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)

Clinical observation was made on 238 dengue fever cases during an epidemic in Taiwan from September to November 1988. Dengue virus infection type 1 was responsible for all cases. The majority of patients had acute onset of fever with abdominal pain, diarrhoea, and vomiting. Gastrointestinal haemorrhage with manifestation of haematemesis and/or melena was observed in 28 (11.8%) of our patients. The clinical gastrointestinal features in patients with a peptic ulcer history were not different from those in patients without it. There was no significant difference in incidence of gastrointestinal manifestations between premedication and non-premedication patients. Sixty-six non-premedication patients in our series were examined by gastroduodenoscopy. Haemorrhagic gastritis was the most common finding in 27 (40.9%) patients. The incidence of gastric and/or duodenal ulcerations was higher in patients with a peptic ulcer history compared with those without it (P less than 0.01). However, the incidence of upper gastrointestinal bleeding was similar between these two groups (19.2% vs 9.8%). Thrombocytopenia in patients with gastrointestinal haemorrhage was more prominent than in those without it (P less than 0.005). This implied that thrombocytopenia might be one of the predisposing factors for gastrointestinal haemorrhage.
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PMID:Clinical and upper gastroendoscopic features of patients with dengue virus infection. 212 43

Twenty evaluable patients with minimal residual ovarian cancer at second look laparotomy were treated with human recombinant interferon alpha-2b (IFN) intraperitoneally. The dose administered was 50 x 10(6) units once weekly for 8 weeks. Seventeen patients were evaluated by a relaparotomy: five had a pathological complete remission, four a partial response, six patients disease stabilization and two patients had progression. Three patients, two stable and one with clinical progression, had no laparotomy. Nine of the 11 patients with residual tumor smaller than 5 mm had a response, while no response was found in six patients with residuals over 5 mm. The median duration of CR is 11+ months (6-13+ months) after evaluation. For toxicity, 156 treatment cycles could be studied. Fever was seen in 80% of all cycles within 24 h following administration of IFN, in 58 cycles (37%) over 38 degrees C and in 65 cycles (43%) over 39 degrees C. Abdominal pain was slight in 32% and moderate in 3% of all cycles. The peripheral blood leukocyte counts dropped after 52% of all cycles, in 27% below 4.0, in 22% below 3.0, and in one patient below 2.0 x 10(9)/l. IFN dosage was not reduced for leukopenia, but in one patient reduction was necessary for thrombopenia, resulting from insufficient marrow reserve after a previous autologous bone marrow transfusion. Pharmacokinetic studies showed i.p. IFN levels 50-100 times the blood levels. Blood levels were still elevated 2 days after i.p. infusion, but normalized within 1 week on repeated administration. At the second instillation, lower peak serum levels were reached. In conclusion, high doses of i.p. IFN appear to be active in patients with minimal residual disease, with ongoing response in CR patients. Apart from general malaise on the day of treatment, toxicity was acceptable. IFN may be active in patients with minimal residual ovarian cancer through local as well as systemic effects.
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PMID:Intraperitoneal human recombinant interferon alpha-2b in minimal residual ovarian cancer. 214 93

Autologous lymphokine-activated killer (LAK) cells and recombinant human interleukin-2 (rIL-2) were administered intraperitoneally (IP) to 24 patients with malignancies limited to the peritoneal space. Ten patients had ovarian cancer, 12 had colorectal cancer, and one patient each had endometrial carcinoma and primary small-bowel adenocarcinoma. All ovarian cancer patients, three of twelve colorectal cancer patients, and one patient with endometrial carcinoma had received prior therapy. Patients received IL-2 100,000 U/kg every 8 hours intravenously (IV) for 3 days, and 2 days later underwent daily leukapheresis for 5 days. LAK cells were generated in vitro by incubating the peripheral blood mononuclear cells in IL-2 for 7 days and were then administered IP daily for 5 days through a Tenckhoff catheter (Davol, Inc, Cranston, RI) together with IL-2 25,000 U/kg IP every 8 hours. All but one patient completed at least one cycle of therapy. Toxic side effects included minor to moderate hypotension, fever, chills, rash, nausea, vomiting, abdominal pain and distension, diarrhea, oliguria, fluid retention, thrombocytopenia, and minor elevations of liver function tests; all of these rapidly improved after discontinuation of IL-2. One patient had a grand mal seizure, and one suffered a colonic perforation; these were felt to be treatment-related. IP fibrosis developed in 14 patients and limited repeated cyclic administration of this therapy in five patients. Two of 10 (20%) ovarian cancer patients and five of 12 (42%) colorectal cancer patients had laparoscopy- or laparotomy-documented partial responses. We conclude that LAK cells and rIL-2 can be administered IP to cancer patients, resulting in moderate to severe short-term toxicity and modest therapeutic efficacy. Further investigation of this form of adoptive immunotherapy modified to address the problem of IP fibrosis and with lower IP IL-2 doses is justified by these initial results.
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PMID:Intraperitoneal lymphokine-activated killer-cell and interleukin-2 therapy for malignancies limited to the peritoneal cavity. 221 99

