Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High prevalence of deep vein thrombosis (DVT) in disaster shelters has been reported in the aftermath of earthquakes in Japan. Calf DVT was examined using sonography in the shelters after the Great East Japan earthquake on March 11, 2011. By the end of July 2011, 701 out of 8,630 evacuees suspected with calf DVT, judged by inspections or medical interviews, were examined in 32 shelters, and 190 evacuees were confirmed to have calf DVT. The prevalence of DVT was 2.20%, which was 200 times higher than the usual incidence in Japan. The DVT prevalence seemed to decrease with time. By the end of May, a significantly higher prevalence of DVT was found in tsunami-flooded shelters (109 of 3,871 evacuees; 2.82%) than in non-flooded shelters (53 of 3,155 evacuees; 1.68%). After June, its prevalence was still higher (18/541; 3.33%) in tsunami-flooded shelters than in non-flooded shelters (10/1063; 0.94%). The cause of the high prevalence of DVT was supposed to be dehydration due to the delay in supplying drinking water, vomiting, and diarrhea experienced by the evacuees because of a shortage of clean water to wash their hands. Dehydration was especially noticed in women because they restricted themselves of water intake to avoid using unsanitary toilet facilities. Moreover, crowded shelters restricted the mobility of elderly people, which would exacerbate the prevalence of DVT. Those deteriorated and crowded shelters were observed in tsunami-flooded areas. Therefore, long-term shelters should not be set up in flooded areas after tsunami.
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PMID:High prevalence of deep vein thrombosis in tsunami-flooded shelters established after the great East-Japan earthquake. 2272 76

A 42-year-old man presented to clinic with 1-week history of cough, malaise, loss of appetite and fever. Symptoms started acutely with cough and generalised weakness followed by fever, chills, nausea, vomiting and diarrhoea. He has been healthy before with no chronic illnesses. Further workup disclosed, leucocytosis with 87% eosinophilia, bilateral lung infiltrate, deep venous thrombosis, pulmonary embolism and both right and left biventricular mural thrombi. Extensive workup was done and was consistent with hypereosinophilic syndrome, which explained all his clinical findings. The patient was started on high-dose steroids and responded very well with a complete resolution of symptoms over the course of a few weeks.
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PMID:Loeffler's endocarditis with biventricular mural thrombi. 2408 24

We report a case of an inadvertent increase in the international normalized ratio (INR) after the addition of bismuth subsalicylate for the treatment of diarrhea in an enterally fed patient receiving warfarin therapy. A 56-year-old Caucasian female presented to the trauma intensive care unit (ICU) with multiple lower extremity fractures. Warfarin was initiated for deep vein thrombosis prophylaxis due to the patient's inability to ambulate. The target INR was 2-3. Continuous intragastric enteral feeding was withheld 1 hour before and 1 hour after intragastric administration of warfarin. Bismuth subsalicylate 30 mL every 4 hours was prescribed for diarrhea. Within 3 days after starting bismuth subsalicylate therapy, the patient's INR increased from 2.56 to 3.54 and minor bleeding was noted from the patient's tracheostomy site. No significant change in warfarin dosage, variability in vitamin K intake, or medications that potentially alter warfarin metabolism were present during the unexpected rise in INR. When the bismuth subsalicylate was discontinued, the patient's INR stabilized into the target range on the same warfarin dose given at the time of the supratherapeutic INR. Salicylate displaces warfarin from plasma protein binding sites and may result in a significant increase in INR secondary to redistribution of warfarin to the free active form. Evaluation of this case report using the Drug Interaction Probability Scale and Naranjo Adverse Drug Reaction Probability Scale yielded scores consistent with a probable adverse drug interaction. Bismuth subsalicylate exaggerates warfarin's anticoagulant response and its concurrent use during warfarin therapy should be avoided.
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PMID:Inadvertent exaggerated anticoagulation following use of bismuth subsalicylate in an enterally fed patient receiving warfarin therapy. 2416 22

Primary eosinophilic diseases of the gastrointestinal tract are increasingly being recognised in adults. Bosinophilic colitis is even less understood and presents with highly variable symptoms depending on the depth of mucosal involvement. We are presenting a case of primary eosinophilic colitis presenting with diarrhoea and localized caecal perforation. Pre-operative computed tomography suggested caecal malignancy and possible livier mnetastasis. Patient underwent an emergency laparoscopic right hemicoloectomy and histology revealed eosinophilic colitis. Post- operative period was complicated by pulmonary embolism and deep vein thrombosis. Secondary causes of eosinophilia were appropriately investigated and excluded. She made a good recovery and a post-operative colonoscopy looking for other areas of eosinophilia was normal.
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PMID:Eosinophilic colitis mimicking caecal malignancy. 2567 61

