Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 investigated the indications for and findings of gastrointestinal (GI) endoscopy in all children < or = 16 years old referred for the procedure to the endoscopy unit at Soba University Hospital, Khartoum from January 2004 to January 2006. Thus 113 children were enrolled; 73% underwent upper GI endoscopy, 27% lower GI endoscopy (15% colonoscopy, 12% flexible sigmoidoscopy). Indications for upper GI endoscopy included haematemesis (24%), portal hypertension (21%), abdominal pain (16%) and vomiting (15%). Diagnoses included oesophageal varices (16%), gastritis (7%) and hiatus hernia (6%). Indications for lower GI endoscopy included rectal bleeding (87%), diarrhoea (19%) and anaemia (10%).
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PMID:Paediatric gastrointestinal endoscopy: experience in a Sudanese university hospital. 2018 56

N-butyl-2-cyanoacrylate is widely used to sclerose bleeding gastric varices. We report the case of a 65-year-old lady, known case of cirrhosis secondary to hepatitis C infection, who presented to the emergency department with coffee ground vomiting and melena for four days. Gastroscopy showed non-bleeding small esophageal varices, mild portal hypertensive gastropathy and a large gastric fundal varix. Injection sclerotherapy was completed successfully and haemostasis was secured. During the procedure, she was hemodynamically stable with an oxygen saturation of 98%. Immediately after the procedure, she went into cardiopulmonary arrest; cardiopulmonary resuscitation (CPR) was started, but she could not be revived. A provisional diagnosis of pulmonary embolism was made. X-ray chest showed linear hyperdense shadows in both pulmonary arteries and in some of their branches, which were not seen on pre-procedural chest X-ray. The patient died of massive pulmonary embolism as confirmed on X-ray chest.
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PMID:Glue embolism: a rare cause of pulmonary embolism. 2191 21

Nodular regenerative hyperplasia (NRH) of the liver is associated with noncirrhotic portal hypertension, rheumatologic and hematologic disorders, administration of certain drugs, and other underlying conditions. This report describes a 64-year-old man with clinically presumed cirrhosis who presented to our institution with coffee-ground emesis, esophageal varices, ascites, and encephalopathy. Eleven years earlier he had been treated for breast cancer with mastectomy and chemo-radiotherapy. He died suddenly, and the autopsy showed no evidence of cirrhosis but instead demonstrated NRH with extensive emboli of recurrent breast carcinoma within the portal vein and its intrahepatic branches. Neoplastic occlusion of the portal vein as a cause of presinusoidal noncirrhotic portal hypertension has not previously been reported for metastatic breast carcinoma. This case highlights the importance of obstructive portal venopathy in the pathogenesis of NRH as well as the diagnostic difficulties that may be encountered in determining the cause of portal hypertension.
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PMID:Portal Hypertension, Nodular Regenerative Hyperplasia of the Liver, and Obstructive Portal Venopathy due to Metastatic Breast Cancer. 2398 49

Bleeding from gastric varices (GVs) is generally considered more severe than that from esophageal varices (EVs) but occurs less frequently. We review the risk factors for bleeding EVs and GVs. GVs were divided into 2 groups: cardiac varices (CVs, Lg-c) and fundal varices (FVs), i.e., varices involving the fundus alone (Lg-f) or varices involving both the cardia and fundus (Lg-cf). Elevated pressure in the portal vein is a risk factor for bleeding EVs. The portal pressure in patients with GVs and a gastrorenal shunt is lower than that in patients with EVs. The large size of varices is a risk factor for bleeding EVs. Red color signs are elevated red areas that are important for predicting the risk of variceal bleeding, and red wale markings, dilated venules oriented longitudinally on the mucosal surface, have been considered to be the sign with the highest risk. Red color signs are rare in FVs, possibly because of the pronounced thickness of the mucosal layer. Bleeding EVs are not associated with use of antiulcer drugs or nonsteroidal anti-inflammatory drugs (NSAIDs). Although, in patients with bleeding GVs, "occasional" use of an oral NSAID is an important step leading to variceal hemorrhage, especially from FVs, even if the mucosa is protected by antiulcer drugs. Constipation, vomiting, severe coughing, and excessive consumption of alcohol may precipitate rupture of EVs.
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PMID:Risk factors for bleeding esophagogastric varices. 2399 67

Cases of splanchnic venous thrombosis have not been described in Cameroon. Their prevalence in acute pancreatitis is variable. With the emergence of acute intra-abdominal infections including typhoid fever and peritoneal tuberculosis in situations of acquired immunodeficiency syndrome, these cases will become frequent. We report the case of a portosplenomesenteric venous thrombosis related to necrotizing acute pancreatitis associated with proteins C and S deficiency, in a 46-year-old Cameroonian man, without particular past medical history. He was admitted for abdominal pain which had been evolving for 3 weeks and accompanied by vomiting. In the absence of hemorrhagic risk factor, the patient received low molecular weight heparin followed by oral warfarin. The abdominal ultrasound check on the 12th day showed a partial recanalization of venous thrombosis. The abdominal contrast-enhanced CT scanner at day 30 on oral anticoagulation therapy showed collateral vessels and small bowel edema. At the same time the upper gastrointestinal endoscopy showed grade II esophageal varices. We have maintained oral anticoagulation therapy. This case highlights that an early effective anticoagulation heparin therapy is needed for a clear benefit in case of suspected PSMVT. It is certain that the sooner the treatment is given, the better outcome will be.
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PMID:Clinical Outcome of a Portosplenomesenteric Venous Thrombosis in Necrotizing Acute Pancreatitis with Protein C and S Deficiency Treated by Anticoagulation Therapy Alone. 2644 85

