Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Budd-Chiari syndrome (BCS) with hepatic vein occlusion is a rare disorder that can effectively be treated in advanced stages with orthotopic liver transplantation. We report on 16 patients who received 18 liver grafts and were followed up for at least 2 years. In 7 patients a hematological disorder was confirmed by bone marrow biopsy. One patient died after 4 months due to cytomegalovirus pneumonia; another patient died after 2 years due to progressive liver failure after portal vein thrombosis. The actuarial 5-year survival rate is 87.5% compared to 85.3% in all other 710 orthotopic liver transplantations performed from September 1988 to December 1995 at our institution. Anticoagulation consisted of intravenous heparin and overlapping continuation with dicoumarin. Three patients received hydroxyurea for thrombocytosis, one patient for 1 week only early after the transplantation. Two postoperative abdominal hemorrhages required laparotomy. Two patients had to be retransplanted, one for thrombosis of the hepatic artery and portal vein after discontinuation of dicoumarin due to GI bleeding and one for hepatic vein thrombosis after insufficient dicoumarin intake. Terminal BCS represents a good indication for orthotopic liver transplantation; however, life-long, closely monitored anticoagulation is essential.
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PMID:[Treatment of advanced Budd-Chiari syndrome by liver transplantation]. 1002 64

We investigated to clarify the clinical findings, course and therapeutic effect in the patients with MPO (myeloperoxidase)-ANCA (anti-neutrophil cytoplasmic antibody) associated vasculitis syndrome. We analyzed clinical findings and data of 19 cases of MPO-ANCA associated vasculitis. These patients were diagnosed with clinical symptoms (fever, arthralgia, body weight loss, etc.), laboratory data (high titer of CRP, leukocytosis, thrombocytosis, and high titer of MPO-ANCA) and pathologic findings of necrotizing vasculitis. They were 14 male and 5 female aged 18 to 84 years (mean 65 years) and were treated with prednisolone and immunosuppressive agents, and additional therapy included pulse therapy and plasma exchange. Seven cases were dead within 3 months. Post-mortum examination showed that these cases died of pneumonitis, cerebral events and gastric bleeding. There was no mortal case induced by over-immunosuppression. In survival cases, the MPO-ANCA levels decreased rapidly after these therapies and these antibodies were maintained low levels (360 to 25 EU/l). Comparison of fatal cases and survival cases, there were difference in the initial dose of prednisolone (27 mg/day vs. 56 mg/day), the ratio of double filtration plasmapheresis (14% vs. 42%), and the ratio of immunosuppressive therapy (14% vs. 83%). The measurement of MPO-ANCA is useful makers of the diagnosis and effectiveness of the therapy in patients with MPO-ANCA associated vasculitis. We recommend the aggressive therapy, including prednisolone, immunosuppressive agents and plasma exchange for MPO-ANCA associated vasculitis. We believe that the aggressive therapy improve the survival rate of the patients with MPO-ANCA associated vasculitis.
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PMID:[Therapeutic effect and clinical findings in patients with MPO-ANCA associated vasculitis syndrome]. 1078 59

Recently, new broad spectrum carbapenem has been investigated on a world-wide scale for the treatment of moderate to severe infections. In the neonatal intensive care units the extensive use of third generation cephalosporins for therapy of neonatal sepsis may lead to rapid emergence of multiresistant gram-negative organisms. We report the use of meropenem in 35 infants with severe infections due to Acinetobacter baumanii and Klebsiella pneumoniae. All gram negative bacteria were resistant to ampicillin, amoxicillin, ticarcilin, cefazoline, cefotaxime, ceftazidime, ceftriaxone and aminoglycosides. Eighty two percent of the cases (29/35) were born prematurely. Assisted ventilation was needed in 85.7% (30/35). All infants deteriorated during their conventional treatment and were changed to meropenem monotherapy. Six percent (2/35) died. The incidence of drug-related adverse events (mostly a slight increase in liver enzymes) was 8.5%. No adverse effects such as diarrhea, vomiting, rash, glossitis, oral or diaper area moniliasis, thrombocytosis, thrombocytopenia, eosinophilia and seizures were observed. At the end of therapy, overall satisfactory clinical and bacterial response was obtained in 33/35 (94.3%) of the newborns treated with meropenem. Clinical and bacterial response rates for meropenem were 100% for sepsis and 87.5% for nosocomial pneumonia. This report suggests that meropenem may be a useful antimicrobial agent in neonatal infections caused by multiresistant gram negative bacilli. Further studies are needed to confirm these results: Meropenem, newborn, sepsis and nosocomial infection.
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PMID:Meropenem in neonatal severe infections due to multiresistant gram-negative bacteria. 1123 30

