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)

Nontraumatic intramural duodenal hematoma (IDH) is rare disease and it is generally related to coagulation abnormalities. Reports of nontraumatic IDH associated with pancreatic disease are relatively rare, and various conditions including acute or chronic pancreatitis are thought to be associated with nontraumatic IDH. However, the association between IDH and acute pancreatitis remains unknown. We report the case of a 45-year-old man who presented with vomiting and right hypochondrial pain. He had no medical history, but was a heavy drinker. The diagnosis of IDH was established by computed tomography, ultrasonography and endoscopy, and it was complicated by acute pancreatitis. The lesions resolved with conservative management. We discuss this case in the context of previously reported cases of IDH concomitant with acute pancreatitis. In our patient, acute pancreatitis occurred concurrently with hematoma, probably due to obstruction of the duodenal papilla, or compression of the pancreas caused by the hematoma. The present analysis of the published cases of IDH with acute pancreatitis provides some information on the pathogenesis of IDH and its relationship with acute pancreatitis.
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PMID:Acute pancreatitis secondary to intramural duodenal hematoma: Case report and literature review. 2116 Jun 69

Cystic dystrophy of duodenal wall and duodenal dystrophy (DD)--is a rare disease which is based on chronic inflammation of the pancreas tissue (PT), malrelated in the wall of the duodenum (DU). The principal method of surgical treatment of this disease is Pancreaticoduodenectomy (PRD), although it was presented several reports of successful use sandostatin or endoscopic treatment in some patients. Analysis of demographic, clinical and instrumental data, methods of surgical treatment of DD showed that all patients with persistent or recurrent abdominal pain was noted in all patients, weight loss--51%, vomiting--at 26%, jaundice--in 20% of patients. The most accurate diagnostic methods were CT, endo-ultrasound and MRI. The diagnosis of duodenal dystrophy installed in 35 patients. Operations were performed on 22 patients: Implemented PRD (10), removal of pancreatic head resection with a vertical branch of the PT and duodenoduodenoanastomosis (2), pancreatic head resection with excision of the cyst wall of the first portion of duodenum (2), gastric resection (1), resection of the vertical branch of the duodenum with duodenoduodenoanastomosus (2), duodenectomia (1) and resection of the vertical branch of the duodenum with reconstruction of the intestinal insert (2). Four patients fulfilled draining intervention on pancreatic ductal system--pankreatico and cystoenteroanastomoses. Postoperative and late mortality--0.77% of patients the disappearance of pain and 23%--a decrease in its intensity. In two cases, after the PRD against the background of pronounced chronic pancreatitis observed impaired glucose tolerance. Cystic dystrophy of duodenal wall without the expressed "orthotopic" pancreatitis clearly shows pathogenetic, clinical, diagnostic and therapeutic aspects of this disease, causing the possibility of an effective surgical treatment, only limited intervention by the KDP, without resection of the pancreas.
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PMID:[Diagnosis and treatment of cystic forms of duodenal dystrophia]. 2126 28

A parahiatal hernia, that occurs from muscular diaphragmatic defects causing separation from the esophageal hiatus, is rare. We treated a 68-year-old Japanese woman with the symptom of vomiting. Based on imaging studies (upper gastrointestinal studies, gastroscopy, contrast-enhanced computed tomography) we diagnosed parahiatal hernia. On laparoscopic surgery, the hernial orifice was separated from the esophageal hiatus and the crus of the diaphragm was between the hiatus and the orifice. We closed the hernial orifice with mesh. Parahiatal hernia is rare and is difficult to diagnose preoperatively. We present a case and the clinical discuss the characteristics and management of this rare disease.
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PMID:[A case of parahiatal hernia with vomiting, and a review of the literature]. 2130 30

