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)

Lately, myeloprolipherative disorders are frequently reported as causes of portal vein thrombosis, probably due to the early detection of latent cases of this condition. We report two patients with portal vein thrombosis that presented with abdominal pain, nausea, vomiting and clinical consequences of portal hypertension such as variceal hemorrhage, splenomegaly and ascites. Diagnosis was made by a CAT scan in one patient and doppler ultrasound in the other. Both patients had high platelet counts and an essential thrombocytosis in the bone marrow.
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PMID:[Portal vein thrombosis associated with essential thrombocytosis. Clinical cases and review of the literature]. 900 49

Splenic infarct is a rare complication of portal hypertension. It has been reported as an early complication after successful liver transplantation when portal pressure returns to normal and the splenic size progressively declines. It has not been reported as a late complication of liver transplantation. We describe the case of a 19-year-old patient with a splenic infarct which occurred 11 months after successful orthotopic liver transplantation for decompensated cryptogenic liver cirrhosis. Following transplantation, the patient was in excellent general health, liver function tests were normal, there was no clinical evidence of portal hypertension and the splenic size had decreased significantly compared to the pre-transplantation period, although it remained increased. The patient presented with high fever, left pleuritic pain and vomiting. The splenic size had not changed and left pleuritic exudate fluid collection was detected. A hypoechoic region of the spleen was demonstrated in the ultrasound examination corresponding to a hypodense lesion in the computerized tomography scanning. The patient recovered completely, with the disappearance of the infarct in the imaging studies in 2 months time. This case report indicates that a symptomatic splenic infarct can occur late following successful liver transplantation for liver cirrhosis despite lack of any evidence of residual portal hypertension at a time that splenomegaly has not yet regressed. The differential diagnosis from a splenic abscess in transplanted patients can be difficult but the final prognosis seems to be good.
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PMID:Splenic infarct as a late complication of liver transplantation. 983 Dec 79

It is now recognised that Helicobacter pylori, like most enteric infections, is mainly acquired in childhood. Adults rarely become infected, with seroconversion rates varying between 0.33and 0.5% per person year. The age at which children are most likely to become infected is still unclear, but findings in a number of cross-sectional studies suggest that infection is acquired before the age of five. The prevalence of infection is highest in children in the developing world where up to 75% of children may be infected by the age of 10. In the developed world the prevalence of infection is noticeably increased among socially deprived children. The diagnosis of H pylori infection in childhood is most often made at endoscopy, for which there are many indications. Symptoms such as abdominal pain, vomiting, and haematemesis may be associated with duodenal ulcer and H pylori infection. However, in the case of children undergoing endoscopy for assessment of oesophagitis, failure to thrive, coeliac disease, Crohn's disease, or portal hypertension, the finding of H pylori infection is likely to be incidental. How should we manage these children with a diagnosis of H pylori infection? Currently, there are no consensus guidelines for the management of H pylori infected children. In 1994 the National Institutes of Health consensus statement recommended that adults with gastric or duodenal ulcer disease, who are infected with H pylori, should receive antimicrobial treatment. The European Maastricht Consensus Report suggested broader indications for treatment of infected adults. It states that treatment is advisable for all H pylori infected dyspeptic patients diagnosed non-invasively under 45 years of age at a primary care level. Patients older than 45 years with dyspeptic symptoms should be treated for H pylori infection but only after endoscopy to rule out any other underlying pathology. The European guidelines also recommend treatment for infected patients with mucosa associated lymphoid tissue lymphoma and patients who are found to have intestinal metaplasia and gastric atrophy.
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PMID:How should Helicobacter pylori infected children be managed? 1045 35

An 18-month-old male Labrador retriever was referred for investigation of chronic intermittent diarrhoea and vomiting of two months duration. A diagnosis of hepatic arteriovenous fistulae was made. These are extremely rare hepatic vascular anomalies which confer arterial pressure to the portal vein. Liver atrophy, portal vein hypoplasia, portal hypertension and multiple acquired portosystemic collateral vessels are the main complications. Surgical excision is a challenge as resection of large lesions may be associated with significant blood loss. In this dog, persistence of portal vein hypoplasia and extensive collateral pathways following surgery led to a reserved prognosis.
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PMID:Hepatic arteriovenous fistulae and portal vein hypoplasia in a Labrador retriever. 1130 58

