Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparative controlled study was carried out in 40 patients suffering from rheumatoid arthritis, osteoarthrosis or ankylosing spondylitis to assess the efficacy of ketoprofen and ibuprofen. Patients were allocated at random to receive either 100 mg ketoprofen twice daily or 400 mg ibuprofen 3-times daily over a period of 3 months. Subjective overall assessments of symptoms, based on rating scale scores for pain, duration of morning stiffness and inflammation, showed that there was a greater, more rapid and more sustained improvement in those patients treated with ketoprofen. Measurements of inflamed joint size and of grip strength also improved more with ketoprofen than with ibuprofen. Side-effects, notably nausea, epigastric discomfort and abdominal pain, were more frequent and severe with ketoprofen, leading to the withdrawal of 2 patients in the early stage of the trial, and were probably related to the high dosage used. Three patients receiving ibuprofen needed 7 injections of ACTH to control their symptoms.
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PMID:A comparative trial of ketoprofen and ibuprofen in patients with rheumatic disease. 35 May

We described here a seventy-one year-old male, who had repeated disseminated intravascular coagulation related to atherosclerosis and aneurysm of the aorta, and was successfully treated with self-subcutaneous injection of heparin sodium. He developed gingival bleeding and purpura in 1977. He was first treated with prednisolone (30 mg/day) and ACTH-Z under the diagnosis of idiopathic thrombocytopenic purpura associated with chronic thyroiditis, since platelet count (0.2 x 10(4)/microliters) was markedly decreased and megakaryocytes in the bone marrow were increased. By the treatment, platelet count recovered to 16.7 x 10(4)/microliters, while fibrin-degradation product levels were increased and hypofibrinogenemia developed, suggesting disseminated intravascular coagulopathy. Additional treatment with heparin was effective, and the coagulation studies became normal. In 1980, he again developed the episode with thrombocytopenia. At this time, prednisolone did not improve the episode, but heparin was effective. Since 1983, an enlargement of abdominal aorta had been recognized and gradually progressed. In 1983, he developed lumbago and abdominal pain, and received an emergency operation using artificial Y-graft vessel under the diagnosis of rupture of the aneurysm. There was no evidence of consumption coagulopathy at that time. He had been well until 1987, when he developed the third episode of thrombocytopenia with gingival bleeding. Thrombocytopenia was controlled with the treatment of heparin, but needed a continuous treatment with heparin. Thereafter, he has been well managed with self-injection of the anticoagulant, heparin sodium.
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PMID:[Disseminated intravascular coagulation related to atherosclerosis and aneurysm of aorta: successful management with subcutaneous self injection of heparin sodium]. 259 49

A 9 1/2-year-old girl is presented who had cyclical attacks of abdominal pain, vomiting, emotional disturbance, and marked weight change for two years. Associated findings were facial plethora, hypertension, transient hyperglycemia and glycosuria, elevated plasma ACTH, cortisol, and urinary 17-OHCS excretion, and low plasma osmolality with hyponatremia. Urinary excretion of catecholamines and porphyrin metabolites was not increased. Between episodes, she showed no abnormal clinical signs or laboratory data. The attacks were effectively suppressed with the administration of chlorpromazine. The disorder appears to be due to the periodic release of excessive ACTH; the cause remains unknown.
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PMID:Periodic ACTH discharge. 624 2

We encountered a patient with siolated ACTH deficiency accompanying dementia. A 69-year old man was admitted because of abdominal pain. A decrease of serum Na level (114mEq/l) due to increased urinary Na excretion suggested the existence of adrenal insufficiency. While serum cortisol and urinary 17-OHCS, 17-KS excretions were reduced, plasma ACTH level remained below the normal range. Since daily ACTH injections increased both serum cortisol level and urinary 17-OHCS excretion, the patient was diagnosed as having isolated ACTH deficiency. The severity of dementia was measured by using the Hasegawa Dementia Scale. Both cerebral blood flow and metabolism, assessed with Positron Emission Computed Tomography (PET), decreased even after the start of 20mg/day cortril administration. An increase of the cortril supplement dose to 30mg/day attenuated the reduction of cerebral blood flow with the improvement of dementia from score point "1" to "27" (Hasegawa scale). The present case raised the possibility that loss of glucocorticoid may involve the development of dementia, resulting from decreased cerebral blood flow and metabolism.
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PMID:[A case of isolated ACTH deficiency with dementia]. 785 24

