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)

Out of 1229 patients operated on according to Harrington there were eight with clinical deep venous thrombosis (DVT) confirmed by phlebography or at autopsy. One patient died from massive pulmonary embolism. All eight DVT were located proximally on the left side. In two cases the first symptom was abdominal pain. At follow-up two patients had slight complaints. One had edema in hot weather and one swelling of the left leg. Another patient had no complaints but venography showed pathological collateral veins. There may be a considerable risk of development of a postthrombotic syndrome.
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PMID:Thromboembolic complications following scoliosis surgery in Scandinavia. 43 80

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

Sixteen patients with mesenteric venous thrombosis were reviewed retrospectively during a period from 1983 to 1987. Twelve patients had progressive abdominal pain, three had gastrointestinal bleeding, and one had general malaise. Seven of these 16 patients had previous deep-vein thrombosis. After negative routine gastrointestinal and hepatobiliary evaluation, 11 patients underwent an infusion computerized tomographic scan. Of these, 10 had superior mesenteric vein thrombosis; three of these 10 patients had portal vein thrombosis. Selective arteriography was done in two patients because of gastrointestinal bleeding, and a diagnosis of mesenteric vein thrombosis was made on the venous phase of the examination. The remaining four patients developed acute abdominal symptoms requiring surgical exploration, at which time mesenteric venous thrombosis was discovered. An identifiable coagulopathy was detected in nine patients (protein C deficiency in six, protein S deficiency in two, and factor IX deficiency treated with factor IX concentrate in one). No case of congenital antithrombin-III deficiency was identified. Six of these nine patients had a past history of deep venous thrombosis. Of five patients who underwent surgical exploration, all required bowel resection. In follow-up, two patients died of intestinal necrosis and a third died of associated pancreatic cancer. Thirteen patients were discharged from the hospital. Treatment of coagulopathy was by heparin in three patients and sodium warfarin (Coumadin) in four patients. Long-term anticoagulation was not instituted because of gastrointestinal bleeding in three and cirrhosis in three patients. Mesenteric venous thrombosis can occur without gangrenous bowel. Diagnosis should be suspected when acute abdominal symptoms develop in patients with prior thrombotic episodes and a coagulopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mesenteric venous thrombosis. 172 86

Careful interpretation of the vascular pathology is important in cases of intestinal ischemia caused by primary mesenteric vein thrombosis because it suggests antithrombin III (AT III) deficiency. This deficiency, an autosomal dominant hereditary disorder, predisposes the patient to venous thrombosis. Similar or acquired deficiencies may also predispose the patient to thrombosis. In hereditary AT III deficiency, 90% of the cases have thrombosis of the leg or iliac veins; 8.3% of the cases, thrombosis of the mesenteric veins. Additionally, some families have a tendency to develop mesenteric vein thrombosis specifically. In this case report, a daughter with probable AT III deficiency had a history of 3 episodes of deep vein thrombosis in the previous 5 years while taking oral contraceptives. Her father, with the same deficiency, died from massive intestinal infarction resulting from portal and mesenteric vein thrombosis. The 19-year old woman developed gradually worsening abdominal pain, signs of peritonitis, and hematemesis. A laparotomy revealed peritonitis that was due to segmental small-bowel infarction; the underlying pathologic condition was mesenteric vein thrombosis. Coagulation study results revealed AT III activity by chromogenic assay, 0.48 u/mL; AT III antigen, 0.5 u/mL; and protein C antigen, 1.15 u/mL. 10 days after discharge, she developed a hemicranial headache with nausea, vomiting, neck tenderness, and photophobia; she was readmitted. A CT scan showed a left posterior parietal cerebral infarct. Repeat AT III activity by chromogenic assay was 0.51 u/mL and AT III antigen level was 0.50 u/mL. Before anticoagulant therapy could be initiated, the patient died 7 days after readmission. The combined lowering of AT III activity and antigen levels to half of normal suggests AT III deficiency. Earlier diagnosis of this deficiency could have been made in light of the patient's own history of thrombosis and the paternal history.
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PMID:Mesenteric venous thrombosis due to antithrombin III deficiency. 333 17

