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)

A 12-year-old girl was admitted to our hospital with signs of an acute abdomen with paralytic ileus. The previous and family history were without abnormalities. Abdominal pain and vomiting had started two days earlier. On palpation the swollen abdomen was painful and there was an increased tension in the left upper part. The clinical diagnosis of acute pancreatitis was confirmed by an increased serum level of lipase (4480 U/l). Clinical chemical investigations further revealed a permanent hypercalcemia in the range of 6.4 to 8.3 mval/l. This, together with concomitantly reduced levels of serum phosphate and a threefold increased level of parathyroid hormone (343 pg/ml, upper limit of reference = 100 pg/ml) were consistent with a hyperparathyroidism. In fact, sonography of the cervical organs revealed a solitary adenoma of the parathyroid glands. After surgery serum levels of calcium returned to normal. Hypercalcemia as a consequence of primary hyperparathyroidism has to be included in the differential diagnosis of acute pancreatitis in childhood.
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PMID:[Acute pancreatitis as an initial manifestation of hypercalcemia in primary hyperparathyroidism in childhood]. 265 77

A 47-year-old female patient with a primary carcinoma of the jejunum combined with colon polyp is presented. Having had an attack of vomiting, she visited our hospital. Oral small intestine radiography revealed a localized stricture with ulceration in the jejunum. Small intestinal endoscopy showed a tumor with an irregular surface and hemorrhagic ulceration. Selective superior mesenteric arteriography revealed a stenosis and deviation of arteries. These findings strongly indicated cancer of the jejunum, and a barium enema study and a colonoscopic examination revealed a polyp in the ascending colon. The resected tumor was histologically diagnosed as a well differentiated adenocarcinoma. CEA-positive cells also were observed. Further, a polypoid lesion in the colon was histologically diagnosed as an adenoma.
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PMID:[Primary carcinoma of the jejunum combined with colon polyp--report of a case]. 272 51

A 48-year-old man was admitted for treatment of Cushing's syndrome due to right adrenal adenoma, associated with chronic renal failure (CRF) with a blood urea nitrogen level of 64.2 and serum creatinine level of 3.9 mg/dl. After removal of the adrenal adenoma, the CRF deteriorated with progressive symptoms of anorexia, vomiting and hypertension, and the patient was placed on hemodialysis. Prior to adrenalectomy, the 17 OHCS and 17 KGS in the urine were not so high. However, the urinary 17 KS was high with an elevated 11-oxy fraction. In comparison with 2 patients suffering from adrenal Cushing's syndrome with normal renal function, there were no large accumulated quantities of glucuronic conjugated and unconjugated metabolites in the plasma of the CRF Cushing's syndrome, with confirmation ascribable to the radioimmunoassayable cross-reactivity of the cortisol antiserum used in the radioimmunoassay kit. In the Cushing's syndrome with CRF, almost all the cortisol, which was hypersecreted from the adenoma, was presumed to be converted to the 11-oxy fraction of 17 KS, possibly by activation of hepatic enzymes.
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PMID:Cortisol and its metabolites in the plasma and urine in Cushing's syndrome with chronic renal failure (CRF), compared to Cushing's syndrome without CRF. 279 94