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death in Taiwan. In order to delineate the unique demographic features and clinical profile of terminal HCC, we conducted a retrospective study in a hospital-based hospice in Taiwan. Of a total of 991 terminally ill cancer patients (654 men and 337 women, mean age 66.1 years) admitted to our palliative care unit during a three-year period, 110 patients (11.1%) were diagnosed as having HCC (93 men and 17 women, mean age 60.5 years). The most common metastatic sites were bone and lung. Eighty-five HCC patients (77.3%) also had associated liver cirrhosis. The most common symptoms of HCC patients upon admission to the hospice ward were pain, fatigue or weakness, anorexia/vomiting, peripheral edema, cachexia, and ascites. Hypoalbuminemia, anemia, hyponatremia and jaundice were common laboratory abnormalities. Eighty-four patients (76.4%) required opiates for pain management. Upper gastrointestinal bleeding or varices bleeding developed in 76 patients (69.1%). Ninety-four patients (85.5%) died at the hospital, and the overall median survival time at hospice ward was 12 days. Because of more severe underlying portal hypertension and deteriorated liver function, terminal HCC patients with decompensated liver cirrhosis (Child-Pugh class C) had a significantly higher prevalence of peripheral edema, ascites, dyspnea, jaundice, thrombocytopenia, and stage III-IV hepatic encephalopathy than noncirrhotic or Child-Pugh class A and B terminal HCC patients. Symptoms and signs resulting from these portal hypertensions frequently complicated the symptomatic management of terminal HCC patients in the hospice ward. The treatment of these complications is mostly empirical in hospice ward, where intensive laboratory or diagnostic tests are usually not performed. In conclusion, symptoms and signs of terminally ill HCC patients in hospice are unique and should be managed appropriately.
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PMID:Hospice palliative care for patients with hepatocellular carcinoma in Taiwan. 1504 5

Left-sided portal hypertension due to splenic vein stenosis is a very rare disease. We report a case of this condition in a 21-year-old woman who suffered from a first episode of tarry stool passage with fresh blood vomiting. Panendoscopy showed isolated gastric varices while sonography showed a normal liver but the presence of splenomegaly with prominent collateral circulations. Further imaging studies, including abdominal computed tomography, splenoportography and percutaneous transhepatic portography, revealed a focal stenotic proximal splenic vein resulting in left-sided portal hypertension. The collateral circulation ran from the short gastric veins via the left gastric veins into the main portal vein. The intraportal venous pressure was within normal limits. Splenectomy was performed and near normal wedge liver biopsy pathology confirmed non-cirrhotic extrahepatic portal hypertension. The patient had no further variceal bleeding after surgery.
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PMID:Isolated gastric varices due to focal splenic vein stenosis. 1534 Jun 66

Arterio-venous fistulas may develop spontaneously, following trauma or infection, or be iatrogenic in nature. We present a rare case of a jejunal arterio- venous fistula in a 35-year-old man with a history of pancreatic head resection that had been performed two years previously because of chronic pancreatitis. The patient was admitted with acute upper abdominal pain, vomiting and an abdominal machinery-type bruit. The diagnosis of a jejunal arterio-venous fistula was established by MR imaging. Transfemoral angiography was performed to assess the possibility of catheter embolization. The angiographic study revealed a small aneurysm of the third jejunal artery, abnormal early filling of dilated jejunal veins and marked filling of the slightly dilated portal vein (13-14 mm). We considered the presence of segmental portal hypertension. The patient was treated with coil embolization in the same angiographic session. This case report demonstrates the importance of auscultation of the abdomen in the initial clinical examination. MR imaging and color Doppler ultrasound are excellent noninvasive tools in establishing the diagnosis. The role of interventional radiological techniques in the treatment of early portal hypertension secondary to jejunal arterio-venous fistula is discussed at a time when this condition is still asymptomatic. A review of the current literature is included.
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PMID:A rare case of jejunal arterio-venous fistula: treatment with superselective catheter embolization with a tracker-18 catheter and microcoils. 1557 44

