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)

We reported clinical and neuropathological observations of a 41-year-old man with Degos disease. He first noted painless skin lesions over the upper extremities in January, 1982. Three years later he was diagnosed as Degos disease by skin biopsy, and treatment with aspirin was started. In September, 1985, he complained of paresthesia on his right arm, followed by a series of new neurological manifestations suggesting multifocal spinal cord lesions. On October 28, examination of admission showed papules with central umblication over the whole body except the head, face, palms, soles and scrotum. Neurological examination revealed no weakness, diminished right biceps reflex, exaggerated patellar reflexes and Achilles reflexes, left extensor plantar reflex, hypesthesia and hypalgesia to the level of Th8, mild left spastic gait, and retention of urine. In November, he had paraparesis, loss of vibration sense of lower extremities, hypesthesia and hypalgesia to the level of TH4, and weakness of right upper extremity. In December, he showed tetraplegia, left-sided facial palsy, and hypesthesia and hypalgesia to the level of C5. In January, 1986, he showed right facial palsy, left facial hypesthesia, pseudobulbar palsy. In February, he had bilateral abducens nerve palsy and hiccups. On February 18, he died of intracranial hemorrhages. He had episodic abdominal pain several times during admission. His condition deteriorated progressively in four months after the first manifestation of neurological symptoms, despite the therapy with heparin, urokinase, ticlopidine, dipyridamole, and prednisolone. Laboratory studies showed gradual increase of CSF proteins (from 156 mg/dl to 602 mg/dl) and extremely increased platelet aggregation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of Degos disease with neurological symptoms--neuropathological observations and increased platelet aggregation]. 162 33

Thirteen patients with acute occlusion of superior mesenteric artery are presented. Eight of them presented with sudden abdominal pain as the initial complaint while the others did with vomiting, abdominal distension or general fatigue. Arterial blood gas and deficit determinations revealed metabolic acidosis in 45.5% and large deficit in 100%, which was considered to be a reliable method for accurate early diagnosis of acute mesenteric arterial occlusion. Eleven patients underwent laparotomy and massive bowel resection, two of which had treatment with selective intraarterial infusion of urokinase prior to operation. One of two remaining patients did not need operation because she went on to complete recovery after fragmentation of embolus in the superior mesenteric artery by the percutaneously inserted catheter on angiography. The other one was inoperable because of poor general condition. The overall mortality in this series was 53.8%.
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PMID:[A clinical study on acute mesenteric arterial occlusion]. 785 74

A 77-year-old man with a history of multiple surgically treated malignancies presented with increasing abdominal pain after eating. Computerized tomographic scan showed superior mesenteric vein and portal vein thrombosis. The patient was treated with selective superior mesenteric artery infusion of urokinase resulting in clinical improvement and near complete resolution of the mesenteric venous thrombosis. An underlying gastric malignancy was found and is believed to be the cause of the patient's hypercoagulable state. Direct infusion of urokinase into the superior mesenteric artery for treatment of mesenteric venous thrombosis is an alternative to surgery in selected patients and an alternative to the much more complicated delivery systems presently used.
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PMID:Mesenteric venous thrombosis treated with urokinase via the superior mesenteric artery. 861 72

A case of significant proteinuria occurred as a result of bilateral renal vein thrombosis secondary to dehydration, which resolved after treatment with urokinase. The patient developed nausea and vomiting from viral gastroenteritis with subsequent volume contraction. He later noted the onset of aching lower abdominal and flank pain. On admission, he was noted to have a serum creatinine of 1.7 mg/dL, and 4+ proteinuria on urinalysis. A 24-hour urine collection showed 2.34 g protein. A renal venogram showed bilateral renal vein thrombosis (RVT) without involvement of the inferior vena cava. Therapy was initiated with heparin at 1,000 U/hr, followed by intravenous (IV) urokinase, 4,400 U/kg bolus, followed by 4,400 U/kg/hr with continuous infusion for 12 hours. A repeat renal venogram done at this time showed partial resolution of thrombosis bilaterally. A second 12-hour infusion of urokinase at 5,000 U/kg/hr was performed; at this time, the patient reported resolution of his flank and abdominal pain. A repeat 24-hour urine collection showed 60 mg protein with a normal creatinine clearance. Levels of antithrombin III, protein C, and protein S were all normal. A renal biopsy was performed and showed normal histology on light, immunofluorescent, and electron microscopic evaluation. The patient has done well on no therapy and has had no recurrence of thrombosis or proteinuria after 2.5 years. This is a US government work. There are no restrictions on its use.
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PMID:Resolution of proteinuria secondary to bilateral renal vein thrombosis after treatment with systemic thrombolytic therapy. 910 53

Idiopathic suppurative pylephlebitis is quite rare and only a few cases have been reported. Conservative systemic administration of antibiotics and urokinase is reported to be effective. In this report, surgical drainage was performed on an 18-year-old man who complained of fever and abdominal pain. He had no past history of abdominal inflammatory disease or abdominal surgery. Ultrasonography and computed tomography showed wide spread thrombosis of the portal vein. Laparotomy was performed and the occluded superior mesenteric vein was incised. Massive pus was removed. Thereafter, a drain was placed at the opened mesenteric vein. Drainage resulted in a dramatic decrease in fever. Postoperative radiographic studies of the colon, the small intestine, and other organs did not show any abnormalities. Emergency surgical drainage was performed successfully, instead of systemic administration of antibiotics and urokinase. Surgical drainage may be useful for wide spread pylephlebitis and pylethrombosis.
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PMID:Surgical drainage for idiopathic suppurative pylephlebitis. 945 3