A 77-year-old man was referred to our hospital because of elevated LDH and leukoblastosis in the peripheral blood in June 2002. Physical examination revealed neither hepatosplenomegaly nor superficial lymphadenopathy. A bone marrow film showed dysmegakaryocytopoiesis with many micromegakaryocytes and MPO-positive blasts appearing in 20-30% of NCC. A diagnosis of MDS (RAEB-t) was made. Blastic cells were positive for CD13, 33, 34 and HLA-DR. Karyotypic analysis at diagnosis revealed 46XY, inv(3) (q21q26), t(9;22) (q34; q11) and minor-BCR/ABL chimeric m-RNA was detected by RT-PCR. Mild chemotherapy (low dose Ara-C etc) was given but the disease progressed to the AML stage with thrombocytosis in August. In September imatinib was given because of Ph positivity, but the effect was transient. In October massive leukocytosis with myeloblastosis was uncontrollable. In December 2002 the patient died of pneumonia, after a total course of 7.5 months. This rare case with Ph chromosome and 3q21q26 syndrome showed a poor prognosis as previously reported.
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PMID:[3q21q26 syndrome with minor-BCR/ABL type Ph chromosome]. 1497 33

The authors report the case of a young 35 year-old male patient, investigated due to thrombocytosis for three years. First the diagnosis of chronic myeloproliferative disease was made. The diagnosis of familial adenomatous polyposis was only evident in advanced stage of the disease. Upper abdominal US, abdominal CT, double-contrast barium enema examination and colonoscopy proved advanced synchronous colorectal cancers (sigmoid and descending colon) with liver metastases along with polyposis throughout the whole large bowel. Days after the diagnosis was made the patients condition deteriorated rapidly and he died with septic symptoms suggesting bowel perforation and pneumonia. Beside the case report the authors try to give a short overview of the current literature of relatively rare but potentially fatal hereditary colon cancer syndromes to awake the attention of the clinicians to investigate more cautiously the background of unexplained clinical-laboratory signs in young adults.
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PMID:[Familial adenomatous polyposis coli--case report]. 1518 36

We report a case of unresolved streptococcal pneumonia in a patient taking anagrelide for essential thrombocythaemia. Resolution only occurred after discontinuing anagrelide and the institution of corticosteroid therapy, which resulted in dramatic improvement. There has been only one previous case report of anagrelide causing hypersensitivity pneumonia. We postulate this patient suffered a 'double hit' from streptococcal infection and anagrelide.
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PMID:'Double hit' from streptococcal pneumonia and hypersensitivity pneumonitis associated with anagrelide. 1643 Apr 63

Amoxicillin/Clavulanate related extreme thrombocytosis during the treatment of pneumonia has never been reported. We present a 54-year-old patient who was admitted due to pneumonia, and was treated with amoxicillin/clavulanate IV and 3-day course of 500 mg azithromycin. Despite clinical and radiological evidence showing that pneumonia improved, thrombocytes increased rapidly. After stopping the antibiotic, the thrombocytes returned gradually to normal. Considering the clinical course, we propose that this extreme thrombocytosis was caused by the administration of amoxicillin/clavulanate. We describe this rare and unique patient and review the literature.
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PMID:Extreme thrombocytosis under the treatment by amoxicillin/clavulanate. 1711 Dec 42

When an infected patient suffers from thrombocytosis, it is very difficult to identify beta-lactam antibiotic induced cases of the disease and separate these from the possibility that the disease is an acute-phase reaction in the infected patient. We present the case of a 54-year-old man who was treated with ceftazidime for pneumonia and developed thrombocytosis during the treatment course. Thrombocytosis persisted until ceftazidime was discontinued, despite clinical and radiological evidence showing that the pneumonia had greatly improved. The Naranjo probability scale indicates ceftazidime as the possible cause of the thrombocytosis in our patient. Although no obvious complications occur in most patients, we should pay close attention to the possibility of adverse reactions and evaluate whether the infection is treated with the appropriate antibiotics.
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PMID:Marked thrombocytosis during treatment with ceftazidime for pulmonary infection. 1761 67