Posterior reversible encephalopathy syndrome (PRES) is a rare disease characterized by altered mental status, seizures, headache, vomiting and visual disturbances, most often described after transplantation and immunosuppressive therapy. PRES is commonly first diagnosed by the neuroradiologist, rather than the clinician, as it is characterized by very typical magnetic resonance imaging (MRI) features, i.e., hyperintense lesions in the territories of the posterior cerebral artery. Here we report our experience in the Intensive Care Unit (ICU) with a case of tacrolimus-related PRES after liver transplant, presenting with sudden neurological deterioration and diffuse and massive hyperintensities upon brain MRI. Discontinuation of tacrolimus, as prompted by the established literature, permitted the patient to eliminate tacrolimus-associated toxicity, whereas its substitution with everolimus and mycofenolic acid allowed the maintenance of immunosuppression while avoiding acute organ rejection and reducing the dosage of corticosteroids. The lowering of blood pressure with drugs reported in the literature for use in PRES proved to be effective but challenging, requiring the use of multiple drugs and only slowly leading to proper control of hypertensive peaks. Nonetheless, hypertension management and supportive therapy allowed for a complete neurological restitutio ad integrum of the patient. In conclusion, tacrolimus-related brain adverse events need to be promptly recognized, especially during the first months after transplantation. When tacrolimus-related PRES occurs, immunosuppressive therapy may be safely and efficiently switched to everolimus and mycofenolic acid. This strategy may help not only to avoid acute organ rejection but also to reduce the dosage of corticosteroids, which might interfere with proper control of hypertension.
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PMID:Posterior reversible encephalopathy syndrome in the Intensive Care Unit after liver transplant: a comparison of our experience with the existing literature. 2317 27

Spontaneous esophageal rupture is a comparatively rare disease, and thought to be a severe emergency disease clinically. Most patients of spontaneous esophageal rupture complained of chest pain after vomiting, which required an appropriate diagnosis. Emergency operation for the extra-mediastinal rupture type and intra-mediastinal rupture type, also conservative treatment for the intra-mediastinal rupture type achieved satisfactory results. The procedure consisted of closure of the perforation site with left thoracotomy and gastric fundic patch via the transhiatal approach. To prevent post-operative empyema and mediastinal abscess formation, insertion of a conventional thoracic drainage tube and another fixed drainage tube from the posterior diaphragm to the lateral border of the vertebral column along the thoracic descending aorta seemed effective. The patients with spontaneous esophageal rupture underwent continuous irrigation and suction via these drainage tubes after the operation.
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PMID:[Diagnosis and treatment of spontaneous esophageal rupture]. 2191 91

Extrahepatic biliary atresia (EHBA) is a rare disease characterized by progressive and obliterative cholangiopathy in infants and is one of the major causes of secondary vitamin K deficiency bleeding (VKDB) due to cholestasis-induced fat malabsorption. Breast feeding increases the tendency of bleeding in EHBA patients because breast milk contains low amounts of vitamin K. A 2-month-old female infant unexpectedly died, with symptoms of vomiting and jaundice prior to death. She had been born by uncomplicated vaginal delivery and exhibited normal growth and development with breastfeeding. There was no history of trauma. She received vitamin K prophylaxis orally. In an emergency hospital, a CT scan showed a right intracranial hematoma and mass effect with midline shift to the left. In the postmortem examination, severe atresia was observed in the whole extrahepatic bile duct. Histologically, cholestasis, periductal fibrosis, and distorted bile ductules were noted. The gallbladder was not identified. A subdural hematoma and cerebellar tonsillar herniation were found; however, no traumatic injury in any part of the body was observed. Together, these findings suggest that the subdural hemorrhage was caused by secondary vitamin K deficiency resulting from a combination of cholestasis-induced fat malabsorption and breastfeeding. Subdural hemorrhage by secondary VKDB sometimes occurs even when vitamin K prophylaxis is continued. This case demonstrated that intrinsic factors, such as secondary VKDB (e.g., EHBA, neonatal hepatitis, chronic diarrhea), should also be considered in infant autopsy cases presenting with subdural hemorrhage.
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PMID:Subdural hemorrhage: A unique case involving secondary vitamin K deficiency bleeding due to biliary atresia. 2260 80

Chylothorax is a rare disease (1-2 % of pleural effusions), with a prevalence between 1/8600 and 1/15,000 births. It is characterized by the presence of chyle in the pleural cavity. Three categories of chylothorax are known: congenital chylothorax, which can be either idiopathic or the result of a malformation, and traumatic chylothorax (mostly postoperative). We report the observation of a 9-month-old infant with idiopathic chylothorax revealed by respiratory symptoms, with pleural effusion and collapse of the ipsilateral lung on chest X-ray and ultrasound examination. Cytology and chemical analysis of the pleural fluid showed an exudative liquid with a chylous aspect, a high concentration of albumin (52 g/dL), triglycerides (11.42 g/L), and a high number of cells (6600 cells/mL), with lymphocyte predominance (96 %). The culture was sterile. Chylothorax is usually revealed by dyspnea, but also by nausea, vomiting, anorexia and/or malnutrition. The diagnosis is suspected when milky white fluid is obtained from thoracocentesis and is confirmed by the presence of a triglyceride level greater than 1.2 mmol/L and more than 1000 cells/mL, with lymphocyte predominance. The treatment of chylothorax can be either conservative or surgical. Conservative treatment (medical) has four goals: ensure pleural emptiness, decrease production of chyle, restore and/or maintain proper nutritional status, and treatment of the cause when identified. Surgical intervention is indicated when conservative management fails and aims to stop a radical and permanent leakage of chyle.
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PMID:[Idiopathic chylothorax in an infant: management and progression]. 2268 19