A 34-year-old woman with primary antiphospholipid syndrome was admitted to the Gastroenterology Department of our hospital with fever, acute abdomen, watery diarrhea, and extremely high levels of inflammatory parameters. She had a history of left lower limb deep vein thrombosis and pulmonary embolism and was taking warfarin potassium. Acute gastroenteritis was suspected and an antibiotic was administered, but symptoms progressed. Abdominal ultrasonography showed occlusion of the left hepatic vein and the middle hepatic vein and her D-dimer level was high. Accordingly, Budd-Chiari syndrome was diagnosed and high-dose intravenous infusion of heparin was initiated. Her abdominal symptoms improved and the levels of inflammatory parameters and D-dimer decreased rapidly. It is known that antiphospholipid syndrome can be complicated by Budd-Chiari syndrome that usually occurs as subacute or chronic onset, but acute onset is rare. It is difficult to diagnose acute Budd-Chiari syndrome complicating antiphospholipid syndrome and this complication generally has a poor outcome. However, the present case can get early diagnosis and successful treatment with tight anticoagulant therapy.
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PMID:A Case of Acute Budd-Chiari Syndrome Complicating Primary Antiphospholipid Syndrome Presenting as Acute Abdomen and Responding to Tight Anticoagulant Therapy. 2767 72

Inflammatory bowel disease is associated with extraintestinal manifestations. Among these manifestations is the venous tromboembolism which presents a risk three times more than that presented in general population. We report the case of a 61-year-old male with a history of abdominal pain, chronic diarrhea and fever, with leukocytosis, and fecal samples containing leukocytes, partial ileal stenosis with multiple ulcers in the enteroscopy, with histologic findings compatible with Crohn's disease. The patient has a good outcome with prednisone and maintenence azathioprine, presenting at the fifth month deep venous thrombosis of both lower extremities that resolvewith anticoagulation treatment.
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PMID:[Venous tromboembolism in a patient with Crohn disease with ileal stenosis]. 2771 65

The diagnosis of pulmonary thromboembolism (PE) is often delayed because it is usually misdiagnosed as pneumonia or deep vein thrombosis. We report an unusual case of PE misdiagnosed as viral pleuritis on the first arrival at the emergency department (ED) in our hospital. A 14-year-old girl with no previous significant medical history was referred to the ED with pleuritic and chest pain with low-grade fever 4 days before admission. Echography showed a small amount of left pleural effusion. A 12-lead electrocardiogram was normal. She received a diagnosis of viral pleuritis. Two days before admission, she revisited ED with dyspnea and exacerbated pain. Echography showed slight increase in left pleural effusion. She had the same diagnosis. The chest pain remained at the same level. On the day of admission, she presented to ED with vomiting, watery diarrhea, abdominal pain, chest pain, and respiratory distress. Laboratory findings showed hypoalbuminemia and proteinuria. Echography showed a moderate amount of pleural effusion on both sides and no dilatation of the right cardiac ventricle. Contrast-enhanced chest computed tomography was performed to search the cause of the respiratory distress, which showed filling defects with contrast material in pulmonary arteries. A 12-lead electrocardiogram showed an S1Q3T3 pattern. She received a diagnosis of PE caused by nephrotic syndrome. Pulmonary thromboembolism can mimic infectious pleuritis and lead to misdiagnosis and/or delayed diagnosis. Thus, risk factors of PE should be considered in pediatric patients presenting with symptoms suggesting infectious pleuritis.
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PMID:Pulmonary Embolism Mimicking Infectious Pleuritis. 2835 Jul 20