A 29-year-old male patient with Crohn's disease of the terminal ileum and previous abdominal surgery was admitted because of severe abdominal pain and signs of bacterial sepsis. The diagnosis of portal vein thrombosis and multiple liver abscesses due to Streptococcus intermedius septicaemia was made and antibiotic therapy was instituted immediately. As high-dose heparin therapy was ineffective, urokinase was administered intravenously over a total of 7 days. Within 2 days, the patient's symptoms completely subsided. Colour duplex ultrasonography revealed complete recanalization of the main stem of the portal vein; the right branch of the portal vein, however, remained occluded. Other case reports on thrombolytic therapy in patients with portal vein thrombosis are reviewed.
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PMID:Thrombolytic therapy in patients with portal vein thrombosis: case report and review of the literature. 1105 61

Intraperitoneal (IP) administration of either streptokinase (SK) or urokinase (UK) has assumed an adjunctive role to antibiotic therapy in selected patients with relapsing peritonitis. In these circumstances, bacteria may be protected from antibiotics through sequestration in either fibrinous structures or biofilms within the lumen of the peritoneal dialysis (PD) catheter or the peritoneal cavity. In some cases, it appears that disruption of these sheltered microenvironments by thrombolytic agents facilitated eradication of the offending organism and obviated the need for catheter removal, replacement, or interim hemodialysis. Although IP SK has been generally well tolerated as additive therapy in relapsing peritonitis, sporadic reports of significant complications, such as abdominal pain, fever, and severe hypotension, have precluded its more widespread acceptance. The only other thrombolytic agent used in this setting, UK, is presently unavailable because of a manufacturing shortfall. Therefore, adjunctive thrombolytic therapy for relapsing peritonitis is currently restricted. To circumvent these limitations, we devised an IP tissue plasminogen activator (tPA) protocol to eliminate recurring infection in a patient undergoing chronic ambulatory PD. After a third episode of peritonitis caused by Enterobacter cloacae, treated twice previously with an adequate antibiotic regimen, we instilled 6 mL of tPA (1 mg/mL) into the PD catheter for a 2-hour dwell time. The treatment was well tolerated and, in conjunction with a third course of antibiotic therapy, has produced an infection-free interval of 8 months.
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PMID:Successful use of recombinant tissue plasminogen activator in a patient with relapsing peritonitis. 1113 81

Postpartum ultrasound investigation of a woman with unremitting fever and right flank pain after Cesarean section revealed an extensive thrombosis of the right ovarian vein which extended into the inferior vena cava. Computed tomography was required to substantiate the diagnosis. Medical treatment with intravenous urokinase and heparin and antibiotics was successfully performed. During the postpartum period, the possibility of ovarian vein thrombosis should be considered in febrile patients with abdominal pain who are not responding to antibiotics, and imaging studies such as ultrasound and computed tomography should be performed early for prompt diagnosis and therapy.
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PMID:Ultrasound diagnosis of postpartum ovarian vein thrombosis: case report. 1177 1

A 24-year-old Japanese man was admitted because of massive haematemesis and melaena with persistent abdominal pain. Markedly bloody ascites and severely oedematous small intestine were recognized, and angiography then revealed superior mesenteric vein thrombosis. After resection of the necrotic small intestine, continuous intravenous infusion of heparin and urokinase was performed. This patient had no familial or personal history of thrombosis. On the 15th day after operation, an initial search for lupus anticoagulant revealed that the prothrombin time (PT) ratio and dilute activated partial thromboplastin time (aPTT) were positive under heparin treatment, without evidence of rheumatic or connective tissue disease. Thrombocytopenia was observed with a nearly normocellular bone marrow. A follow-up examination 1 year later still revealed an increased aPTT. However, all tests for antiphospholipid antibodies had been negative including dilute aPTT for about 2 years since the 15th day after operation. These findings suggest that, in this patient, superior mesenteric vein thrombosis has not been associated with primary antiphospholipid syndrome but is probably idiopathic. Positive tests for lupus anticoagulant in the initial period may be unreliable due to heparin treatment.
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PMID:Superior mesenteric vein thrombosis presented transient false positivity for lupus anticoagulant under heparin treatment. 1198 2

A 57-year-old man, who had undergone hepatic arterial infusion chemotherapy with right portal occlusion for hepatocellular carcinoma was admitted to our hospital because of severe abdominal pain. Contrast-enhanced computed tomograms revealed that most areas of the liver were not enhanced, a finding suspicious for perfusion disturbance in the liver. Angiography revealed an interrupted right hepatic artery. Arterial portograms revealed complete obstruction of the right portal vein and a small left branch of the portal vein. Despite anticoagulant therapy with urokinase for portal vein thrombosis, the patient died from hepatorenal failure. Autopsy revealed that cholangiocarcinoma occupied almost the entire parenchyma of the right lobe, although the treated hepatocellular carcinoma lesion was completely necrotic. The right hepatic artery was obstructed due to direct invasion of tumor. There were diffuse thrombi in the left portal branches surrounded by tumor infiltrating along Glisson's sheath to the peripheral portion of the left lobe.
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PMID:Portal thrombosis due to intrahepatic cholangiocarcinoma following successful treatment for hepatocellular carcinoma. 1284 99


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