve glandular-fever-like illness and should start prompt diagnosis to contain AIDS spread.
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PMID:[Virus-associated hemophagocytic syndrome (VAHS) as an initial manifestation in HIV infection]. 2191 9

Visceral leishmaniasis (kala-azar) is a disease caused by protozoa of genus Leishmania. It is currently regarded as the second most dreaded parasitic disease, next to malaria. There have been very few case reports of visceral leishmaniasis among the renal transplant recipients. We present a renal allograft recipient with symptoms of fever, sore throat, hoarseness of voice, lymphadenopathy, splenomegaly, and pancytopenia after 7 years post-transplant period. On investigating, he was diagnosed to have extensive visceral leishmaniasis with laryngeal involvement. Despite extensive PubMed literature search, we could not find any case report of postrenal transplant visceral and laryngeal leishmaniasis and to the best of our knowledge this is the first case report of this kind.
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PMID:Postrenal transplant laryngeal and visceral leishmaniasis - A case report and review of the literature. 2316 77

Diphtheria is a rare cause of infection in highly vaccinated populations and may not be recognized by modern clinicians. Infections by nontoxigenic Corynebacterium diphtheriae are emerging. We report the first case of necrotizing epiglottitis secondary to nontoxigenic C diphtheriae. A fully vaccinated child developed fever, poor oral intake, and sore throat and was found to have necrotizing epiglottitis. Necrotizing epiglottitis predominantly occurs in the immunocompromised host. Laboratory evaluation revealed pancytopenia, and bone marrow biopsy was diagnostic for acute lymphoblastic leukemia. Clinicians should be aware of aggressive infections that identify immunocompromised patients. This case highlights the features of a reemerging pathogen, C diphtheriae.
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PMID:A Case of Necrotizing Epiglottitis Due to Nontoxigenic Corynebacterium diphtheriae. 2605 49

T-cell acute lymphoblastic leukemia (ALL) is an aggressive hematological malignancy, accounting for ~25% of all adult cases of ALL. We herein report a case of T-cell ALL exhibiting aberrant CD34, CD56, CD33 and CD117 expression in addition to T-cell markers, which did not respond to induction treatment. A 55-year-old woman was admitted to our hospital with a sore throat unresponsive to medication for 1 month. The laboratory examination revealed pancytopenia and the peripheral blood smear examination revealed blast cells. On flow cytometric analysis, the blast cells were found to be positive for cytoplasmic CD3, CD2, CD5, CD7, CD34, CD56, CD33 and CD117, and negative for myeloperoxidase, CD13, CD11b, CD15, CD19, CD79a, CD22 and CD10. The patient was diagnosed with T-cell ALL according to the 2008 World Health Organisation classification. The patient did not respond to Hyper-cyclophosphamide, vincristine, adriamycin and dexamethasone (CVAD) course A treatment and succumbed to the disease during Hyper-CVAD course B treatment. To the best of our knowledge, this is the first report of aberrant co-expression of the natural killer cell marker CD56, myeloid cell markers CD117 and CD33 and stem cell marker CD34 in a patient with T-cell ALL. This appears to be associated with an unfavorable outcome, despite the use of intensive chemotherapy.
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PMID:T-cell acute lymphoblastic leukemia with co-expression of CD56, CD34, CD117 and CD33: A case with poor prognosis. 2744 73

Ehrlichiosis, caused by transmission of Ehrlichia chaffeensis to humans through the bite of an infected lone star tick, can lead to secondary hemophagocytic lymphohistiocytosis (HLH), a life-threatening condition caused by uncontrolled activation of the cellular immune system. We describe a child with HLH secondary to ehrlichiosis who developed multiorgan failure and was successfully managed with extracorporeal membrane oxygenation (ECMO). A 9-year-old boy developed headaches, fever, and sore throat after suspected tick exposure. He presented with pancytopenia, elevated ferritin, and soluble interleukin-2 receptor levels, all consistent with HLH. Bone marrow biopsy revealed hemophagocytosis. Polymerase chain reaction was positive for E chaffeensis He developed acute kidney injury, coagulation failure, hepatic insufficiency, and progressive respiratory failure requiring intubation. Due to refractory hypoxemia, he was cannulated for veno-venous ECMO. Continuous veno-venous hemofiltration was used to manage acute kidney injury and fluid overload. He received doxycycline and dexamethasone/etoposide for treatment of ehrlichiosis and HLH, respectively. Plasma exchange was used for thrombocytopenia-associated multiple organ failure. The patient was decannulated after 140 hours of ECMO and subsequently transferred for inpatient rehabilitation after extubation. Review of the Extracorporeal Life Support Organization Registry database identified 6 patients with tickborne diseases who received ECMO for organ support (survival in 3 of 6); ehrlichiosis was not reported in any of these cases. ECMO likely allowed a platform for stabilization and additional therapeutic interventions in this patient.
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PMID:Use of Extracorporeal Support in Hemophagocytic Lymphohistiocytosis Secondary to Ehrlichiosis. 2763 21


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