Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Superior mesenteric vein thrombosis (SMVT) is an uncommon but important clinical entity that can induce ischemia or infarction of the small and large bowel. It is rare and accounts for 5-15% of mesenteric vascular occlusions. Bowel infarction due to SMVT can present as an acute abdominal disease, requiring urgent laparotomy with resection of the intestinal segment affected. However, the clinical diagnosis of this event remains difficult and invariably requires specific imaging investigations in order to be able to treat the condition as soon as possible. SMVT without bowel infarction can present as persistent, non-specific abdominal pain and nausea with minimal clinical signs, affecting young individuals without any known predisposing disorder, where laparotomy is not an urgent indication. We report a case of a young adult man with SMVT due to a hypercoagulable state (protein S deficiency), in whom an early diagnosis and appropriate anticoagulant treatment prevented any further extension of the thrombotic process and limited the hemorrhagic infarction of the ileum, which simply required a segmental resection.
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PMID:Spontaneous superior mesenteric vein thrombosis (SMVT) in primary protein S deficiency. A case report and review of the literature. 1083 45

Mesenteric vein thrombosis is generally difficult to diagnose and can be fatal. A case of extensive thrombosis of the mesenteric and portal veins was diagnosed early and successfully treated in a 26-year-old man with Down syndrome who was admitted to hospital because of abdominal pain, severe nausea and high fever. Ultrasonography revealed moderate ascites, and there was minimal flow in the portal vein (PV) on the Doppler examination. Computed tomography (CT) showed remarkable thickening of the walls of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, combined thrombolysis and anticoagulation therapy without surgical treatment was chosen. Urokinase was administered intravenously and later through a catheter in the superior mesenteric artery. Heparin and antibiotics were given concomitantly. The patient's symptoms and clinical data improved gradually. After 10 days, CT revealed that collateral veins had developed and the thrombi in the distal portions of the mesenteric veins had dissolved, although the main trunk of the PV had not recanalized. The only risk factor of thrombosis that was detected was decreased protein S activity.
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PMID:Extensive mesenteric vein and portal vein thrombosis successfully treated by thrombolysis and anticoagulation. 1185 47

A-38-year-old man suddenly developed nausea, vomiting and vertigo during chiropractic neck manipulation. This was followed by right hemiplegia, right deep sensory disturbance and left hypoglossal nerve palsy, consistent with the medial medullary infarction (Dejerine syndrome). The MRI revealed infarction at left medial part of the medulla. The vertebral angiogram and MRA showed marked narrowing of the left vertebral artery. X-rays of the cervical spine showed no spondylosis, dislocation nor osteolysis of the odontoid process. The serological studies, including lupus anticoagulant, protein C, and protein S gave normal results. Although vascular accidents involving the brain stem after chiropractic neck manipulation have been reported since Pratt-Thomas and Berger, previous reports are still rare. In them lateral medullary infarction (Wallenberg syndrome) is probably the most common case. On the other hand, medial medullary syndrome (Dejerine syndrome) is absolutely rare. To our knowledge, the only one report has been made by Watanabe and his colleagues before our present case. The mechanism was suggested that rotation and tilting of the neck stretches and compresses the vertebral artery at the cervical joint causing injury to the vessel, with an intimal tearing, dissection, and pseudoaneurysm formation. Consequently, the present case may be caused by injury to the left vertebral artery with an intimal tearing during neck manipulation sufficient to cause disection and subsequent infarction of the brain stem.
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PMID:[The medial medullary infarction (Dejerine syndrome) following chiropractic neck manipulation]. 1268 91

We report clinical findings, risk factors and neurological and cognitive long-term outcome in three Italian children aged 7, 8 and 5, respectively, who experienced cerebral venous sinus thrombosis (CVST). All children presented with headache, associated to nausea, vomiting and papilloedema. None suffered from epileptic seizures. In two of them a paresis of the sixth cranial nerve with diplopia was found. Diagnosis was confirmed by magnetic resonance imaging angiography (angio MRI) in all cases. In all patients plasma levels of protein C, protein S, antithrombin III (AT III), antiphospholipid antibodies (ApA) and homocysteine were detected. Furthermore, factor V Leiden mutation, prothrombin mutation G20210A and MTHFR mutation were searched for. A Protein C reduction was detected in all patients at onset; this finding, however, was not confirmed at follow-up in all of them. At one-year follow-up, neurological examination was normal in all children and neuropsychological assessment, aimed at excluding linguistic and non-linguistic cognitive deficits, revealed normal performances in two of them. In the third child, cognitive assessment confirmed a previously diagnosed developmental dyslexia.
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PMID:Cerebral venous sinus thrombosis in childhood: clinical aspects and neurological and cognitive long-term outcome in three cases. 1562 88

A 25-year-old man was admitted to our hospital because of abdominal pain, nausea and low-grade fever. An abdominal CT showed remarkable thickening of the wall of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, anticoagulation therapy was chosen. Heparin was administered intravenously and was used alternatively with warfarin later. The patient's symptoms and clinical data improved gradually. Concerning the etiological factors of the thrombosis, only protein S activity definitely decreased. Genetic analysis indicated a variant of protein S, protein S Tokushima.
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PMID:[A case of portal vein thrombosis associated with congenital protein S deficiency]. 1754 50

Protein S (PS), a vitamin K-dependent glycoprotein, performs an important role in the anticoagulation cascade as a cofactor of protein C. Because of the presence of a pseudogene and two different forms of PS in the plasma, protein S deficiency (PSD) is one of the most difficult thrombophilias to study and a rare blood disorder associated with an increased risk of thrombosis. We describe a unusual case of previously healthy 37-year-old man diagnosed with portal-splenic-mesenteric vein thrombosis secondary to PSD. The patient was admitted to the hospital due to continuous nonspecific abdominal pain and nausea. Abdominal computed tomography revealed acute venous thrombosis from inferior mesenteric vein to left portal vein via splenic vein, and laboratory test revealed decreased PS antigen level and PS functional activity. Conventional polymerase chain reaction and direct DNA sequencing analysis of the PROS1 gene demonstrated duplication of the 166th base in exon 2 resulting in frame-shift mutation (p.Arg56Lysfs*10) which is the first description of the new PROS1 gene mutation to our knowledge. Results from other studies suggest that the inherited PSD due to a PROS1 gene mutation may cause venous thrombosis in a healthy young man without any known predisposing factor.
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PMID:[Portal-splenic-mesenteric venous thrombosis in a patients with protein S deficiency due to novel PROS1 gene mutation]. 2516 54