Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old woman who had until recently been healthy, was transferred to our hospital by ambulance with complaints of dyspnea and pain in both lower limbs. She had 1-week history of sore throat, fever and cough. She had been to a neighboring clinic three days previously, and had been prescribed some medication for bronchitis, but her symptoms had not improved. By the time of admission, she was already in shock and had severe respiratory failure. Laboratory data showed renal dysfunction, disseminated intravascular coagulation, CPK elevation and severe metabolic acidosis. Chest x-ray and CT films revealed consolidation of the entire right lung field. The patient was quickly intubated and we began mechanical ventilation. We immediately initiated broad-spectrum antibiotics, immunogloblin, dopamine hydrochloride and gabexate mesilate, but she died 7 hours later. From cultures of blood and sputum taken from the patient, Streptococcus pyogenes was isolated. On the basis of these clinical and bacteriological findings, we confirmed a diagnosis of pneumonia and toxic shock syndrome caused by Streptococcus pyogenes (STSS). Serologically her M protein was serotyped as M1, and with regard to Streptococcal pyrogenic exotoxin genes were identified as speA and speB. These serological findings were consistent with the most frequent type that causes STSS. In spite of the uncommon cause of community-acquired pneumonia, Streptococcus pyogenes can potentially affect healthy individuals. The pneumonia can be complicated with STSS and so the clinical course may be severe and fulminant. The evidence acquired from this case suggests that in the event of severe pneumonia with shock, we should be aware that this may represent the presence of Streptococcus pyogenes and/or toxic shock syndrome.
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PMID:[Case of severe streptococcus pyogenes pneumonia with streptococcus toxic shock syndrome]. 1859 96

The retinoic acid syndrome (RAS) is an unpredictable but frequent complication which may develop after administration of all-trans retinoic acid (ATRA) most commonly in patients with acute promyelocytic leukaemia (APL). In this review, we describe the incidence, predictive factors, clinical course, outcome and treatment of RAS in patients with APL treated with ATRA. The incidence of RAS in patients receiving ATRA is about 14-16%, with an associated mortality of about 2%. Initial high white blood cell (WBC) count, rapidly increasing WBC count and/or the presence of the CD 13 expression on leukaemic cells may help in identifying patients likely to develop RAS. Concurrent chemotherapy will probably decrease the risk of developing RAS but often exacerbates bleeding, leading to leucocytosis, thrombocytopenia, disseminated intravascular coagulation and fibrinolysis. Prophylactic steroids are not recommended but prompt administration of steroids at the first sign of unexplained dyspnea, fever, weight gain or pulmonary infiltrate, is critical. Liposomal ATRA is being investigated to induce haematological cure in APL without chemotherapy and to reduce the incidence of RAS but further validation of its usefulness is necessary.
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PMID:Retinoic acid syndrome: a review. 1861 50

We experienced 2 patients of valvular heart disease in Parkinson's patients taking cabergoline. Patient 1 was a 79-year-old woman who began taking 4 mg cabergoline daily after being diagnosed with Parkinson's disease (PD) in June 2003. She presented with dyspnea in November 2005. The patient had cardiomegaly, pulmonary congestion, and pleural effusion, and an echocardiogram showed valvular heart disease in the form of aortic regurgitation (AR) (grade I), tricuspid regurgitation (TR) (grade I), and mitral regurgitation (MR) (grade III). Cabergoline was thought to have caused these phenomena, so it was replaced with pramipexole, and after administration of diuretics and angiotensin-converting enzyme inhibitors (ACEIs) the patient's symptoms gradually disappeared. MR, AR and TR also disappeared 3 months later. Patient 2 was a 74-year-old woman who presented with sluggish movement in April 2001 and subsequently developed Parkinson's. While being administered 700 mg levodopa (Menesit) and 4 mg cabergoline, the patient presented with shortness of breath in April 2005. An echocardiogram showed valvular heart disease in the form of MR (grade I) and TR (grade I). Heart function improved with the administration of diuretics. However, heart function again worsened in November 2005, and the patient presented with edema of the lungs and lower limbs. An echocardiogram in January 2006 showed worsening MR (grade III) and TR (grade II), and the patient also had pulmonary hypertension. ACEIs were administered along with diuretics and cabergoline was replaced with pramipexole, but the patient also developed malignant syndrome and disseminated intravascular coagulation (DIC) and later died. Patient 2 is the first case in Japan of death due to heart failure caused by the side effects of cabergoline. Caution is usually needed when treating a Parkinson's patient for valvular heart disease due to a dopamine agonist, and periodic checks for heart murmurs and echocardiography are crucial. When signs of heart failure develop during treatment with an ergot preparation of dopamine agonist, it is essential to immediately either stop the administration of the ergot preparation or change to a non-ergot preparation of dopamine agonist.
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PMID:[Two cases of patients with Parkinson's disease developing valvular heart disease while taking cabergoline]. 1871 82

This is a report of 2 cases of Ludwig's angina. An Indonesian young female patient developed severe stridor after oral examination. Then she underwent tracheostomy and developed post decannulation dyspnea due to huge surgical emphysema. The second case regards an Indian young male who developed disseminated intravascular coagulation and died from hemorrhage. The objectives of our cases presentation are to avoid mouth examination of Ludwig's angina if we are not ready for performing tracheotomy and to be aware of the possible development of disseminated intravascular coagulation and post decannulation emphysema.
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PMID:Unusual outcome of Ludwig's angina. 1908 39

