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 report the case of a 28-year-old man who was admitted in an emergency because of severe abdominal pain with gastrointestinal haemorrhage and shock. Laparotomy showed infarction of the small intestine with mesenteric veins thrombosis. Severe thromboembolic complications occurred during the post-operative period: bilateral femoral deep vein thrombosis with pulmonary embolism, axillary and subclavian vein thrombosis associated with an intravenous catheter, portal hypertension related to portal vein thrombosis and cavernoma, thrombosis of the superior longitudinal sinus. Laboratory investigations performed after thrombotic episodes and repeated 5 years later evidenced a type 1 Heparin Cofactor II deficiency (HCII Ag by EID: 40 percent; functional Tollefsen's method: 60 percent). This heterozygous deficiency was also found in one of the patient's sons. This is the first reported case of HCII deficiency associated with mesenteric infarction and cerebral thrombophlebitis. The relationship between these severe venous thrombotic episodes and the HCII deficiency is discussed in relation to the dermatan sulphate-HCII couple physiology. Vascular injury may act as a triggering factor in patients with HCII deficiency.
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PMID:[Recurrent venous thromboembolism caused by heparin cofactor II deficiency. A case]. 183 93

To elucidate further the characteristics, optimal management and ultimate outcome of patients with primary mesenteric venous thrombosis, the records of nine such patients were analyzed. There were seven male and two female patients, with a mean age of 47 years. Abdominal pain, vomiting, fever and hematochezia were the characteristics presenting complaints. Tenderness, distention and diminished intestinal sounds were the prominent abdominal physical findings and were often associated with tachycardia and hypotension. No one of the laboratory findings were specifically diagnostic for mesenteric venous thrombosis, but leukocytosis and hemoconcentration were commonly found. Roentgenographic findings were consistent with intestinal obstruction in six patients. Thrombosis of the mesenteric veins could not be attributed to any specific cause in these nine patients, thereby warranting the classification of primary. At operation, all nine patients were found to have a segment of infarcted small intestine--132 +/- 105 centimeters--with obvious thrombosis of the mesenteric veins but with patent mesenteric arteries. Five patients had bloody ascites. Two deaths occurred in the immediate postoperative period, both being due to sudden and unexpected cardiopulmonary arrest. Neither of these two patients received anticoagulant therapy. Two patients had undergone segmental resection at other hospitals and were referred to our institution because of a recurrence of acute abdominal signs and symptoms. Neither of these patients received anticoagulant therapy. At reoperation, both had recurrent segmental mesenteric venous thrombosis. Familiarity with this condition is essential in making the correct diagnosis, so that resection may be undertaken promptly. Heparin should immediately be administered intravenously after establishing the diagnosis of mesenteric venous thrombosis to prevent recurrent thrombosis and other possible thrombotic complications. If these steps are taken expeditiously, the prognosis of mesenteric venous thrombosis is often favorable.
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PMID:Primary mesenteric venous thrombosis. 705 78

We report a case of a 37-year-old female who suffered from upper abdominal pain, progressive abdominal distention, shortness of breath, palpitation and pitting edema of lower legs for more than one month. Abdominal sonography showed small caliber of hepatic veins, mild hepatosplenomegaly and moderate ascites. Computed tomography of abdomen disclosed extensive thrombi in bilateral femoral veins, ovarian veins and inferior vena cava. Ascites was transudate with normal cell count. Laboratory data showed hypoalbuminemia, mild elevation of total bilirubin and iron deficiency anemia. Anti-cardiolipin antibody was positive and antinuclear antibody was negative. The histopathological features, including sinusoidal dilatation with atrophic change of adjacent hepatocytes, slight congestion and hemosiderin-like material within the cytoplasm of Kupffer cells, were compatible with the criteria of Budd-Chiari syndrome. Heparin was intravenously administered immediately to prevent further progression of thrombosis. The ascites was successfully controlled with diuretics (spironolactone and furosemide). After a two-week course of treatment, she was discharged in good condition and on warfarin anti-coagulant medication.
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PMID:Anticardiolipin antibody-related Budd-Chiari syndrome: report of a case. 951 90