Hemolytic-uremic syndrome (HUS) of childhood is a triad of acute hemolytic anemia, thrombocytopenia, and acute renal failure associated with a gastrointestinal prodrome. From 1977 to 1988, 134 patients with HUS were admitted to this institution. All patients presented with abdominal pain and diarrhea, which was virtually always bloody. Seventy-eight patients (60%) required dialysis. Five patients died (4%). One patient died as a result of colon perforation, the other four patients died of other nonsurgical complications of HUS. Three patients underwent exploratory laparotomy. One patient had a hemoperitoneum from mesenteric and transmural bleeding of the entire intraabdominal colon. Another patient had undergone surgery elsewhere for presumed intussusception with pancolitis found at exploration. Fourteen days postoperatively, he had a spontaneous perforation of the transverse colon. The third patient presented with pancolitis and perforation of the transverse colon. Despite surgical intervention he died on the sixth postoperative day. One other patient was treated conservatively for pancreatitis, which developed 3 weeks after her presentation with HUS. Complications requiring surgical intervention in HUS are rare, potentially lethal, and usually involve the colon.
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PMID:Surgical complications of the hemolytic-uremic syndrome. 227 21

Although restricted transhepatic portal flow is necessary for development of generalized portal hypertension (GPH), increased splanchnic arterial inflow also contributes to GPH and its clinical sequelae. In this context, we describe 7 male and 6 female patients (mean age 48 years) in whom the lesser splanchnic (gastrosplenic) system played a key role in the signs and symptoms of GPH. These 13 patients (9 with hepatic cirrhosis, 3 with primary myeloproliferative disorder, and 1 with extrahepatic portal block) shared common features of massive splenomegaly, huge splenofundic gastric varices, often with a prominent natural shunt to the left renal vein. Total or near total splenectomy alone or combined where appropriate with coronary vein ligation was effective in controlling varix hemorrhage (10 patients), ascites (3), or complications of an enlarged spleen-anorexia and abdominal pain (3), hemolytic anemia (1) and profound thrombocytopenia with severe epistaxis (1). Intraoperative jejunal portal venography was crucial in operative management in order to establish definitively the presence or absence of coronary venous collaterals, and when present, to verify their operative ligation. These distinctive patients illustrate: 1) GPH is a heterogeneous syndrome of divergent splanchnic circulatory patterns, a feature which should be taken into account in selecting operative treatment; 2) one well-defined subgroup displays prominent hyperdynamic lesser splanchnic and specifically, splenic blood flow as a major contributor to clinical complications; and 3) within this subgroup, splenectomy combined with documented absence or surgical interruption of coronary venous collaterals as corroborated by intraoperative portography is effective alternative treatment.
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PMID:Preeminence of lesser splanchnic blood flow in selected patients with generalized portal hypertension. 227 22

Therapeutic efficacy and toxicity were evaluated in 28 children with acute lymphoblastic leukemia, in ten with acute nonlymphoblastic leukemia (ANLL), and in 13 with metastatic neuroblastoma. All were refractory to standard chemotherapeutic agents and 25 were refractory to an investigational drug. The initial dose was 12 mg/m2/day and was based on an established maximal dose tolerated in adults. This dose was found to be intolerable in 5 of 5 children with leukemia. Similarly an initial dose of 9 mg/m2/day was intolerable in 4 of 5 patients with leukemia. The starting dose in the next 28 children with leukemia or neuroblastoma was 3 mg/m2. This drug was gradually increased to the highest tolerated dose by 3-mg/m2 increments. Fifteen children with acute lymphoblastic leukemia, 3 children with ANLL, and 2 children with neuroblastoma received the drug daily. Seven patients with ANLL and 7 patients with neuroblastoma received the drug biweekly. Seventeen patients with acute lymphoblastic leukemia, 6 patients with ANLL, and 5 patients with neuroblastoma had an adequate trial of the drug. An adequate trial was defined as a minimum of 5 weeks of therapy unless progressive disease developed. Side effects of the drug were striking and included fever, hypotension, myalgia, bone pain, arthralgia, arthritis, abdominal pain, liver toxicity, thrombocytopenia, and neurotoxicity. No complete remission occurred although interferon levels above 100 units/ml were induced in nearly 50% of the patients.
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PMID:Phase II trial of a complex polyriboinosinic-polyribocytidylic acid with poly-L-lysine and carboxymethyl cellulose in the treatment of children with acute leukemia and neuroblastoma: a report from the Children's Cancer Study Group. 241 2