A 31-year-old man was admitted to the hospital because of a low-grade fever, general malaise, nausea, vomiting, and a poor appetite. On admission his renal function was severely deteriorated (serum creatinine 16.12 mg/dl, BUN 163 mg/dl), and he had severe anemia (Hb 7.5 g/dl) and thrombocytopenia (67,000/microl). A radiological examination revealed the presence of multiple cysts in his kidneys bilaterally. The patient was diagnosed as having end-stage renal disease due to polycystic kidney disease, and hemodialysis was started on the day of admission. After the initiation of hemodialysis, his symptoms and laboratory tests improved, except for anemia and thrombocytopenia. He was noted to have marked splenomegaly and dilation of the portal vein, raising the suspicion of portal hypertension as the cause of the splenomegaly and pancytopenia. To treat his pancytopenia (anemia and thrombocytopenia) and to determine the reason for his portal hypertension, a splenectomy and open-wedge biopsy of the liver were performed. Histological findings in the liver included extensive fibrosis of the portal areas with an excess of moderately dilated bile ducts, compatible with a diagnosis of congenital hepatic fibrosis. After splenectomy, his red blood cell and platelet counts returned to normal, and he was discharged on maintenance dialysis. Congenital hepatic fibrosis is often associated with autosomal recessive polycystic kidney disease (ARPKD), but not with autosomal dominant polycystic kidney disease (ADPKD). However, both his mother and older brother had multiple renal cysts, indicating that this was an unusual case of ADPKD complicated by congenital hepatic fibrosis.
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PMID:[Case of autosomal dominant polycystic kidney disease associated with congenital hepatic fibrosis]. 1597 90

In advanced stages of polycystic liver disease, often associated with polycystic kidney disease, a curative therapy is liver or combined liver-kidney transplantation. However, little is known about long-term outcome and quality of life. Between 1990 and 2003, 36 patients (32 female, 4 male) with polycystic liver or combined liver-kidney disease underwent liver (n = 21) or liver-kidney (n = 15) transplantation at our center. Main indications for liver transplantation were cachexia, muscle atrophy, loss of weight, recurrent cyst infections, portal hypertension, and ascites. Apart from clinical parameters, 2 anonymous questionnaires (standard short form 36 and self-designed) addressing quality of life and social status were evaluated. Five patients (14 %) died due to sepsis or myocardial infarction with pneumonia, all within 61 days after transplantation. The follow-up time of the remaining 31 patients ranged from 5 to 156 months, with a mean of 62 months. Of the 23 (74%) answered the questionnaires, 91% of patients felt "much better" or "better," only 9% felt "worse" than before, and 52% of patients participated in sports regularly. Fatigue, physical fitness, loss of appetite, and vomiting improved significantly after transplantation. Physical attractiveness and interest in sex increased as well. Professional occupation did not change for 71% of patients. Family situation before and after transplantation changed in 1 case only. Finally, 78% of patients said they would opt for transplantation again, while 17% were undecided; 1 patient would not repeat transplantation. In conclusion, patients with advanced polycystic liver or polycystic liver-kidney disease have an excellent survival rate and an improved quality of life after liver or combined liver-kidney transplantation.
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PMID:Outcome and quality of life in patients with polycystic liver disease after liver or combined liver-kidney transplantation. 1686 56

Sixty four children (38 boys and 26 girls), aged 1 yr to 14 yr, presenting with fever, splenomegaly and positive LD body in splenic smear examination, admitted to pediatric ward of Nalanda Medical college and Child care center between 1st July 03 to 30th June 04 were taken for study. Patients were categorized into two groups: 44 were in Group I (Patients who had not received prior antileishmanial drug) and 20 in Group II (Patients who had received 30 days course of SAG; 20 mg per kg per day). All patients were given Miltefosine in dose of 2.5 per kg per day od or bid per orally to a maximum of 100 mg and were followed at completion of therapy, 1 month and 6 months for clinical response, splenic size and parasite density. 63 patients had parasitological cure with relapse in one patient of Group I during follow up. One patient in Group II had no response with first course but became parasitologically negative with 2nd course of Miltefosine. In Group I, one patient had persistent splenomegaly and found to have associated portal hypertension. GI side effects i.e. diarrhea and vomiting were observed in 26 and 23 patients respectively. Majority of patients had pancytopenia. Elevated ALT (> 3 times of normal) were seen in 28 and 11 patients of Group I and Group II respectively which returned to normal in subsequent follow up. The final cure rates were 93.2 percent and 95 percent in Groups I and II respectively.
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PMID:Miltefosine in children with visceral leishmaniasis. 1720 5


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