Anecdotes and animal experiments alike suggest that physiological and psychological stress can profoundly alter gastrointestinal function. However, few studies have examined, in humans, real-world stress to see if free-living persons exhibit gut alterations similar to those produced in the laboratory. To investigate this possibility, we studied 16 medical and premedical students during final written examinations. As compared to a control day, the examination created a classic stress response: elevated serum cortisol (16 +/- 1 to 21 +/- 3 micrograms/dl; P < 0.05), ACTH (31 +/- 1 to 33 +/- 1 pg/ml; P < 0.05), heart rate (72 +/- 3 to 79 +/- 3 beats/min; P < 0.05), arterial blood pressure (systolic pressure 106 +/- 2 to 120 +/- 2 torr; P < 0.05; diastolic pressure 72 +/- 2 to 77 +/- 1 torr; P < 0.05), and subjective anxiety (raw score 28 +/- 2 to 47 +/- 3; P < 0.0001). In contrast, subjects displayed identical orocecal liquid transit time (of 0.36 g/kg lactulose in a 240-ml, 250-kcal liquid meal) under control (103 +/- 8 min) and examination conditions (106 +/- 8 min; P = NS). Mean subjective reports of gas, diarrhea, and borborygmi were unchanged on the day of the experiment, although the examination did increase reported abdominal pain (from 0.5 +/- 0.4 to 2.1 +/- 0.5 on a 0-5 analog scale; P < 0.05). We conclude that examination stress in humans can increase gastrointestinal symptoms without altering orocecal transit.
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PMID:Increased abdominal pain during final examinations. 828 43

Gastric carcinoid tumors arise from enterochromaffin-like (ECL) cells, these tumors represent 2-41% of all neuroendocrine tumors and 0.3% of malignant gastric neoplasias, being more common in men than in women, and commonly affecting people over 60 years old. These tumors arise from accelerated proliferation of the ECL cells as a consequence of the hypersecretion of gastrin, situation that can be present in atrophic gastritis and the Zollinger-Ellison syndrome. We report the case of a 51 year old hispanic female who presented with a 3 month history of abdominal pain, meteorism and constipation; she was treated with ranitidine and metoclopramide without clinical improvement, thus she underwent upper gastrointestinal endoscopy which showed an atrophic gastritis and gastric polyps. Histopathologic examination revealed a neuroendocrine gastric tumor which was positive to serotonine and gastrin stainings. Hormonal screening showed normal serum levels of LH, FSH, estradiol, ACTH, progesterone, calcitonin and cortisol. The serum level of gastrin was elevated with 500 pg/mL. Gammagraphic scanning with octreotide was negative for metastasis.
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PMID:[Gastric neuroendocrine tumor]. 1006 36

We report a 27-year-old female with Crohn's disease clinically misdiagnosed with intestinal endometriosis. Her complaints were abdominal pain and fullness, which occurred monthly during her menstrual period. Although we had no histopathological evidence, we diagnosed her as bowel endometriosis on the basis of her clinical course. Since nafarelin acetate therapy started, the symptoms due to mechanical subileus have improved. The transverse colon, a 70 cm segment of the ileum, including the terminal ileum, were resected because of repeated symptoms of bowel obstruction despite prolonged nafarelin therapy. Histopathological findings of the resected specimen revealed Crohn's disease without endometrial tissue. In our patient, an increased cortisol and ACTH secretion, a side effect of nafarelin, was noted during the therapy. This case showed that nafarelin therapy could increase serum concentration of ACTH and cortisol, which was considered to suppress the pathology of Crohn's disease by its anti-inflammatory action. We emphasize that intestinal examination must be performed with Crohn's disease in mind, even if nafarelin acetate is effective.
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PMID:Crohn's disease mimicking as bowel endometriosis. Are the symptoms reduced by nafarelin acetate? 1076 42

We experienced two Duchenne muscular dystrophy patients with advanced congestive heart failure, who showed abrupt severe hyponatremia, hyperkalemia and metabolic acidosis. Two patients received respiratory management, parenteral nutrition, and drugs including angiotensin converting enzyme inhibitors (ACEI). The patient 1 who was 19 years old showed abdominal pain, hematuria, diarrhea and disorientation. Laboratory findings were as follows; Na 120 mEq/L, K 7.3 mEq/L, BUN > 140 mg/dl (scale over), ACTH 20.2 pg/ml, cortisol 25 micrograms/dl, renin 40.7 ng/ml/hr and aldosterone 203 ng/dl. Arterial blood gas analysis (ABG) showed metabolic acidosis (pH 7.232). Combination therapy with hydrocortisone, glucose-insulin therapy (GIT) and NaHCO3 successfully rescued this patient. The patient 2 (28 years of age) was admitted to our hospital because of congestive heart failure. Laboratory findings were as follows; Na 129 mEq/L, K 5.5 mEq/L, BUN 60 mg/dl, cortisol 21 micrograms/dl, renin 36 ng/ml/hr and aldosterone 47 ng/dl. He complained abdominal discomforts from the next day of admission. Ten days after the admission Na, K and BUN were 111 mEq/L, 6.2 mEq/L and 154 mg/dl, respectively. ABG showed compensated metabolic acidosis. He fell into shock during GIT therapy. Laboratory findings at that time were as follows; Na 108 mEq/L, K 3.2 mEq/L, ACTH 77.6 pg/ml, cortisol 24 micrograms/dl, renin 58 ng/ml/hr and aldosterone 24 ng/dl. Although hydrocortisone was introduced, he could not recover and died. There are some reports about life-threatening electrolyte abnormalities and metabolic acidosis in the patients receiving ACEI. These phenomena were more frequent in patients with renal dysfunction and/or congestive heart failure. Hyponatremia, hypovolemia, combination therapy with nonsteroidal anti-inflammatory drugs (NSAID) and/or potassium sparing diuretics were reported as risk factors. We could not prove the correlation between the acute changes in our cases and ACEI. However ACEI is suspicious, because many of these risk factors were observed in our cases. Aldosterone was extremely elevated in the patient 1 when potassium was severely elevated. On the other hand, the patient 2 showed lower aldosterone level after correction of potassium than that on admission. Potassium is regarded as a major secretion factor of aldosterone for patients receiving ACEI. The fact the patient 2 fell into shock during GIT, tells us that we should use steroid simultaneously when we try to correct potassium quickly in severe cases, because acute reduction of potassium may decrease aldosterone. Today, ACEI is a common drug for CHF, so we should pay attentions that ACEI could cause such acute changes. To prevent such acute changes, excessive restriction of water and sodium intake should be avoided. If possible, NSAID and potassium sparing diuretics also should be avoided. Steroid therapy must be introduced rapidly when needed.
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PMID:[Electrolyte abnormalities and metabolic acidosis in two Duchenne muscular dystrophy patients with advanced congestive heart failure]. 1100 25

