Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
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Cerebral venous thrombosis is a clinical condition of difficult diagnosis, and poor prognosis when treatment is not started early. There is a long list of causes, and hereby we describe a case associated to prothrombin G20210 mutation. A 53-year-old man, white, was admitted with status epilepticus. After seizures control, he developed intracranial hypertension, with headache and vomiting, and bilateral papilledema. His past medical and familial history were unremarkable. He was a nonsmoker, no drug and alcohol user. CT scan and MRI showed right temporal and parietal infarct with hemorrhagic transformation. Spinal tap with opening pressure of 500 mmH2O showed normal CSF examination. MRI angiography disclosed superior sinus, right transverse and sigmoid sinus complete thrombosis. He was started with heparin and oral warfarin. In spite of anticoagulation, two months later he developed deep right inferior limb thrombosis. All the initial tests were normal, and test for prothrombin G20210 mutation was positive. He needed a much higher than conventional daily dose of warfarin to keep him asymptomatic.
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PMID:[Cerebral and systemic venous thrombosis associated to prothrombin G20210 mutation: case report]. 1476 16

In this report we describe a case of extensive cerebral venous thrombosis in a patient with Evans syndrome. A 19-year-old male patient with Evans syndrome was admitted to the hospital with the complaints of headache, convulsive seizure, and vomiting. The cerebral venous thrombosis including left lateral, left sigmoid, straight sinus, and vena jugularis interna was diagnosed by cerebral magnetic resonance angiography. When the thrombosis developed, he was in hematological remission and he was not receiving any medications except lamivudine for chronic hepatitis B infection. As a genetic prothrombotic risk factor, he had heterozygous prothrombin G20210A gene mutation. His clinical and radiologic findings improved after unfractionated heparin and subsequently with coumadin therapy. On follow-up, cerebral venous thrombosis reoccurred in different localizations, but complete recanalization could be obtained with antithrombotic therapy. We present the case since the association of cerebral venous thrombosis and Evans syndrome is very rare.
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PMID:Cerebral venous thrombosis in a patient with Evans syndrome: a rare association. 1552 99

A 39-year-old white woman presented with a history of aortoiliac occlusive disease diagnosed in 1992 attributed to oral contraceptive use. Shortly thereafter, aortoiliac replacement was performed. Mild hyperlipidemia was diagnosed in 2001. At the current clinic visit, she presented to her primary care physician with a 3-month history of postprandial midepigastric abdominal pain relieved by vomiting and a 30-pound weight loss. Her evaluation included an esophagogastroduodenoscopy, a colonoscopy, and an abdominal ultrasound, all of which were within normal limits. Because of her medical history, the patient underwent an arteriogram, which revealed brachiocephalic stenosis (Figure 1), occlusion of the left subclavian artery (Figures 2a and 2b), and narrowing of the superior and inferior mesenteric arteries (not shown). Since she had discontinued her oral contraceptives in 1992 and her hyperlipidemia was mild, the rheumatology service was consulted to evaluate this patient. On physical examination, she had decreased left brachial and radial pulses and a right carotid bruit. Laboratory evaluation revealed a normal complete blood count, comprehensive metabolic panel, erythrocyte sedimentation rate, and C - reactive protein. Subsequent testing included a prothrombin time, activated partial thromboplastin time, protein S, protein C, reptilase time, antithrombin III, anticardiolipin antibody, antiphospholipid antibody, lupus anticoagulant, homocysteine, RPR, and a lipid profile. All test results were within normal limits. Due to the severity of her abdominal pain, the patient underwent superior mesenteric artery (SMA) bypass surgery. Sections from the aorta resected in 1992 are shown in Figures 3 and 4.
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PMID:Pathology case of the month. 39-year-old woman with abdominal pain and weight loss. Takayasu's arteritis (TA). 1555 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

The vast majority of acute iron toxicity cases occur in children less than 5 years of age. Moreover, clinical hepatic injury is uncommon with most symptoms stemming from the intestinal tract (eg, nausea, vomiting, diarrhea). Therefore, physicians, particularly those who do not routinely treat pediatric patients, are often unfamiliar with hepatotoxicity related to iron overdose. Nevertheless, hepatotoxicity caused by acute iron poisoning is associated with a high mortality rate. We report a case of severe hepatic injury in an adult who overdosed on iron tablets with suicidal intent. Tests for other hepatotoxins (eg, acetaminophen), hepatatrophic viruses, and other causes of acute liver injury were negative. Although peak serum iron level (340 microg/dL) was significantly lower than that reported to cause hepatotoxicity (>1,700 microg/dL), rapid and significant elevations in aminotransferases (>4,000 U/L), total bilirubin (5 mg/dL), and prothrombin time (50 seconds) occurred within 48 hours. Treatment with deferoxamine was prompt and followed by empiric N-acetylcysteine once liver injury was apparent. The patient was minimally symptomatic and she eventually had a full recovery.
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PMID:Acute liver failure due to iron overdose in an adult. 1575 60