Celiac artery compression syndrome (CACS) or median arcuate ligament (MAL) syndrome is a rare vascular disease. The clinical manifestations of CACS include the triad of postprandial pain, vomiting, and weight loss. The pathogenesis of CACS is the external compression of celiac artery by the MAL or celiac ganglion. Moreover, some authors also reported the compression with different etiologies, such as neoplasms of pancreatic head, adjacent duodenal carcinoma, vascular aneurysms, aortic dissection, or sarcoidosis. In the literature, most cases of CACS were reported from Western countries. In contrast, this disease was seldom reported in Oriental countries or regions, including Taiwan. Superior mesenteric artery syndrome (SMAS) is also a rare disease characterized by compression of the third portion of the duodenum by the SMA. The clinical features of SMAS are postprandial pain, vomiting, and weight loss. To date, there are no guidelines to ensure the proper treatment of patients with CACS because of its low incidence. Thus, tailored therapy for patients with CACS remains a challenge as well as the prediction of clinical response and prognosis. The aim of our present study was to investigate the clinical features, the association with SMAS, treatments, and outcomes of patients with CACS in a single institution in Taiwan.
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PMID:Celiac artery compression syndrome: an experience in a single institution in taiwan. 2298 53

Genetic mutations in complement components are associated with the development of atypical hemolytic uremic syndrome (aHUS), a rare disease with high morbidity rate triggered by infections or unidentified factors. The uncontrolled activation of the alternative pathway of complement results in systemic endothelial damage leading to progressive development of renal failure. A previously healthy 8-month-old boy was referred to our hospital because of onset of fever, vomiting, and a single episode of nonbloody diarrhea. Acute kidney injury with preserved diuresis, hemolytic anemia, and thrombocytopenia were detected, and common protocols for management of HUS were followed without considerable improvement. The persistent low levels of complement component C3 led us to hypothesize the occurrence of aHUS. In fact, the child carried a specific mutation in complement factor H (Cfh; nonsense mutation in 3514G>T, serum levels of Cfh 138 mg/L, normal range 350-750). Given the lack of response to therapy and the occurrence of kidney failure requiring dialysis, we used eculizumab as rescue therapy, a monoclonal humanized antibody against the complement component C5. One week from the first administration, we observed a significant improvement of all clinical and laboratory parameters with complete recovery from hemodialysis, even in the presence of systemic infections. Our case report shows that complement inhibiting treatment allows the preservation of renal function and avoids disease relapses during systemic infections.
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PMID:Preservation of renal function in atypical hemolytic uremic syndrome by eculizumab: a case report. 2302 68

Angioedema due to the acquired deficiency of C1-inhibitor is a rare disease known as acquired angioedema (AAE), which was first described in a patient with high-grade lymphoma and is frequently associated with lymphoproliferative diseases, including expansion of B cell clones producing anti-C1-INH autoantibodies, monoclonal gammopathy of uncertain significance (MGUS) and non-Hodgkin lymphoma (NHL). AAE is clinically similar to hereditary angioedema (HAE), and is characterized by recurrent episodes of sub-cutaneous and sub-mucosal edema. It may affect the face, tongue, extremities, trunk and genitals. The involvement of the gastrointestinal tract causes bowel sub-occlusion with severe pain, vomiting and diarrhea, whereas laryngeal edema can be life-threatening. Unlike those with HAE, AAE patients usually have late-onset symptoms, do not have a family history of angioedema and present variable response to treatment due to the hyper-catabolism of C1-inhibitor. Reduced C1-inhibitor function leads to activation of the classic complement pathway with its consumption and activation of the contact system leading to the generation of the vasoactive peptide bradykinin, which increases vascular permeability and induces angioedema. Lymphoprolipherative diseases and AAE are tightly linked with either angioedema or limphoprolyferation being the first symptom. Experimental data indicate that neoplastic tissue and/or anti-C1-inhibitor antibodies induce C1-inhibitor consumption, and this is further supported by the observation that cytotoxic treatment of the lymphoproliferative diseases associated with AAE variably reverses the complement impairment and leads to a clinical improvement in angioedema symptoms.
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PMID:Acquired C1-inhibitor deficiency and lymphoproliferative disorders: a tight relationship. 2349 Mar 22


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