To describe the clinical and immunologic characteristics of patients with adrenal involvement and antiphospholipid syndrome (APS), we conducted a computer-assisted (PubMed) search of the literature to identify all cases of primary adrenal insufficiency associated with antiphospholipid antibodies published in English, French, and Spanish from 1983 (when APS was first defined) through March 2002. We reviewed 86 patients (80 from the literature plus 6 from our cohort); 55% were male, and the mean age at presentation was 43 +/- 16 years. Sixty-one (71%) patients had primary APS, and 14 (16%) had systemic lupus erythematosus. In 31 (36%) patients, adrenal insufficiency was the first clinical manifestation of APS. Abdominal pain was present in 55% of patients, followed by hypotension (54%), fever (40%), nausea or vomiting (31%), weakness or fatigue (31%), and lethargy or altered mental status (19%). The main finding in imaging techniques was compatible with adrenal hemorrhage (59%) and in histopathologic study was a hemorrhagic infarction with vessel thrombosis (55%). Lupus anticoagulant was detected in 97% of patients and the anticardiolipin antibodies titer was positive in 93% of patients. Most patients (95%) were positive for the IgG isotype of anticardiolipin antibodies, whereas 40% were positive for the IgM isotype. Baseline cortisol levels were decreased in 98% of patients, ACTH hormone levels were increased in 96% of patients, and the cosyntropin stimulation test was positive in 100% of patients tested. Steroid replacement therapy was the most frequent treatment (84%), followed by anticoagulation (52%) and aspirin (6%). Thirty-two of 35 (91%) patients with prolonged anticoagulant therapy were in good health with a mean follow-up of 25 months, whereas 25 of the 69 (36%) patients with outcome data available had died. The results of the present review stress the clinical importance of systematic screening for lupus anticoagulant and anticardiolipin antibodies in all cases of adrenal hemorrhage or infarction. An initial screening for hypoadrenalism is mandatory in any antiphospholipid antibody-positive patient who complains of abdominal pain and undue weakness or asthenia.
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PMID:Adrenal involvement in the antiphospholipid syndrome: clinical and immunologic characteristics of 86 patients. 1264 Jan 87

We present a 54-yr-old woman with ectopic corticotropin syndrome caused by a neuroendocrine tumor of the pancreas. At initial presentation, the patient suffered from diarrhea, heartburn, and nonspecific abdominal pain. There was no evidence of Cushing's syndrome. A neuroendocrine tumor in the head of the pancreas with metastases into peripancreatic lymph nodes was diagnosed and completely resected. Fourteen months later, abdominal computed tomography and scintigraphy with (111)In-labeled octreotide suggested relapse of the tumor. The patient again had no evidence of Cushing's syndrome. A second in toto tumor resection was performed. Another 8 months later, the patient developed forgetfulness, depressive episodes, muscle weakness, new-onset hypertension, hypokalemia, plethora, diabetes mellitus, polyuria, and weight loss. Endocrine testing suggested a source of ectopic ACTH production. An octreotide scan showed an intense uptake ventromedial of the left kidney, an area that showed a mass lateral of the superior mesenteric artery on abdominal magnetic resonance imaging. A complete pancreatectomy with splenectomy and left-sided adrenalectomy were performed. At this second relapse, this neuroendocrine tumor clinically had changed its hormonal profile. Immunohistochemically, in contrast to primary tumor and first relapse, we found strong immunostaining for ACTH in tumor cells of the second relapse and a MIB-1 index greater than 20%. To our knowledge, this is the first report describing a pancreatic neuroendocrine tumor that started to secrete ACTH de novo at the time of the second relapse after two former complete tumor resections. This case underscores the pluripotency of neuroendocrine tumor cells and the importance of keeping in mind a possible shift in hormone production during tumor evolution and progression.
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PMID:Pancreatic neuroendocrine tumor with ectopic adrenocorticotropin production upon second recurrence. 1529 97


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