A 24-year-old man with sickle cell anemia presented with fatigue, dark stool, and coffee ground emesis. He was found to have large esophageal varices and experienced massive variceal hemorrhage in the hospital. The varices were caused by diffuse splanchnic venous thrombosis, and his only risk factor for hypercoagulability was sickle cell anemia. Splanchnic venous thrombosis due to sickle cell anemia is exceedingly rare.
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PMID:Massive Esophageal Variceal Bleeding as a Rare Complication of Sickle Cell Anemia. 2695 56

This cross-sectional observational study was conducted in the Department of Gastroenterology, Bangabandhu Sheikh Mujib Medical University, Sir Salimullah Medical College and Mitford Hospital, Holy family Red Crescent Medical College and Hospital and Popular Diagnostic Centre, Shantinagar branch, Dhaka, Bangladesh from January 2012 to July 2013. Study subjects were included in the study irrespective of age and sex having different upper GI tract. Complaints like dysphagia, heart burn, abdominal pain/dyspepsia, nausea, vomiting, haematemesis and/or malena, anorexia, unexplained anemia, weight loss etc. All the findings of oesophagus, stomach and duodenal lesions were observed and data were recorded. The results were considered positive based on the macroscopic appearance using standard diagnostic criteria. During the study period endoscopy was performed in 5608 subjects. Among which 2968(52.92%) were male and 2640(47.07%) were female. The patients age range from 7 years to 108 years. The majority of the patients were from 40-50 years. Normal findings were observed among 3321(59.21%) cases. Gastroduodenal erosions were present among 684(12.19%) cases, Oesophageal varices in 444(7.91%) cases, duodenal ulcer diseases in 415(7.40%) cases and gastric ulcer in 184(3.28%) cases. Ca stomach was found among 165(2.94%) cases. A number of diseases were identified through this procedure. Current study observed a large proportion of patients (40.79%) had positive upper GI endoscopy.
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PMID:Pattern of Changes in the Findings among the Patients Undergoing Diagnostic Esophagogastroduodenoscopy in Bangladesh. 2794 38

BACKGROUND Cholesteryl ester storage disease (CESD), also known as lysosomal acid lipase deficiency (LAL-D), is a rare autosomal-recessive inheritable lysosomal storage disease. Since 2015, a causal treatment with sebelipase alfa, which replaces the missing LAL enzyme, has been approved. We report a fatal course of LAL-D in a female patient. CASE REPORT In 1979, CESD was first diagnosed in a 13-year-old female with marked hepatomegaly. At that time, no specific treatment for CESD was available and the spontaneous course of the disease had to be awaited. In 2013, a laparoscopic cholecystectomy for symptomatic gallstones was performed. The patient's CESD had caused a Child-Pugh A/B and Lab-MELD 14 cirrhosis with esophageal varices (grade III), a solitary fundal varix, as well as hepatosplenomegaly with thrombocytopenia. In 2016, the patient was admitted with compensated cirrhosis and splenomegaly for a ligature of esophageal varices which was complicated by vomiting of blood followed by severe coagulopathy and hemorrhagic shock. The dried blood test showed reduced acid lipase (0.03 nmol/spot*3 hours; reference range 0.2-2) and beta-galactosidase (0.08 nmol/spot*21 hours; reference range 0.5-3.2). Then 15 days after the esophageal varices bleed, the patient died due to multiorgan failure as a sequelae of advanced liver disease. CONCLUSIONS LAL-D should be included in the differential diagnosis of lipid metabolism disorder, hepatomegaly, and non-alcoholic fatty liver disease with fibrosis or cirrhosis. Causal treatment with sebelipase alfa should be introduced even in patients who have LAL-D and many years of clinically mild symptoms of this disease to prevent the serious sequelae of cirrhosis or cardiovascular complications.
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PMID:Cholesteryl Ester Storage Disease: Fatal Outcome without Causal Therapy in a Female Patient with the Preventable Sequelae of Progressive Liver Disease after Many Years of Mild Symptoms. 2977 83

Polycythaemia Vera (PV) is a myeloproliferative disorder in which bone marrow has increased production of red blood cells, white blood cells and platelets. The hallmarks of the disease are veno-occlusive events, secondary to increased blood viscosity. Polycythaemia Vera rarely presents with portal vein thrombosis below age of 55 years especially in absence of any chronic liver disease. We report a case of 30-years-old South Asian male presenting with abdominal pain, weight loss and vomiting for 3 months. On evaluation, he was found to have oesophageal varices. Furthermore, CT scan showed infiltration at porta-hepatis and portal venous thrombosis. Polycythaemia Vera was diagnosed with a positive JAK2 mutation and increased haemoglobin. Laparoscopy was done to perform biopsy of the porta-hepatis mass. Biopsy showed engorged vessels with no sign of malignancy. Patient underwent repeated sessions of upper GI endoscopy for band ligation and multiple sessions of venous phlebotomy which drastically improved his blood indices. He was started on lifelong aspirin and was advised regular follow-ups. With early recognition and prompt management patients can be prevented from potential complications which can prove to be detrimental.
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PMID:Polycythaemia Vera Presenting As A Porta Hepatis Mass. 3193 24


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