May-Thurner syndrome is an uncommon process in which the right common iliac artery compresses the left common iliac vein, resulting in left iliofemoral deep vein thrombosis and severe leg edema. We report the case of a 41-year-old female who presented with severe left leg edema present for 1 day. One week earlier she had experienced acute shortness of breath and pleuritic chest pain. Duplex ultrasound revealed a left iliofemoral deep vein thrombosis. A computed tomography (CT) scan performed for abdominal pain revealed thrombosis of the entire left common and external iliac veins. A ventilation-perfusion scan diagnosed a pulmonary embolism. The patient was treated with systemic intravenous heparin and catheter-directed thrombolysis of the iliofemoral deep vein thrombosis. Complete thrombolysis and iliofemoral vein patency was achieved over 5 days. A persistent stenosis in the left common iliac vein consistent with May-Thurner syndrome was alleviated with percutaneous balloon angioplasty and placement of a Wallstent. Heparin therapy was terminated at the time of stenting because of suspected heparin-induced thrombocytopenia. The patient was started on a continuous infusion of 10% dextran 40, and warfarin therapy was initiated. Heparin-induced antibodies were confirmed by a C-14 serotonin release assay. The endovascular reconstruction remains patent 4 months later. Heparin-induced thrombocytopenia complicating endovascular reconstruction of the iliofemoral venous system in a patient with May-Thurner Syndrome is an uncommon occurrence. This case and a review of the literature are discussed.
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PMID:Treatment of May-Thurner syndrome with catheter-directed thrombolysis and stent placement, complicated by heparin-induced thrombocytopenia. 1039 65

Hypertriglyceridaemia is thought to be the aetiology in 3% of patients with acute pancreatitis, often associated with poorly controlled diabetes mellitus or chronic alcohol abuse. However, in patients with non-biliary pancreatitis, chylomicronaemia is an underrated cause of acute pancreatitis. The activity of lipoprotein lipase (LPL) is crucial in removing triglycerides from the plasma; LPL gene mutations combined with secondary alterations in plasma lipoproteins, such as occur in pregnancy, diabetes mellitus, and alcohol abuse can cause severe hypertriglyceridaemia and pancreatitis. Heparin and insulin stimulate LPL activity. During a 12 months' period we consecutively screened all patients with the diagnosis of acute non-biliary pancreatitis for hypertriglyceridaemia, to evaluate the prevalence of hypertriglyceridaemia-induced pancreatitis and to assess the outcome under standardised treatment with intravenous heparin and insulin. Hypertriglyceridaemia-induced pancreatitis was diagnosed in 5 out of 46 patients (11%) with acute pancreatitis. In 2 patients hypertriglyceridaemia was associated with diabetes mellitus, in one patient with pregnancy and in another with chronic alcohol abuse. Four patients had to be referred to the intensive care unit. Plasma concentrations of triglycerides were (median +/- range) 43 mmol/l (14.7 to 80.4); pancreas amylase was 574 U/l (155 to 1606), and lipase was 1003 U/l (330 to 3010). All patients had oedematous pancreatitis demonstrated by CT scan. Treatment with i.v. heparin and i.v. insulin decreased trigylceride levels to less than 10 mmol/l within 2.8 days (1 to 6), the amylase and lipase levels returned to normal after 3 and 4 days respectively, and the abdominal pain was resolved. Hypertriglyceridaemia is a common and under-diagnosed etiology of acute non-biliary pancreatitis. Intravenous heparin and insulin is safe and effective in the treatment of hypertriglyceridaemia-induced pancreatitis. Low fat diet, supplements of (n-3) fatty acids ("fish oil") and fibrates are recommended for long-term maintenance therapy.
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PMID:[Heparin and insulin in the treatment of acute hypertriglyceridemia-induced pancreatitis]. 1049 50

