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)

Hyponatremia, albeit common in chronic renal insufficiency, necessitates a detailed search of the underlying hidden causes. We report on a 67-year-old woman with chronic kidney disease (creatinine 230 micromol/L) and hypertension who suffered from general fatigue, dizziness, nausea, vomiting and abdominal fullness off and on for 6 months. Hyponatremia (plasma Na(+) 106-125 mmol/L) on 4 occasions during the past 6 months was noticed. Her extracellular volume status was apparently normal. Plasma Na(+) concentration 110 mmol/L was the most striking laboratory abnormality with mild metabolic acidosis (HCO(3)- 19.8 mmol/L). Her urine Na(+) concentration and osmolality were inappropriately high. Her hyponatremia was refractory to normal saline, hypertonic NaHCO(3) and 0.1-microg 9 alfa-fludrocortisone. Despite normal plasma cortisol and thyroid hormone concentrations, a provocation test with cosyntropin (250 microg) showed a blunted cortisol (<579 nmol/L) but intact aldosterone response. Magnetic resonance imaging of her brain displayed a normal pituitary gland and hypothalamus. A history of intermittent intravenous steroid therapy to treat her allergic rhinitis for 3 years was uncovered. Steroid supplements induced water diuresis and corrected hyponatremia to 135 mmol/L in 5 days. With nonspecific clinical symptoms, glucocorticoid insufficiency must be kept in mind as a cause of hyponatremia even in patients with impaired renal function and normal plasma cortisol concentration.
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PMID:Recurrent hyponatremia in a patient with chronic kidney disease. 1687 5

This study involved longitudinal evaluations of symptom severity and describes the symptom patterns of 77 terminal cancer patients (median age: 62 years; 61% female), selected from 537 consecutive patients admitted to the Palliative Care Unit of the National Taiwan University Hospital. The most common primary cancer sites in these patients were lung (23.4%), liver (15.6%), and stomach (13%). Nineteen physical and psychological symptoms were assessed using different scales. The median number of symptoms was 11 (range: 1-18) on admission, among which weakness, fatigue, anorexia, pain, and depression were the most common. A comparison of the initial symptom severity scores with those at one week after admission and two days before death suggested six symptom change patterns: A: continuous static (restless/heat, abdominal fullness, constipation, dizziness, and insomnia); B: static-increase (fatigue, weakness, nausea/vomiting, taste alteration, dysphagia, diarrhea, dry mouth, and night sweats); C: decrease-static (pain and depression); D: decrease-increase (anorexia and dyspnea); E: static-decrease (aggression); and F: gradually decrease (anxiety). These six symptom patterns can be divided into two categories on the basis of the relative severity of symptoms between one week after admission and two days before death. The first category included patterns A, C, E and F, and the symptoms improved with palliative care. However, the symptoms in the second category (patterns B and D), which were associated with the anorexia-cachexia syndrome and dyspnea, did not show improvement. As symptom management is an essential component of palliative care, holistic care, which encompasses physical, psychosocial and spiritual aspects, represents a rational approach for the relief of these incurable symptoms at the end stage of life for these patients.
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PMID:Symptom patterns of advanced cancer patients in a palliative care unit. 1706 Feb 55

A 56-year-old woman with obesity and poorly controlled diabetes mellitus presented with a two-day history of abdominal fullness and vomiting. No fever, flank pain or dysuria was present. On admission, her blood urea nitrogen concentration was 74 mg per deciliter and the serum creatinine concentration was 3.5 mg per deciliter. Laboratory data revealed an elevated white blood cell count (11.72 x 10(3)/ml), blood sugar (826 mg/dl), pyuria (WBC 30-50/HPF) and negative urine ketone. A plain abdominal radiograph revealed right renal stones and localized air accumulation at the left upper abdominal area.
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PMID:Emphysematous pyelonephritis with acute renal failure. 1861 55

Spontaneous rupture of the short gastric artery is an extremely rare event that can cause abdominal apoplexy or spontaneous hemoperitoneum. For the emergency physician, simultaneous restoration of circulatory volume and a rapid diagnosis remain central to a successful outcome in such critical cases. We reported a 21-year-old man who initially presented with watery diarrhea and abdominal fullness followed by vomiting after the ingestion of alcohol but was later diagnosed with hemoperitoneum, resulting in hemorrhagic shock due to spontaneous rupture of the small branches of the short gastric artery. The patient underwent emergency exploratory laparotomy with a good outcome. Abdominal apoplexy should be considered in the differential diagnosis of unexplained hemorrhagic shock with an abrupt onset of severe abdominal pain associated with vomiting.
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PMID:Spontaneous rupture of the short gastric artery after vomiting. 2135 50

Gastroparesis is a disorder characterized by a delay in gastric emptying of a meal in the absence of a mechanical gastric outlet obstruction. Diagnosis of gastroparesis is based on the presence of symptoms ( nausea, vomiting, postprandial abdominal fullness), excluded mechanical obstruction (endoscopy) and on objectively determined delay in gastric emptying. Gastric emptying can be assessed by scintigraphy and stable isotope breath tests. The true prevalence of gastroparesis is unknown. The aetiology of gastroparesis is diverse. In approximately one third of cases, gastroparesis is related to the presence of diabetes mellitus; one third of case is of unknown cause (idiopathic). Mild disease will respond to dietary and life style measures and prokinetics (domperidone, metoclopramide, erytromicyne). Severe disease can benefit from intrapyloric botulinum toxin injection, gastric pacing or more radical surgical interventions (partial or total gastrectomy).
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PMID:[Gastroparesis--diagnosis and treatment]. 2149 37

