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)

Careful interpretation of the vascular pathology is important in cases of intestinal ischemia caused by primary mesenteric vein thrombosis because it suggests antithrombin III (AT III) deficiency. This deficiency, an autosomal dominant hereditary disorder, predisposes the patient to venous thrombosis. Similar or acquired deficiencies may also predispose the patient to thrombosis. In hereditary AT III deficiency, 90% of the cases have thrombosis of the leg or iliac veins; 8.3% of the cases, thrombosis of the mesenteric veins. Additionally, some families have a tendency to develop mesenteric vein thrombosis specifically. In this case report, a daughter with probable AT III deficiency had a history of 3 episodes of deep vein thrombosis in the previous 5 years while taking oral contraceptives. Her father, with the same deficiency, died from massive intestinal infarction resulting from portal and mesenteric vein thrombosis. The 19-year old woman developed gradually worsening abdominal pain, signs of peritonitis, and hematemesis. A laparotomy revealed peritonitis that was due to segmental small-bowel infarction; the underlying pathologic condition was mesenteric vein thrombosis. Coagulation study results revealed AT III activity by chromogenic assay, 0.48 u/mL; AT III antigen, 0.5 u/mL; and protein C antigen, 1.15 u/mL. 10 days after discharge, she developed a hemicranial headache with nausea, vomiting, neck tenderness, and photophobia; she was readmitted. A CT scan showed a left posterior parietal cerebral infarct. Repeat AT III activity by chromogenic assay was 0.51 u/mL and AT III antigen level was 0.50 u/mL. Before anticoagulant therapy could be initiated, the patient died 7 days after readmission. The combined lowering of AT III activity and antigen levels to half of normal suggests AT III deficiency. Earlier diagnosis of this deficiency could have been made in light of the patient's own history of thrombosis and the paternal history.
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PMID:Mesenteric venous thrombosis due to antithrombin III deficiency. 333 17

Recent cohort and case control studies of low-dose combined oral contraceptives (COCs) containing the new generation of progestogens have allowed classification of adverse effects into those which are rare but serious and should be considered risks and those which are more frequent but are less of a threat to health. Low-dose COCs continue to affect coagulation in a complex way, but the risk is less than with the older preparations, and it can be minimized by screening women for a personal or familial history of early or unusual thrombosis and for levels of protein C, S, and antithrombin III. Women with true migraine with focal signs should also avoid using COCs. The relative risk of myocardial infarction (MI) may increase from 4:1 in women with one risk factor (age, smoking, hypertension, hyperlipidemia, and diabetes) to 20:1 with two risk factors and 128:1 with three or more risk factors. In the absence of all risk factors, a recent study indicated that the relative risk of MI with COC use was 1.9 for current and past use. COC use also causes a slight increase in hypertension in most women, especially those who are older or have a family history of hypertension. While the COC can affect carbohydrate and lipid metabolism, the new generation of progestogens has reduced these effects. The COC may accelerate presentation of gallbladder disease in predisposed women. The COC protects against benign breast disease but may increase the risk of breast cancer and cervical cancer slightly. There is a strong link between hepatocellular adenoma and COC use, but the incidence is low. Return to fertility after use has not been a problem. Both estrogenic adverse effects (nausea, dizziness, irritability, weight gain, bloating) and progestogenic adverse effects (vaginal dryness, acne, hirsutism, weight gain, depression, loss of libido) can occur in 50% of women, but these generally disappear after a few months of use. In conclusion, the low-dose, third generation COCs are associated with minimal risks in the absence of other risk factors and have many beneficial effects such as the prevention of ovarian and endometrial cancer; a decrease in pelvic inflammatory disease and ectopic pregnancies; and protection from anemia, primary dysmenorrhea, functional ovarian cysts, and benign breast disease as well as from the morbidity and mortality associated with pregnancy.
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PMID:The combined oral contraceptive. Risks and adverse effects in perspective. 776 40

We report the successful treatment of envenoming by the Gaboon viper (Bitis gabonica) and include results of in vitro investigations of the haemostatic properties of the whole venom. The patient was admitted to casualty soon after the bite with chest tightness, dizziness, nausea and swelling at the site of the bite and was treated immediately with polyspecific antivenom, hydrocortisone, chlorpheniramine and antibiotics. Results of haemostatic investigations were essentially normal on admission but on day 3 the thrombin time became prolonged and was associated with significant hypofibrinogenaemia and elevated D-dimers. Factors V and VIII, antithrombin III and protein C levels and platelet number were not significantly reduced. The haemostatic disturbances persisted for more than 24 h despite treatment with blood products (16 units of cryoprecipitate, 2 units of fresh frozen plasma and 6 units of platelet concentrate). Resolution of the abnormalities occurred only after administration of a further dose of antivenom. The period of hypofibrinogenaemia occurred at a time when venom antigen was undetectable in plasma by enzyme-linked immunosorbent assay. Studies in vitro with whole venom and a panel of amidolytic substrates commonly employed for measurement of haemostatic proteins revealed significant activity of venom with substrates sensitive to kallikrein and plasmin. The venom inhibited washed platelet aggregation induced by collagen, thrombin, arachidonic acid and the calcium ionophore A23187 in a dose-dependent manner.
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PMID:Accidental envenoming by a Gaboon viper (Bitis gabonica): the haemostatic disturbances observed and investigation of in vitro haemostatic properties of whole venom. 846

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

Portal vein thrombosis secondary to protein C deficiency is a rare finding. Diagnosing a portal vein thrombosis itself is difficult due to nonspecific symptoms such as nausea, vomiting, anorexia, and weight loss. Proving that a protein C deficiency is the cause of a portal vein thrombosis is even more difficult as an extensive and thorough workup is required to rule out malignancies, myeloproliferative disorders, and hypercoaguable states which can all lead to thromboses. Patients require anticoagulation to prevent two dangerous complications of portal vein thrombosis; portal hypertension leading to esophageal varices with massive hemetemesis and extension of thrombus from the portal vein into the mesenteric veins leading to intestinal ischemia and death. In this case report, we present a patient with the complaint of painless jaundice who was found to have an incidental finding of portal vein thrombosis secondary to protein C deficiency. The different etiologies of portal vein thrombosis, along with diagnosis and treatment options will be discussed and highlighted.
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PMID:A rare incidental finding in a case of painless jaundice. 3071 33

We report a patient with combined thrombophilia--protein C deficiency and mild hyperhomocysteinemia with total spontaneous thrombosis of a basilar tip aneurysm after subarachnoid hemorrhage, without neurological deficit. At admission, the patient had headache, drowsiness, and nausea, with no neurological deficit. Computed tomography (CT) did not show the presence of subarachnoid blood, and magnetic resonance examination revealed discrete remains of a subarachnoid hemorrhage in projections of temporal, frontal and occipital lobes, with no vascular abnormalities. Initial angiography showed a small basilar tip aneurysm and the patient was scheduled for endovascular treatment. A second angiography, performed before the planned endovascular treatment, did not show the aneurysm and complete thrombosis was suspected. A follow-up angiogram, 6 months after this event, showed preserved posterior cerebral circulation with no aneurysm present. The patient was discharged in good condition, without neurological deterioration. We did not find any previous reports of similar conditions.
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PMID:Spontaneous thrombosis of basilar artery aneurysm after subarachnoidal hemorrhage in a patient with thrombophilia and recurrent deep venous thrombosis. 2054 47

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