Enoxaparin is a low-molecular-weight heparin used for prophylaxis against deep venous thrombosis. Indications include hip and knee replacement surgery, risk of deep venous thrombosis during abdominal surgery, and prevention of ischemic complications of unstable angina and non-Q-wave myocardial infarction. Its efficacy in the prevention of the above complications has been previously studied; however, the liberal use of enoxaparin is not without incident. Complications of enoxaparin include hemorrhage, thrombocytopenia, and local reactions. Since 1993 there have been more than 40 reports of epidural or spinal hematoma formation with the concurrent use of enoxaparin and spinal/epidural anesthesia or spinal puncture. Herein reported are two cases of abdominal wall hematomas in patients receiving prophylaxis with enoxaparin. Both patients sustained an unexplained fall in the hematocrit and abdominal pain. A CT scan confirmed the diagnosis. One patient recovered uneventfully; however, the other patient, on chronic hemodialysis, became hemodynamically unstable and hyperkalemic and sustained a fatal cardiac arrhythmia. An extensive review of the literature revealed no similar cases of abdominal wall hematomas associated with enoxaparin although other complications, including spinal and epidural hematomas, psoas hematomas, and skin necrosis have been reported. The extended use of enoxaparin as an anticoagulant requires the physician to be vigilant of these rare complications. Bleeding can occur at any site during therapy with enoxaparin. An unexplained fall in the hematocrit or blood pressure should lead to a search for a bleeding site.
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PMID:Enoxaparin associated with hugh abdominal wall hematomas: a report of two cases. 1096 44

Mesenteric vein thrombosis is generally difficult to diagnose and can be fatal. A case of extensive thrombosis of the mesenteric and portal veins was diagnosed early and successfully treated in a 26-year-old man with Down syndrome who was admitted to hospital because of abdominal pain, severe nausea and high fever. Ultrasonography revealed moderate ascites, and there was minimal flow in the portal vein (PV) on the Doppler examination. Computed tomography (CT) showed remarkable thickening of the walls of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, combined thrombolysis and anticoagulation therapy without surgical treatment was chosen. Urokinase was administered intravenously and later through a catheter in the superior mesenteric artery. Heparin and antibiotics were given concomitantly. The patient's symptoms and clinical data improved gradually. After 10 days, CT revealed that collateral veins had developed and the thrombi in the distal portions of the mesenteric veins had dissolved, although the main trunk of the PV had not recanalized. The only risk factor of thrombosis that was detected was decreased protein S activity.
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PMID:Extensive mesenteric vein and portal vein thrombosis successfully treated by thrombolysis and anticoagulation. 1185 47

We report the case of a 28-year-old secundipari with a history of severe hypertriglycideremia-induced pancreatitis 3 years ago who was admitted in the 37th week of gestation with abdominal pain. A blood sample had a milky aspect and plasma concentrations were as follows: triglycerides 8,5g/l, cholesterol 1000 mg/dl, amylase 574 IU/l, lipase 1310 IU/l. Acute pancreatitis was diagnosed, a caesarean was performed under spinal anaesthesia. The diagnosis was confirmed by CT-scan. Treatment with 15,000 IU heparin per day and intravenous nutrition decreased triglycerides level to less than 1g/l within 48 h. She was discharged 28 days later. Heparin could be a low-cost alternative to plasmapheresis in hypertriglycideremia-induced pancreatitis.
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PMID:[A case of hypertriglycideremia-induced pancreatitis in pregnancy: value of heparin]. 1534 58

Heparin induced thrombocytopenia (HIT) is associated with serious and sometimes devastating thrombotic events. We report a case of bilateral adrenal hemorrhage (BAH) associated with HIT after prophylactic use of low molecular weight heparin. The vague presenting symptoms of acute adrenal insufficiency offers a diagnostic challenge, which if delayed may be life threatening. A high index of suspicion for adrenal hemorrhage is required in patients receiving any form of heparin therapy presenting with new onset thrombocytopenia, abdominal pain, and fevers.
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PMID:Bilateral adrenal hemorrhage associated with heparin induced thrombocytopenia. 1726 58

A 25-year-old man was admitted to our hospital because of abdominal pain, nausea and low-grade fever. An abdominal CT showed remarkable thickening of the wall of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, anticoagulation therapy was chosen. Heparin was administered intravenously and was used alternatively with warfarin later. The patient's symptoms and clinical data improved gradually. Concerning the etiological factors of the thrombosis, only protein S activity definitely decreased. Genetic analysis indicated a variant of protein S, protein S Tokushima.
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PMID:[A case of portal vein thrombosis associated with congenital protein S deficiency]. 1754 50


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