Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 67 years old man was admitted on July 1979 for nausea, dysphagia and rectal pain. At age 64 he had undergone radiotherapy on the lower lip for an epidermoid carcinoma. He remained then healthy. His medical history was negative with the exception of chronic bronchitis. He had never been exposed to toxic agents or drugs and had never left Europe. A few days after admission he suffered acute intestinal obstruction but at laparostomy no etiology was found. At the same time the patient complained of pain in all four limbs and he was found to have diffuse wasting of muscles, areflexia and distal sensory loss. No sign of dysautonomia was present. Physical examination was negative with the exception of a cervical lymphadenopathy. The lymph node biopsy showed an undifferentiated metastatic carcinoma. Negative investigations included: blood cells count; serum ionogram and immunoelectrophoresis; thyroid function tests; serological test for Chagas' disease. The following abnormalities were found: ESR: 55-105; CSF protein: 145 mg/100 ml and 1 cell mm3; whole blood folic acid: 1,7 mg/ml; Hbs antigen was present in blood; EMG showed evidence of denervation but motor conduction velocities were normal. By September the patient's weakness had increased and complete intestinal obstruction persisted. At oesophageal, gastric and duodenal fibroscopy no contraction was visible, and biopsies were negative. The patient died of peritonitis on October 5th, 1979. At necropsy peritonitis secondary to multiple perforation of the large bowel was found. No recurrence of the lip carcinoma or metastase or evidence of a primary carcinoma was found. Light microscopy showed no evidence of amyloidosis or scleroderma. Examination of the alimentary tract showed abnormalities restricted to the myenteric plexuses which varied from one level to another. In the small bowel there was hyperplasia of the smooth muscle and the myenteric plexuses were enlarged by marked proliferation of Schwann cells. Severe neuronal loss and nodules of Nageotte were also noted. Schwann cells proliferation was less marked in the stomach and large bowel. Lympho-histiocytic infiltration strictly confined to the region of the myenteric plexuses was present in oesophagus, stomach, large bowel and rectum. Mild chronic inflammatory lesions were also found in anterior and posterior spinal roots and semi-lunar ganglia. The striking feature of this case is the association of an undifferentiated carcinoma and a polyradiculoneuritis with a complete alimentary tract palsy of rapid onset, secondary to lesions restricted to the myenteric plexuses. The low folate level was insufficient to explain the neuropathy. Investigations showed no evidence of the usual causes of intestinal pseudo-obstruction: muscular, dysautonomic, toxic, plexic (idiopathic, familial, inflammatory), Chagas' disease). The clinical course, the pathological pictures of the alimentary tract and spinal roots and the association with a carcinoma suggest that our case may represent a paraneoplastic syndrome...
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PMID:[Paralysis of digestive tract with lesions of myenteric plexuses. A new paraneoplastic syndrome (author's transl)]. 729 42

In this descriptive study, 20 midlife women experiencing chronic distressing gastrointestinal (GI) symptoms recorded GI symptom severity in a symptom diary for a 30-day period and dietary intake in a 9-day food record. A wide variability in GI symptom severity was noted. Significant negative relationships were present between dietary fiber intake and abdominal pain, awakening with abdominal pain, nausea, awakening with nausea, and awakening with rectal pain. No significant relationships were noted between amount of caffeine or alcohol intake and distressing GI symptoms.
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PMID:Dietary fiber and distressing gastrointestinal symptoms in midlife women. 797

The objective of this study was to test the efficacy and safety of salmon calcitonin (sCT) suppository in post-menopausal women with previous hip fractures as an inhibitory agent of bone loss. The study was a single blind, randomized, and placebo-controlled trial comparing three parallel groups of patients. Fifty-four healthy women were randomly allocated to 1 year's treatment with either sCT 100 IU/6 times a week, 200 IU/3 times a week, or placebo/6 times a week. All groups received a calcium supplement of 500 mg daily. Fifteen patients left the study before its end, six of those due to adverse events, such as abdominal and rectal pain, nausea, headache, and diarrhea. Bone mineral density of the spine and the femoral neck was measured every 26 weeks, and biochemical markers of bone turnover were measured at baseline and week 12, 26, and 52. There were no significant changes in bone mineral density in the spine and in the hip in any of the treatment groups. No significant changes were observed in serum alkaline phosphatase, serum osteocalcin, urine hydroxyproline, and urine pyridinoline or deoxypyridinoline. Conclusively, we did not observe any significant effect on bone metabolism in women with postmenopausal osteoporosis after 1 year of treatment with sCT suppositories at the doses used.
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PMID:Effects of salmon calcitonin suppositories on bone mass and turnover in established osteoporosis. 811 46

The combination of leucovorin [(6d,l)-5-formyl-tetrahydrofolate] and 5-fluorouracil (5-FU) has increased efficacy compared to 5-FU alone as treatment of advanced colorectal cancer. Leucovorin is metabolized to methylene tetrahydrofolate, which potentiates the antitumor actions of 5-FU by forming a ternary complex of thymidylate synthase, fluorodeoxyuridine and methylene tetrahydrofolate. Only l-leucovorin is metabolized to methylene tetrahydrofolate and forms this ternary complex. However, d-leucovorin may not be inert. d-Leucovorin may impair cellular uptake and metabolism of l-leucovorin, thereby inhibiting the actions of l-leucovorin. Because of this possible limitation to the effectiveness of racemic leucovorin, we have begun to explore the effects of the pure, biologically active isomer, l-leucovorin. In this phase I trial, patients with advanced gastrointestinal malignancies were treated with a 5-day continuous infusion of l-leucovorin and daily intravenous boluses of 5-FU at 370 mg/m2. The dose of l-leucovorin was escalated in groups of three patients at four doses, 200 mg/m2 per day, 400 mg/m2 per day, 700 mg/m2 per day and 1000 mg/m2 per day. Treatment was repeated every 28 days. Seventeen patients with advanced gastrointestinal cancers entered the trial. Sixteen patients were evaluable for toxicity. Toxicity was similar to that expected for leucovorin plus 5-FU. The most common severe toxicities (and the number of patents affected) were: diarrhea (2), mucositis (2), nausea/vomiting (1), and abdominal/rectal pain (2). The maximum tolerated dose of l-leucovorin was 700 mg/m2 per day. Twelve patients were evaluable for response. One complete, one partial and one minor response were observed. All responses occurred among the nine patients with colorectal carcinomas. The combination of l-leucovorin and 5-FU is well tolerated by patients and appears active for treatment of advanced colorectal carcinomas. Additional clinical trials are necessary to determine if l-leucovorin is more effective than d,l-leucovorin for modulating the effectiveness of 5-FU.
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PMID:Phase I trial of a 5-day infusion of L-leucovorin plus daily bolus 5-fluorouracil in patients with advanced gastrointestinal malignancies. 850 Feb 27