Amniotic fluid embolism is one of the most catastrophic complications of pregnancy. First described in 1941, the condition is exceedingly rare and the exact pathophysiology is still unknown. The etiology was thought to be embolic in nature, but more recent evidence suggests an immunologic basis. Common presenting symptoms include dyspnea, nonreassuring fetal status, hypotension, seizures, and disseminated intravascular coagulation. Early recognition of amniotic fluid embolism is critical to a successful outcome. However, despite intensive resuscitation, outcomes are frequently poor for both infant and mother. Recently, aggressive and successful management of amniotic fluid embolism with recombinant factor VIIa and a ventricular assist device, inhaled nitric oxide, cardiopulmonary bypass and intraaortic balloon pump with extracorporeal membrane oxygenation have been reported and should be considered in select cases.
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PMID:Amniotic fluid embolism. 1937 42

Obstetric crisis includes hemorrhagic shock, embolisms and difficult airway. Life will be rapidly threatened with disseminated intravascular coagulation, multiple organ failure or systemic inflammatory response syndrome in these crises. In the face of the crisis, repeated evaluation of parturients and differential diagnosis are necessary along with fetal heart monitoring. For evaluation of bleeding, one should notice that the visual estimation of vaginal bleeding does not reflect the extent of intravascular volume deficit. Treatments for hemorrhagic shock include fluid replacement, blood transfusion as well as fresh frozen plasma, platelet, anticoagulants, anti-thrombin III, and protease inhibitors. When bleeding is still uncontrollable, arterial embolization or hysterectomy will be considered. Embolic disorders are another cause of maternal mortality. The signs and symptoms are all similar (dyspnea, cyanosis and sudden cardiovascular collapse). Strategies against the embolism will be basically symptomatic therapy. The physiological change with pregnancy results in the need of careful pre-anesthetic airway evaluation for parturients. A difficult or failed intubation drill is also extremely important. Recently, laryngeal mask airway has been successfully used in these parturients. During resuscitation of a pregnant woman, left uterine displacement is essential. For a patient who has not responded after 4 to 5 minutes of ACLS, immediate cesarean delivery should be considered.
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PMID:[Crisis management during obstetric surgery]. 1946 96

We report the case of a primary gastrointestinal stromal tumor (GIST) found in the greater omentum of an extremely elderly woman. A 99-year-old woman with a history of heart failure and renal failure presented with dyspnea and disturbance of consciousness. A tumor located between the stomach and spleen had been detected by abdominal computed tomography three years previously. After admission, she received oxygen supplementation and diuretics. However she died of heart failure and disseminated intravascular coagulation on the 31st day of hospitalization. Autopsy was performed on the same day. A large mass measuring 12.5 x 7.0 x 7.5 cm was revealed, originating from the greater omentum. Histopathologically, it was composed of spindle cells with the nuclei showing a focal palisading pattern, however there were no mitoses. Immunohistochemically, the tumor was positive for c-kit. The tumor was diagnosed as a primary GIST of the greater omentum.
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PMID:[A case of a primary gastrointestinal stromal tumor (GIST) found in the greater omentum of a 99-year-old woman]. 1949 25

A 76-year-old woman was admitted to our hospital with infiltrations evident in the right lower lobe on chest computed tomography. Bronchoscopic biopsy showed lymphoma of mucosa-associated lymphoid tissue (MALT). Lymphoma of the pulmonary MALT became enlarged at 8 months after diagnosis and dyspnea developed. Four courses of chemotherapy(rituximab+ cladribine)resulted in a partial response. However, 14 months after the chemotherapy, she developed multiple lung and liver tumors accompanied by disseminated intravascular coagulation syndrome. A histological examination of bone marrow aspiration showed small cell carcinoma. We administered one course of carboplatin and etoposide, but bone marrow suppression was so severe that further chemotherapy was precluded. To our knowledge, this is a rare case of small cell lung cancer arising from the treatment of lymphoma of pulmonary MALT.
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PMID:Small-cell lung cancer arising after chemotherapy for a patient with lymphoma of pulmonary mucosa-associated lymphoid tissue-a case report. 1983 33

An 80-year-old woman was admitted with dyspnea. She had been treated with oral prednisolone for bronchial asthma. She was intravenously treated with dexamethasone. On the 9th day, she presented oliguria and thrombocytopenia. She was diagnosed as dehydration and disseminated intravascular coagulation, and was treated with hydration and heparin infusion. On the 12th day, she presented macroscopic hematuria and melena. Cystoscopy revealed hemorrhagic cystitis. Bone marrow aspiration showed hemophagocytosis. Serum antigen of cytomegalovirus (CMV) was positive. CD4+ T cell count was very low (40/microL). She was diagnosed as disseminated CMV infection, and was treated with gancyclovir and immunoglobulin infusion. On the 14th day, she died of pneumonia. This is the first report of fatal CMV infection during corticosteroid therapy for bronchial asthma.
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PMID:Fatal cytomegalovirus infection with CD4+ T-lymphocytopenia during corticosteroid therapy for bronchial asthma. 2015 55

An 82-year-old woman was admitted to the hospital with dyspnea and fatigue. She had been given amlodipine, furosemide, candesartan, pravastatin and roxatidine acetate for two months in an other hospital. Chest CT showed patchy consolidations throughout the entire lungs. We suspected drug-induced pneumonia, and treated her with prednisolone under mechanical ventilation. The pulmonary consolidations eventually improved, but on the 15th hospital day the patient developed thrombocytopenia and disseminated intravascular coagulation (DIC). Heparin flushes had been performed since the first hospital day. After these were stopped, her platelet count became normal and the patient recovered from DIC. The clinical course, and the fact that testing for heparin-induced thrombocytopenia (HIT) antibodies was positive, supported the diagnosis of HIT and DIC. We report a rare case of HIT and DIC during treatment for drug-induced pneumonia.
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PMID:[Heparin-induced thrombocytopenia and disseminated intravascular coagulation in a patient with drug-induced pneumonia]. 2018 49


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