The diagnostic features and operative results of six patients with spontaneous aorto-caval fistula associated with abdominal aortic aneurysm were analyzed. Abdominal pain, pulsatile abdominal mass and haematuria were constant preoperative findings in all patients. Radiological signs of congestive heart failure of various degrees were present in five, abdominal bruit in four and preoperative renal failure in three patients. As preoperative diagnostic examinations i.v. pyelography was done in two patients and ultrasound scanning and angiography of the abdominal aorta in a further two patients. In one ultrasound scanning a dilated inferior vena cava and hepatic veins were seen as an indirect sign of ACF, while in both angiograms the ACF was seen. In these two cases the diagnosis of ACF was made preoperatively, while in four other cases the diagnosis was made during the operation. Three patients survived the operation and were still alive after eight months, four years and six years respectively. Postoperative complications developed in two patients: postoperative ileus in one and deep venous thrombosis and pneumonia in another. Because of its rarity aorto-caval fistula is difficult to diagnose. The presence of haematuria in a patient suffering from abdominal aortic aneurysm should strongly suggest the diagnosis of an aorto-caval fistula.
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PMID:Diagnosis and treatment of spontaneous aorto-caval fistula. 355 68

Seventeen women with thrombosis during pregnancy were studied prospectively. The deep venous thrombosis (DVT) was diagnosed objectively with phlebography, plethysmography and thermography. In many cases (13/17) the dominant symptom was diffuse pain in the lower abdomen and/or leg which in several cases caused a delay in the diagnosis. The traditionally typical thrombotic signs were often missing. Proximal thrombi were predominant (13/17) as were left-sided ones (14/17). During pregnancy and lactation the patients were treated with heparin which, after the initial parenteral administration, was given subcutaneously by self-administration. In conclusion, DVT must be suspected and non-invasive diagnostic tests be liberally performed in cases of uncharacteristic lateral and/or declive abdominal pain or leg pain during pregnancy. The DVT must always be objectively verified before treatment. In patients with pregnancy DVT there is no indication for early labor induction and the patients can be delivered by the normal vaginal route. It is recommended that patients with DVT during pregnancy should be treated with heparin subcutaneously which can be self-administered. The post-partum treatment may be continued for 2-3 months with heparin subcutaneously or peroral anticoagulants.
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PMID:Deep vein thrombosis during pregnancy. A prospective study. 666 57

A nationwide surveillance of mortality associated with sterilization led to the identification of the death of a woman who was using oral contraceptives (OCs) prior to operation and died as a result of mesenteric venous thrombosis after tubal sterilization. This case is reported as a reminder of the increased risk of postoperative thromboembolism associated with OC use and to suggest how this risk can be decreased. The patient was a healthy, 24-year-old, white woman with 2 living children. She did not smoke and had no history of thromboembolic disorders. She had been using OCs for several years and continued their use until the time of hospitalization for operation. The specific OC preparation she was using is unknown. The first 48 hours following the operation the patient did well except for some mild to moderate lower abdominal pain. On the 4th day, she developed severe, acute abdominal pain and suffered a cardiovascular collapse for which she required resuscitation. She was considered to be septic and dehydrated; thus, treatment with intravenous fluids and antibiotics was initiated. An echogram obtained on the 5th day after sterilization suggested the possibility of an abdominal mass on the right sight, and an exploratory laparotomy was performed. There was 2000 ml of clear fluid in the peritoneal cavity. The cecum and ascending colon were necrotic with thrombosis of the colic and ileocolic veins. The pelvis and the appendectomy stump appeared normal. A right hemicolectomy and resection of the distal ileum were performed followed by a primary side-to-side ilecolostomy. The patient's condition deteriorated after laparotomy despite vigorous management, and she died the next morning, 7 days after the sterilization operation. Significant findings at postmortem examinations were thrombosis of both the ileocolic vein and the superior mesenteric vein and inflammation in the area of colon adjacent to the anastomosis. The cause of death was determined to be endotoxic shock secondary to large bowel necrosis which resulted from thrombosis of the mesenteric veins. This patient was at increased risk for postoperative venous thrombosis because she continued to use OCs during the month before the operation. 2 carefully conducted case-control studies have shown that OCs increase by more than 3-fold the risk of postoperative thromboembolism. It is unclear how much the knowledge of this risk has altered preoperative management of women having elective operation in the U.S. At least 1 prospective study has found no difference in incidence of idiopathic deep venous thrombosis with increasing estrogen doses, but the risk of postoperative thromboembolism associated with OCs containing a lower estrogen content has not been studied.
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PMID:Oral contraceptives and postoperative venous thrombosis. 708 37