The effects of dihydroergocriptine (DHECP), a dihydrogenated ergot alkaloid with dopaminergic agonistic and alpha-adrenergic antagonistic properties, were studied in 22 women with PRL-secreting microprolactinomas and compared with those recorded in 36 previously studied patients treated with bromocriptine (BRC). After acute administration of 5 mg DHECP, orally, serum PRL decreased by 61 +/- 18% (+/- SD); only 1 patient was unresponsive. The nadir was reached at 300 min. Long term treatment with increasing DHECP doses caused a progressive PRL fall from 125 +/- 142 (+/- SD) to 81 +/- 159 micrograms/L after 1 week of a 3 mg twice daily regimen, to 64 +/- 88 micrograms/L after 1 week of 5 mg twice daily, 46 +/- 57 micrograms/L after 1 week of 10 mg twice daily, and 28 +/- 34 to 33 +/- 45 micrograms/L throughout 9 months of treatment with 10 mg DHECP 3 times daily. Seventy-seven percent of patients had normal serum PRL levels during chronic treatment. All women, including those with supranormal serum PRL levels, resumed regular menses, and 16 had ovulatory cycles; 1 woman became pregnant. Galactorrhea disappeared in all. During treatment the PRL response to TRH, initially absent in all patients, became positive in 10. In 7 patients, after DHECP treatment for 9 months, high definition computed tomographic scan no longer showed the focal lesions initially seen. After drug withdrawal, serum PRL increased again in all except 1 patient. Two patients had regular menses for 6 months, and 3 still had no adenoma imaged by high definition computed tomography. In BRC-treated patients the serum PRL changes and clinical results were very similar to those in the DHECP-treated patients, except for the persistence of normal serum PRL levels in 4 patients after drug withdrawal. On the other hand, side-effects were negligible during DHECP treatment, but remarkable during BRC. Systolic and diastolic blood pressures decreased by only 5.4 and 3.0 mm Hg, respectively, after acute 5 mg DHECP administration, but decreased by 12.8 and 14 mm Hg after acute 2.5 mg BRC administration. Orthostatic hypotension and peripheral vasomotor phenomena occurred in the long term DHECP treated patients except one, but they occurred in 9 and 3 of those treated with BRC, respectively. Gastric discomfort or mild nausea occurred in 12 DHECP-treated patients, while mild or severe nausea or vomiting were observed in 18, 11, and 2 of those taking BRC, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dihydroergocriptine in management of microprolactinomas. 311 32

Cecal perforation was diagnosed in a dog with a history of acute vomiting. The dog also had an adrenocortical adenoma. Intestinal perforation can be a serious complication of cortico-steroid treatment in the dog, but has not been attributable to hyperadrenocorticism. Fever and an inflammatory CBC were not observed, which could have been secondary to adrenal-dependent hyperadrenocorticism. The acute abdominal crisis associated with peritonitis required quick resolution in an attempt to save the dog, but also precluded any further diagnostic procedures for possible hyperadrenocorticism. The signs that suggested hyper-adrenocorticism in this dog included alopecia, lymphopenia, eosinopenia, high liver enzyme activities, hypercholesterolemia, and one large and one small adrenal gland. This latter finding presumably indicated negative feedback suppression and atrophy attributable to a functional adrenocortical adenoma.
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PMID:Cecal perforation and adrenocortical adenoma in a dog. 361 Jul 87

The case of a 60-year-old woman with pheochromocytoma and concomitant adrenocortical adenoma in the same gland is presented. She complained of episodic headache, palpitation, nausea, vomiting and sweating. Physical examination revealed that the patient has generalized obesity, wet skin and paroxysmal hypertension, but no signs of Cushing's syndrome. Elevated levels of urinary noradrenaline, adrenaline and total metanephrine were sequentially observed. In addition, urinary 17-OHCS was also slightly elevated, but plasma cortisol was normal and suppressed after oral administration of 0.5 mg of dexamethasone. Abdominal echography and CT scanning demonstrated a left adrenal tumor, which took up both 131I-meta-iodobenzylguanidine and 75Se-scintadoren in the same region. A left adrenalectomy was performed and the tumor was found to consist of two parts, pheochromocytoma (2.5 X 2.5 X 2.5 cm) and cortical adenoma (2.5 X 3 X 5 cm). A total of 23 reported cases showing evidence of hyperfunction of the adrenal cortex and the medulla were noted. So far as we know, this patient was the second case of pheochromocytoma with adrenocortical adenoma in Japan.
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PMID:Pheochromocytoma associated with adrenocortical adenoma: case report and literature review. 372 Jun 79