Gastroparesis is a disorder characterized by a delay in gastric emptying of a meal in the absence of a mechanical gastric outlet obstruction. The most common etiologies include diabetes, postsurgical and idiopathic. Idiopathic Gastroparesis is at least as common as diabetic Gastroparesis in most case series. Diagnosis of Gastroparesis is based on the presence of symptoms such as nausea, vomiting, postprandial abdominal fullness, and on an objectively determined delay in gastric emptying. The true prevalence of Gastroparesis is unknown. Gastric emptying can be assessed by scintigraphy and stable isotope breath tests. Management of Gastroparesis consists of dietary and lifestyle measures, possible pharmacological interventions (prokinetics, antiemetics, intrapyloric botulinum toxin injection) and/or interventions that focus on adequate nutrient intake either through a nasoduodenal tube, percutaneous gastrostomy, or jejunostomy. New advances in drug therapy and gastric electrical stimulation techniques have been introduced and might provide new hope to patients. Presented here is an interesting case of idiopathic Gastroparesis along with its management and review of the literature.
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PMID:Idiopathic gastroparesis: case report and literature review of diagnostic and treatment modalities. 2179 94

Gastroparesis is a condition characterized by delayed gastric emptying and the most common known underlying cause is diabetes mellitus. Symptoms include nausea, vomiting, abdominal fullness, and early satiety, which impact to varying degrees on the patient's quality of life. Symptoms and deficits do not necessarily relate to each other, hence despite significant abnormalities in gastric emptying, some individuals have only minimal symptoms and, conversely, severe symptoms do not always relate to measures of gastric emptying. Prokinetic agents such as metoclopramide, domperidone, and erythromycin enhance gastric motility and have remained the mainstay of treatment for several decades, despite unwanted side effects and numerous drug interactions. Mechanical therapies such as endoscopic pyloric botulinum toxin injection, gastric electrical stimulation, and gastrostomy or jejunostomy are used in intractable diabetic gastroparesis (DG), refractory to prokinetic therapies. Mitemcinal and TZP-101 are novel investigational motilin receptor and ghrelin agonists, respectively, and show promise in the treatment of DG. The aim of this review is to provide an update on prokinetic and mechanical therapies in the treatment of DG.
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PMID:Diabetic gastroparesis: Therapeutic options. 2212 72

Hydatid disease is a parasitic infestation caused by the tapeworm Echinococcus granulosus. Echinococcosis occurs worldwide and can affect multiple organs. The liver (75%) and the lungs (15%) are the most common sites of occurrence followed by the spleen, kidney, bones and brain. Peritoneal hydatidosis commonly occurs secondary to a ruptured hydatid cyst of the liver or the spleen. Primary peritoneal hydatidosis is an extremely rare entity accounting for just 2% of all intra-abdominal hydatid disease. Most patients remain asymptomatic for years before presenting with vague abdominal symptoms such as non-specific pain, abdominal fullness, dyspepsia, anorexia and vomiting. We successfully treated a 55-year-old woman with primary peritoneal hydatidosis. The role of imaging and immunological tests in the diagnosis is highlighted. The patient was managed by a combination of preoperative and postoperative antihelminthic therapy along with laparotomy, cyst deroofing, toileting and omentoplasty. The patient is asymptomatic at 1-year follow-up.
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PMID:Primary peritoneal hydatidosis. 2391 61

An 80-year-old man presented with abdominal fullness and vomiting. Laboratory data revealed severe anemia, an inflammatory response, and elevated white blood cell counts. Abdominal computed tomography indicated ileus caused by a jejunal tumor measuring 8cm in diameter. Although small-bowel endoscopy enabled visualization of the tumor, adequate biopsy specimens could not be obtained for accurate diagnosis. The patient's condition rapidly deteriorated, because of which surgical treatment could not be initiated. The patient died approximately 3 weeks after admission. High serum granulocyte colony-stimulating factor (G-CSF) levels were detected at autopsy. Immunohistochemical staining of the autopsy specimen indicated positive G-CSF levels in the jejunal tumor. On the basis of these findings, a final diagnosis of undifferentiated carcinoma of the jejunum producing G-CSF was made.
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PMID:[Undifferentiated carcinoma of the jejunum producing granulocyte colony-stimulating factor]. 2450 Mar 20

The patient was a 58-year-old man diagnosed with type 2 advanced gastric cancer located at the fundus with multiple liver, lung, and lymph node metastases(Stage IV). Examination of an endoscopically obtained biopsy specimen revealed poorly differentiated adenocarcinoma (por), which stained positive for human epidermal growth factor receptor 2 (HER2) on immunohistochemistry. We started chemotherapy with S-1 plus cisplatin (CDDP) plus trastuzumab. The treatment was effective, as the tumor had reduced in size by 22.5% and 36.2%(partial response[PR])after 3 and 6 courses, respectively. Adverse events related to the treatment were limited to grade 1 fever, nausea, vomiting, and diarrhea. The patient's chief complaints of right upper abdominal pain and abdominal fullness remarkably improved after treatment initiation. Although the therapy was effective against the multiple liver metastases and could be continued for 11 courses, the lymph nodes metastases did not respond to therapy (progressive disease [PD]), and the patient died 9 months after the start of treatment. Chemotherapy with S-1 pus CDDP plus trastuzumab may be effective for HER2-positive advanced gastric cancer with liver metastasis.
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PMID:[A case of advanced gastric cancer with multiple liver, lung, and lymph node metastases treated with S-1, CDDP, and trastuzumab]. 2524 5


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