Lupus anticoagulant has been described in association with many autoimmune disorders. Here we describe its occurrence in a patient with ANCA-associated microscopic polyarteritis with medium vessel involvement. A 62-year-old man presented with mononeuritis multiplex and abdominal pain and was demonstrated to have multiple aneurysms on visceral angiography, consistent with the diagnosis of medium vessel vasculitis or classical polyarteritis nodosa. In addition he had active tuberculosis. He developed a deep venous thrombosis at this admission and, on one occasion, had a prolonged APTT but this was not confirmed to be due to a lupus anticoagulant. Two years later when the patient was readmitted with fevers, headaches and nasal discharge, both ANCA and a lupus anticoagulant were demonstrated in his serum, although there was no evidence of a venous thrombosis. Six months later the patient was demonstrated for the first time to have dysmorphic urinary RBC consistent with glomerular bleeding; at the same time he developed a deep venous thrombosis. ANCA was still present, but the lupus anticoagulant could not be detected. The patient was treated with cyclophosphamide and prednisolone and a Greenfield filter inserted into his inferior vena cava.
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PMID:Lupus anticoagulant in anti-neutrophil cytoplasmic antibody-associated polyarteritis. 773 54

Pneumatic tourniquet and hone cement are often applied in orthopaedic surgery. In lower limb surgery, deep vein thrombosis may occur after release of tourniquet, causing embolism of lungs and vital organs. Paradoxical embolism may develop if the patients present extracardiac or intracardiac right to left shunt, such as atrial septum defect, etc. A 60-year-old female patient suffered from osteoarthritis of both knees was admitted for total knee replacement (TKR). Pneumatic tourniquet was inflated on the operated leg for the orthopaedic surgery which lasted for 2h. Dyspnea, sinus tachycardia and abdominal pain were noted after TKR. Blood gases analysis showed arterial hypoxemia and respiratory alkalosis. Chest X-ray revealed diffused bilateral pulmonary infiltration, pulmonary trunk engorgement, and decreased lung markings. Two days after TKR under the impression of peritonitis, she received exploratory laparotomy in which ischemic bowel and gall bladder were found. Pulmonary and paradoxical embolism were diagnosed, both of which were the well-known complications of TKR with tourniquet and bone cement application. The patient finally succumbed because of multiple organ failures.
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PMID:[Pulmonary and paradoxical embolism after total knee replacement--a case report]. 908 31

Azathioprine is a drug commonly used for the treatment of inflammatory bowel disease, organ transplantation and various autoimmune diseases. Hepatotoxicity is a rare, but important complication of this drug. The cases reported to date can be grouped into three syndromes: hypersensitivity; idiosyncratic cholestatic reaction; and presumed endothelial cell injury with resultant raised portal pressures, venoocclusive disease or peliosis hepatis. The components of azathioprine, 6-mercaptopurine and the imidazole group, may play different roles in the pathogenesis of hepatotoxicity. The strong association with male sex, and perhaps with human leukocyte antigen type, suggests a genetic predisposition of unknown type. Many of the symptoms of hepatotoxicity, such as nausea, abdominal pain and diarrhea, can be nonspecific and can be confused with a flare-up of inflammatory bowel disease. As well, the subtype resulting in portal hypertension can occur without biochemical abnormalities. A 63-year-old man with Crohn's disease who is presented developed the rare idiosyncratic form of azathioprine hepatotoxicity, but also had a severe disabling steroid myopathy, peripheral neuropathy, resultant deep venous thrombosis and pulmonary embolism related to immobility, and a nosocomial pneumonia. His jaundice and liver enzyme levels improved markedly on withdrawal of the drug, returning to almost normal in five weeks. Treating inflammatory bowel disease effectively while trying to limit iatrogenic disease is a continuous struggle. Understanding the risks of treatment is the first important step. There must be a low threshold for obtaining liver function tests, especially in men, and alertness to the need to discontinue the drug or perform a liver biopsy should patients on azathioprine develop liver biochemical abnormalities, unexplained hepatomegaly or signs of portal hypertension.
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PMID:Cholestatic hepatocellular injury with azathioprine: a case report and review of the mechanisms of hepatotoxicity. 981 67


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