Atypical community-acquired pneumonia (CAP) may be caused by zoonotic or nonpulmonary pathogens. However, atypical pathogens are systemic infectious disease accompanied by pneumonia in contrast with typical bacterial pathogens with infection limited to the lungs and absent extrapulmonary findings. Clinically and radiologically, the atypical CAP pathogens that most closely resemble each other are psittacosis, Q fever, and Legionnaires' disease. Psittacosis can usually be readily suspected or eliminated on the basis of a recent psittacine bird contact history. The 2 atypical pneumonias that most closely resemble each other clinically are Q fever and Legionnaires' disease. The epidemiology of Q fever is related to livestock, and sporadic cases are related to contact to parturient cats. In nonendemic areas, Q fever CAP mimics Legionnaires' disease most closely. Both Q fever and Legionella CAP have several clinical and laboratory features in common. However, there are subtle but important differences that allow the astute clinician to differentiate between these 2 disorders on the basis of clinical and nonspecific laboratory findings before definitive diagnostic tests results are reported. We report a case of severe Q fever CAP mimicking Legionnaires' disease in a young adult normal host. Her initial zoonotic contact history was negative, and her clinical presentation suggested Legionnaires' disease as the most likely diagnosis. Against the diagnosis of Legionnaires' disease was the patient's age and occurrence of the disease in spring time. In contrast, Legionnaires' disease is usually an infection of older individuals and occurs in late summer/fall. Although the patient did not have splenomegaly, a common finding in Q fever CAP, she did have mild hepatomegaly. Hepatomegaly is a uncommon in Q fever CAP but is not a feature of Legionnaires' disease. In the absence of a positive zoonotic contact history, the cardinal findings pointing to the diagnosis of Q fever in this case were "multiple round opacities" on chest computed tomography scan and thrombocytosis during her hospitalization. Against the diagnosis of Legionnaires' disease was the absence of hypophosphatemia and highly elevated ferritin levels. In patients with atypical pneumonias in whom the clinical presentation and nonspecific laboratory findings suggest Legionnaires' disease, but in addition have findings not associated with Legionnaires' (eg, hepatomegaly, thrombocytosis), Q fever serology should be ordered. We conclude that Q fever may closely mimic Legionnaires' disease. Severe atypical CAP with "multiple round opacities" on chest x-ray/computed tomography chest scan with elevated anti-smooth muscle antibodies or thrombocytosis should suggest the diagnosis of Q fever and prompt specific testing for Q fever. Rarely, Q fever CAP may be associated with elevated cold agglutinin titers.
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PMID:Severe Q fever community-acquired pneumonia (CAP) mimicking Legionnaires' disease: Clinical significance of cold agglutinins, anti-smooth muscle antibodies and thrombocytosis. 1957 8

The most common cause of nonzoonotic atypical community-acquired pneumonia (CAP) is Mycoplasma pneumoniae. M. pneumoniae CAP is most common in young adults but may occur at any age. Like other atypical CAPs, M. pneumoniae is associated with a characteristic pattern of extrapulmonary organ involvement and nonspecific laboratory tests. M. pneumoniae CAP is frequently accompanied by gastrointestinal manifestations (eg, loose stools/diarrhea), nonexudative pharyngitis, or skin involvement (ie, erythemamultiforme). Central nervous system involvement with M. pneumoniae is rare and accompanied by highly elevated cold agglutinin titers. Cardiac, hepatic, and renal involvement are not features of M. pneumoniae CAP. Because M. pneumoniae CAP is most frequent in ambulatory young adults, it is an easily overlooked diagnosis in elderly patients hospitalized with CAP. The hallmark clinical finding of M. pneumoniae CAP is protracted nonproductive cough. The characteristic nonspecific laboratory test finding uniquely associated with M. pneumoniae CAP is elevated cold agglutinin titers. Seventy-five percent of patients with M. pneumoniae infection have elevated cold agglutinin titers. However, the absence of elevated cold agglutinin titers does not argue against the diagnosis of M. pneumoniae. If cold agglutinins are present in a patient with CAP, the higher the cold agglutinin titer is (>1:64), the more likely the cold agglutinins are due to M. pneumoniae. Q fever is the only other atypical CAP that is rarely associated with cold agglutinins. We present a hospitalized patient with CAP in whom all microbiologic and serologic diagnostic test results were negative during the first week of her hospitalization. M. pneumoniae CAP was not suspected because of her age. Her initial M. pneumoniae immunoglobulin-M and cold agglutinin titers were negative. During the second week of hospitalization, an increased platelet count was noted. It is a common misconception that acute thrombocytosis is an acute phase reactant. Her acute thrombocytosis increased and persisted. The diagnostic clue to the cause of this hospitalized patient with CAP was acute thrombocytosis. In a patient with CAP, acute thrombocytosis is usually associated with Q fever pneumonia and less commonly with M. pneumoniae. If Q fever can be excluded on the basis of a recent/proximate zoonotic vector contact history, then acute thrombocytosis is an important clue to M. pneumoniae CAP. Acute thrombocytosis due to M. pneumoniae and Q fever occurs during weeks 1 and 2 of the infection. In patients with CAP, acute thrombocytosis that occurs during weeks 1 and 2 of the illness should suggest M. pneumoniae in patients without recent zoonotic vector contact history.
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PMID:Mycoplasma pneumoniae community-acquired pneumonia (CAP) in the elderly: Diagnostic significance of acute thrombocytosis. 1975 96


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