We report on the course of disease in a young woman, originally admitted with suspected refractory infectious tropical traveler's diarrhea. However, symptoms did not resolve upon either symptomatic or subsequent antibiotic therapy. When neurologic deterioration was observed, imaging studies revealed a dramatic series of thromboembolic events, including intracranial hemorrhage caused by extensive sinus vein thrombosis as well as thrombi of the right cardiac ventricle. Colonic mucosal biopsy samples finally led to the histologic diagnosis of ulcerative colitis. Having excluded thrombophilia or any other disease potentially related to a prothrombotic state, we interpreted the thromboembolic events as secondary to the primary manifestation of the underlying inflammatory bowel disease.The increased risk of thromboembolic complications-especially deep vein thrombosis and pulmonary embolism-in inflammatory bowel disease is well documented in the literature. However, sinus vein thrombosis and cardiac thrombi represent a remarkable dimension of this risk and a rare course of coagulopathy secondary to an acute flare of ulcerative colitis. Still, there is a lack of awareness of this risk, resulting in poor implementation of preventive measures modifying risk factors and allowing for pharmacological prophylaxis. We therefore emphasize that-in line with the 2014 German S3 Guideline-thromboprophylaxis in the setting of an acute flare of inflammatory bowel disease is mandatory and should not be restricted because of safety concerns.
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PMID:Traveler's Diarrhea, vision abnormalities and unsteady gait in a young woman. 2842 9

Antiphospholipid syndrome is characterized by multiple arterial and/or venous thrombotic events, recurrent fetal losses in the presence of antiphospholipid antibodies (aPL). Catastrophic antiphospholipid syndrome is a life-threatening, rare subset of antiphospholipid syndrome when the thrombotic events affect at least three organs, and clinical manifestations develop simultaneously or within a week. Diagnostically, small vessel occlusions can be detected by histopathology in the presence of aPL. Our case report describes an 18-year-old man who has been treated for antiphospholipid syndrome associated with systemic lupus erythematosus (SLE) since 2011. The clinical findings were dominated by recurrent deep vein thrombosis, and severe proteinuria caused by lupus nephritis, accompanied by mild serological and laboratory findings. The patient was hospitalized in March 2014 because of severe thrombocytopenia and infective diarrhoea. At this time the renal functions deteriorated rapidly. Simultaneously, left upper extremity paresis was observed; computed tomography showed ischaemic lesions in the territory of the middle cerebral artery. Abdominal discomfort and pain occurred. On computed tomography scan ischaemic lesions were seen in the spleen, the right kidney and the coeliac trunk. Laboratory and serological findings verified the presence of aPL and anti-DNA antibodies, anaemia and thrombocytopenia. Based on the above-mentioned clinical and laboratory findings, the diagnosis of catastrophic antiphospholipid syndrome was established. Anticoagulation, corticosteroids and plasma exchange treatment, as well as haemodiafiltration were initiated. Although the thrombotic cascade decelerated following these interventions, we could not see an improvement in the renal function. Rituximab treatment was started, leading to a significant improvement in renal function. After 5 weeks of treatment the patient was discharged from hospital.
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PMID:Microthrombotic renal involvement in an SLE patient with concomitant catastrophic antiphospholipid syndrome: the beneficial effect of rituximab treatment. 2963 99

Glucagonoma is a rare and slow-growing pancreatic tumor that usually manifests as glucagonoma syndrome. It is mainly characterized by a typical Dermatosis named necrolytic migratory erythema (NME), Diabetes and glucagon oversecretion. Deep vein thrombosis and Depression complete this set. We report the case of an advanced glucagonoma with liver spread, where all these 4D symptoms occurred but a chronic secretory Diarrhea was the most relevant feature. A 65-year-old man was referred to our center to investigate multiple hepatic nodules evidenced by abdominal tomography. He had a recent diagnosis of diabetes and complained of significant weight loss (25 kg), crusted skin lesions and episodes of a large amount of liquid diarrhea during the past 6 months. On admission, there were erythematous plaques and crusted erosions on his face, back and limbs, plus angular cheilitis and atrophic glossitis. The typical skin manifestation promptly led dermatologists to suspect glucagonoma as the source of our patient's symptoms. A contrast-enhanced abdominal computed tomography showed a hypervascularized pancreatic lesion and multiple hepatic nodules also hypervascularized in the arterial phase. Despite initial improvement of diarrhea after subcutaneous octreotide, the patient's impaired nutritional status limited other therapeutic approaches and he died of respiratory failure due to sepsis. His high levels of serum glucagon were not yet available so we performed an autopsy, confirming the diagnosis of metastatic glucagonoma with NME on histology. Chronic diarrhea is not a common feature in glucagonoma syndrome; however, its severity can lead to serious nutritional impairment and set a poor outcome.
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PMID:Diarrhea: a missed D in the 4D glucagonoma syndrome. 3180 36


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