Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 99 cases of viridans streptococcal endocarditis encountered during the period of 1973 and 1990 at the Veterans General Hospital-Taipei were reviewed to evaluate its prognostic factors. Applying strict clinical and laboratory criteria, 24 cases were categorized as definite, 44 probable, 23 possible and 8 likely. The symptoms were frequently subtle and atypical but initial laboratory tests gave useful indications: 69.1% with leukocytosis, 78% with anemia, 58.5% with elevation of LDH level, 88.9% with elevation of ESR value and 100% with elevation of CRP level. Furthermore, 32.4% of the cases demonstrated proteinuria and 67.4% microscopic hematuria. Seventy-three of the subjects had a history of underlying heart disease, predominantly rheumatic heart disease. Histological examination and echocardiography revealed that 51 patients suffered from vegetative endocarditis, 7 (13.7%) of whom were found to have anatomically confirmed vegetations without initial echocardiographic evidence, Vascular events were seen in 61 cases (61.6%): peripheral stigmata (32 cases), cerebral vascular accidents (17 cases), pulmonary embolism (10 cases) and others (2 cases). The overall mortality rate was 18.2%. Congestive heart failure with embolization was the most common cause of death in this group. The presence of vegetation was not well correlated with embolic events. There was no statistically significant association between the mortality and the following characteristics: age, sex, underlying heart disease, evidence of echocardiographically detected vegetations, major surgical intervention and recurrent cases except for embolic events (p less than 0.01). In conclusion, viridans streptococcal endocarditis complicated embolic events usually presented with a fulminant course and a grave outcome.
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PMID:Overview of viridans streptococcal endocarditis: clinical analysis of 99 cases. 165 35

The patient was a 29-year-old woman. She was well until autumn 1983, when she presented with polyarthralgia, fever above 39 degrees C, hepatosplenomegaly, swelling of lymphnode and salmon pink rash. Laboratory tests revealed marked leucocytosis with shift to the left, elevated ESR, strong positivity of CRP and abnormal liver function tests. However, anti-nuclear antibody and RA factor were negative. She was diagnosed as adult onset Still's disease (AOSD) by characteristic clinical course and laboratory data. During her disease course these abnormal findings could be well controlled neither by nonsteroidal anti-inflammatory drugs, immunosuppressive agents nor corticosteroids. Two and half years after the first admission, she began to complain of dry cough, dyspnea on efforts. Auscultation revealed an increased pulmonic sound and systolic murmur of cardiac apex. Chest X-Rays showed enlarged main pulmonary arteries. The lung fields were normal. Pulmonary function tests gave no evidence of a significant obstructive or restrictive defect but showed the low DLco and hypoxemia. Ventilation-perfusion lung scanning failed to reveal pulmonary embolism. Finally, right heart catheterization confirmed the pulmonary precapillary hypertension. Her pulmonary hypertension has progressed rapidly, strongly suggesting poor prognosis. Her pulmonary hypertension associated with no apparent parenchymal involvement was thought to be caused by a pulmonary vascular change probably related to AOSD. This case is a first case of AOSD with pulmonary hypertension.
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PMID:[A case of adult Still's disease with pulmonary hypertension]. 237 40

In this hospital based study, we analysed the clinical records of 104 patients having various spinal cord diseases seen between 1988 and 1993 with a view to delineating diagnostic and prognostic features. The patients comprised 80 males and 24 females with a mean age of 45 years. The mean duration of disease at presentation was 11 months and the average duration of stay in hospital was five months. Spondylotic myelopathy (31 subjects) predominated. It showed cervical predilection, infrequent sphincteric dysfunction and low ESR. Tuberculous disease of the spine (26 subjects) was next in frequency. The presentation of the TB cases was similar to those of neoplastic causes but the latter had a worse prognosis. There was a predilection for the dorsal spine and a high ESR. Myelitis occurred in the younger age group, showed dorsal spine predilection and relatively low ESR. The prognostic factors include duration of disease at entry, duration of hospital stay, presence of complication, motor power above grade three and absence of flacidity. The preventable causes of death include: deep vein thrombosis with subsequent pulmonary embolism and septicaemia.
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PMID:Non-traumatic spinal cord diseases in Ibadan, Nigeria: aetiology and prognostic factors. 778 67

A 66-year-old man was admitted to our department with left abducens palsy and pain in the territory of the left trigeminal nerve. He had a history of left mandibular osteomyelitis that had been treated for five years in the dental department. However, the osteomyelitis was resistant to therapy. Two months before this admission, he had an infectious aneurysm of the left extracranial carotid artery with occlusion. On admission, the ESR was 140 mm/hour. P-ANCA and antinuclear antibody were negative. Lumbar puncture revealed elevated cell counts (43% neutrophils) and protein. Microbiological studies were negative. Cranial MR images showed an enhanced lesion in the left cavernous sinus. His condition gradually improved with high dose of penicillin and low dose of corticosteroid. However, he died of pulmonary embolism after 81 days. At autopsy, the left extracranial carotid aneurysm was highly fibrose. The left CCA, ICA, and ECA were occluded from the origin of the left common carotid artery to the ICA in the cavernous sinus. There were also fibrosis, hemosiderin, and macrophages around these arteries, and parts of these arteries were destroyed. The left cavernous sinus lesion was also highly fibrose. These pathological findings indicated that there was old inflammation around the left extracranial carotid aneurysm, left carotid artery, and left cavernous sinus. We believe that the left cavernous sinus syndrome in our patient was caused by left carotid artery vasculitis induced by the left infectious extracranial carotid aneurysm. We also believe that this infectious aneurysm was caused by the left mandibular osteomyelitis.
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PMID:[A case of cavernous sinus syndrome following a mycotic aneurysm of extracranial carotid artery]. 1196 46