Parecoxib (Dynastat) is a parenteral cyclooxygenase-2 inhibitor available in Europe. Clinical trials have reported a benefit in reducing pain following oral, orthopedic, gynecologic and cardiac surgeries. The overall efficacy was dose-related and similar to ketorolac (Toradol). Several trials reported an opioid-sparing effect with parecoxib. No trials have reported significantly fewer opioid-related gastrointestinal side effects (e.g., nausea, vomiting, constipation and intestinal ileus) when opioids were administered with parecoxib versus placebo. Gastroduodenal ulcers, gastric ulcers and duodenal ulcers or erosions were less common with parecoxib than ketorolac. Parecoxib does not affect platelet aggregation, interfere with the antiplatelet affect of aspirin, affect prothrombin and partial thromboplastin time or platelet counts when administered with heparin.
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PMID:Parecoxib: a shift in pain management? 1585 57

Acute fatty liver of pregnancy (AFLP) is a rare disorder of unknown aetiology that is diagnosed typically in the third trimester or early postpartum period. The incidence is estimated to be 1/6692-1/13,328. The obstetric team must have a high index of suspicion of this pathology, particularly in the presence of clinical and laboratory findings, such as nausea, vomiting, jaundice, increased serum transaminase levels, increased prothrombin time and hypoglycaemia. Early diagnosis followed by prompt delivery and supportive care provides significantly improved maternal and perinatal outcome. Delay in diagnosis of this obstetric emergency may lead to rapid progression to hepatic failure, disseminated intravascular coagulation (DIC), haemorrhage, encephalopathy, multiple organ failure and finally death. The case of a 34-year-old woman, gravida 3, para 2, with AFLP complicated with DIC is presented herein with a review of literature and discussion of its origin.
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PMID:Acute fatty liver of pregnancy complicated with disseminated intravascular coagulation and haemorrhage: a case report. 1587 33

Various hematological abnormalities including fall in serial values of hemoglobin or hematocrit, coagulation factor abnormalities, leukocytosis, acute hemolytic anemia, thrombocytopenia, and thrombotic thrombocytopenic purpura or hemolytic uremic syndrome have been reported in patients with acute pancreatitis. Similarly, abnormalities of blood coagulation factors consistent with disseminated intravascular coagulopathy (DIC) have also been noticed in patients with pancreatitis. We report a case of a 33-year-old female with acute pancreatitis who presented with one episode of epistaxis and abnormal prothrombin time and partial prothrombin time. Coagulation work-up revealed thrombin time 24.3 s fibrinogen 110 mg/dl, D-dimers >1 and < 2, and fibrin degradation products >22. Pancultures did not show any evidence of infection. The patient maintained a normal renal and mental status during her illness. Her D-dimers continued to decrease with resolution of acute pancreatitis as evidenced by decreased abdominal pain, relief of nausea, control of vomiting, and decrease in serum amylase and lipase levels. This case report suggests that coagulation abnormalities are encountered in patients with acute pancreatitis. It is hypothesized that such hemostatic abnormalities may be related to early intravascular consumption of coagulation factors secondary to circulating pancreatic enzymes, particularly trypsin, or secondary to vascular injury. Recognition of these hematological complications including DIC is paramount. Physicians caring for these patients should be aware of such a complication of acute pancreatitis.
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PMID:DIC secondary to acute pancreatitis. 1604 98

Reactions after bee or wasp sting are similar to anaphylaxis. Symptoms such as weakness, fatigue, vomiting, diarrhea, urticaria, and hypotension may occur. Serious toxic reactions usually occur after numerous stings. Massive bee envenomations can result in immediate onset of shock, hemolysis, rhabdomyolysis, disseminated intravascular coagulation (DIC), coma, and renal failure. In milder cases, patients may only have isolated prolonged activated partial thromboplastin time (aPTT) and normal prothrombin time (PT), clinically without a tendency to bleed. As a rule, they recover spontaneously without any complication. We report three cases of wasp stings; they all manifested prolongation of aPTT and finally recovered completely. Isolated prolongation of aPTT in cases of wasp stings may be related to an extract from the venom inhibiting the coagulation pathway.
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PMID:Isolated prolongation of activated partial thromboplastin time following wasp sting. 1623 65

The patient was a 57-year-old woman presenting with jaundice as the chief complaint. She began vomiting on July 10, 2003. Jaundice was noted and admitted to our hospital for thorough testing. Tests on admission indicated severe hepatitis, based on: aspartate aminotransferase (AST), 1 076 IU/L; alanine aminotransferase (ALT), 1 400 IU/L; total bilirubin (TB), 20.9 mg/dL; and prothrombin time rate (PT%), 46.9%. Acute hepatitis A (HA) was diagnosed based on negative hepatitis B surface antigen and hepatitis C virus RNA and positive immunoglobulin (Ig) M HA antibody, but elevation of anti-nuclear antigen (X320) and IgG (3 112 mg/dL) led to suspicion of autoimmune hepatitis (AIH). Plasma exchange was performed for 3 d from July 17, and steroid pulse therapy was performed for 3 d starting on July 18, followed by oral steroid therapy. Liver biopsy was performed on August 5, and the results confirmed acute hepatitis and mild chronic inflammation. Levels of AST and ALT normalized, so dose of oral steroid was markedly reduced. Steroid therapy was terminated after 4 mo, as the patient had glaucoma. Starting 3 mo after cessation of steroid therapy, levels of AST and ALT began to increase again. Another liver biopsy was performed and AIH was diagnosed based on serum data and biopsy specimen. Oral steroid therapy was reinitiated. Levels of AST and ALT again normalized. The present case was thus considered to represent AIH triggered by acute HA.
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PMID:Autoimmune hepatitis triggered by acute hepatitis A. 1627 28


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