A Phase II study of poly(I,C)-LC was performed in 28 children and adolescents with acute lymphoblastic leukemia (ALL), 10 with acute nonlymphoblastic leukemia (ANLL), and 13 with metastatic neuroblastoma. All were refractory to standard chemotherapeutic agents and 25 to an investigational drug. Initial doses of 12 mg/m2 and 9 mg/m2 were intolerable. However, 9 mg/m2 was tolerable in the majority of patients when the drug was started at 3 mg/m2 and increased by 3 mg/m2 increments. Fifteen children with ALL, three with ANLL, and two with neuroblastoma received the drug daily. Seven patients with ANLL and seven children with neuroblastoma received the drug biweekly. Twenty-eight patients received an adequate trial, which was defined as a minimum of 5 weeks at the maximal tolerated dose, unless there was progressive disease at the maximal tolerated dose. Side effects of the drug were striking, and included fever, hypotension, myalgia, bone pain, arthralgia, arthritis, abdominal pain, liver toxicity, thrombocytopenia, and neurotoxicity. No complete remissions occurred in spite of interferon levels above 100 U in nearly 50% of patients.
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PMID:Phase II trial of poly(I,C)-LC, an interferon inducer, in the treatment of children with acute leukemia and neuroblastoma: a report from the Children's Cancer Study Group. 241 84

Clinical symptoms and laboratory measures of renal and liver function, coagulation, and inflammatory parameters were prospectively studied in 74 hospitalized patients (14-74 years of age) with serologic evidence of nephropathia epidemica. The most common clinical findings were acute onset of symptoms, fever (greater than or equal to 38 degrees C), thirst, headache, nausea, back pain, vomiting, myalgia, and abdominal pain. Twenty-seven patients (37%) had hemorrhagic manifestations, i.e., epistaxis, melena, hematemesis, petechial bleeding, macroscopic hematuria, or metrorrhagia. Disseminated intravascular coagulation developed in four patients. Fifty-one percent had thrombocytopenia. Proteinuria was recorded for all patients, while hematuria and glucosuria were noted for 85% and 58%, respectively. Serum creatinine levels were elevated in 71 (96%) of the patients. Levels of C-reactive protein or erythrocyte sedimentation rates were elevated in all cases, usually to levels found in serious bacterial diseases. Sixty-six (89%) of the patients were followed for up to 7 months, at which time all had recovered clinically. No patient died or required dialysis. We conclude that nephropathia epidemica in Sweden has a clinical picture similar to that of hemorrhagic fevers in other parts of the world, but with a milder course and a better prognosis.
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PMID:Clinical characteristics of nephropathia epidemica in Sweden: prospective study of 74 cases. 257 3

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

Three cases of acute adrenal haemorrhage complicating heparin induced thrombocytopaenia are described. The patients were 2 men and 1 woman, respectively 62, 74 and 76-year old. They all had orthopaedic problems requiring a treatment by subcutaneous calcium heparinate. Thrombocytopaenia occurred 7 to 10 days after the beginning of treatment, with a progressive return to normal of platelet count on stopping heparin. A syndrome suggestive of adrenal failure appeared on the 10 th to 12 th day consisting of abdominal pain, hyperpyrexia, arterial hypotension, asthenia, altered consciousness. Adrenal hormone levels were decreased. Abdominal scanography demonstrated adrenal haemorrhage in 2 patients. The third patient died before further investigations could be carried out. Hormonal replacement therapy brought things back to normal. Six other similar cases have already been published. The heparin induced thrombocytopaenia probably explains the two paradoxes of adrenal haemorrhage complicating heparin therapy: its occurrence in the absence of excessive anticoagulation, and adrenal venous thrombosis. The presence of abdominal pain, fever, collapse, or hyponatraemia with heparin induced thrombocytopaenia should suggest a possible adrenal haemorrhage. Adrenal CT scans should be carried out rapidly, so that hormone treatment can be initiated without delay.
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PMID:[Heparin-induced thrombocytopenia complicated by hematoma of the adrenal glands and acute adrenal insufficiency]. 263 63


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