Macroprolactinomas have a well-recognized potential for marked expansion during pregnancy. Measures advocated to minimize this risk include prior treatment with dopamine agonists, radiotherapy and pituitary surgery. We describe a patient who underwent transsphenoidal surgery with the removal of an histologically proven prolactin-secreting adenoma with the intention of rendering subsequent pregnancy safe. The patient remained hyperprolactinaemic and received prolonged therapy with metergoline and bromocriptine which suppressed prolactin to normal and she conceived after induction of ovulation with human menopausal gonadotrophin and human chorionic gonadotrophin. At 3 months gestation she developed headaches, vomiting, reduced visual acuity and bitemporal hemianopia caused by massive pituitary expansion. Reintroduction of bromocriptine rapidly abolished features of tumour expansion and after delivery of a full-term normal female infant, repeat CT scan documented tumour shrinkage.
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PMID:Failure of prophylactic surgery to avert massive pituitary expansion in pregnancy. 379 72

An adult Keeshond had clinical signs associated with hypercalcemia, including inappetence, polyuria, polydipsia, and vomiting. Blood biochemical findings and urinary clearance studies were consistent with a diagnosis of primary hyperparathyroidism. Histomorphometric analysis of trabecular bone in an iliac crest biopsy indicated increased bone remodeling activity. Surgical exploration of the neck revealed an oval mass, which was removed by blunt dissection. Histologic diagnosis was parathyroid gland adenoma. The dog died because of renal failure on the eighth postoperative day. This report defines primary hyperparathyroidism in the dog, thus facilitating diagnosis for the veterinary clinician.
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PMID:Primary hyperparathyroidism in a dog: biochemical, bone histomorphometric, and pathologic findings. 380 43

Budd Chiari Syndrome, characterized by massive ascites, hepatomegaly, abdominal pain, and tenderness, nausea, and vomiting, is caused by obstruction of the hepatic venous outflow. Of the known causes of polycythemia rubra vera, hypernephroma, and other tumors invading the inferior vena cava have been most often reported, while pregnancy and oral contraceptives (OCs) have also been held as causes. In this paper the case is presented of a young woman, previously on OCs for 4 months, who developed the syndrome 2 weeks after delivery; she was also found to have multiple hepatic adenomas on laparotomy. The longterm use of OCs has been estimated to be associated with an annual incidence of liver cell adenoma of 3-4/100,000. Evidence suggests that the estrogen components, rather than the progesterone, of OCs seem more likely to cause liver cell adenoma since estrogens are carcinogenic in other organs and promote liver cell regeneration in rats. By interference with the metabolism of oncogenic bile salt derivatives, estrogen may exert its oncogenic effect. The patient is this case was told never to use OCs again since there is also evidence that the tumor may regress on stopping OCs, and she was advised against further pregnancies.
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PMID:Budd-Chiari syndrome and hepatic adenomas associated with oral contraceptives. A case report. 627 27

A 32-year-old woman with a contraceptive history of use of combination contraceptives (Oviston, Non-Ovlon) between 1966 and 1979 (with a 1-year interruption), followed by radical hysterectomy in 1979, complained of dull right upper quadrant pain, nausea, vomiting, and fatigue in 1980. Among various diagnostic studies performed only cholecystography and cholangiography demonstrated clear areas in the gallbladder assumed to be stones. Cholecystectomy performed in 1981 showed chronic inflammation of the gallbladder without stones. The undersurface of the liver revealed a greyish tumor (3 cm in diameter). Frozen section demonstrated mature hepatocellular adenoma. Wedge excision of the tumor and cholecystectomy were performed without complications. CAT-scan follow-up showed no residual pathology. Additional literature search reports 58 cases in western European and American journals. Diagnosis of these benign tumors is difficult because the symptoms are vague. The main complication is intraabdominal hemorrhage necessitating emergency lobectomy. Ligation of a branch of the hepatic artery is done in case of inoperability. CAT-scan and ultrasonography with selective angiography are the best procedures to ascertain the diagnosis. Needle biopsy is contraindicated because of the risk of hemorrhage.
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PMID:[Hepatocellular adenoma following long-term intake of ovulation inhibitors]. 630 51


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