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)

A 26-year-old woman, after cesarean section in the 33rd week of gestation, developed after delivery thrombosis of the popliteal vein, pulmonary embolism and thrombosis of the portal vein. After completion of a six month period of oral anticoagulation, laboratory investigations revealed diminished levels of plasminogen and free protein S antigen as well as APC-resistance due to heterozygous FV R506Q mutation. After six uneventful years, abdominal sonography and magnetic resonance examination, performed because of abdominal pain, showed liver cirrhosis with Budd-Chiari syndrome. Additional hematological investigations led to the diagnosis of polycythemia vera. Association of myeloproliferative disorders, mainly polycythemia vera, with splanchnic venous thrombosis is well known and should always be looked for.
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PMID:[A 26-year-old woman with splanchnic vein thrombosis as the initial manifestation of polycythemia vera]. 1051 20

Mesenteric venous thrombosis is a rare disease with no specific signs. It's major risk is intestinal ischaemia and necrosis. We report the case of a young women who presented with unexplained abdominal pain and subnormal abdominal ultrasound. The diagnosis was made on laparoscopic exploration which allowed anticoagulant therapy followed by proximal and distal divertingostomies of the ischemic bowel. Small bowel continuity was re-established after 3 month of total parenteral nutrition. The patients is doing well 1 year after surgery. She is still under anticoagulant therapy. The etiology found was a hypermegacaryocytosis as seen in myeloproliferative disease.
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PMID:[Extended venous ischemia of the small intestine caused by portal thrombosis. Value of diagnostic celioscopy and intestinal bi-exclusion (Thiry-Vella technique)]. 1063 45

A young female, who had been in excellent health and had used third-generation oral contraceptives, was admitted to hospital because of abdominal pain and ascites. Budd-Chiari syndrome (BCS) was diagnosed by radiographic and histological examination. Tests for myeloproliferative disease, deficiency of coagulation inhibitors and paroxysmal nocturnal haemoglobinuria were negative. DNA investigation showed a double heterozygous defect: the Arg506Gln mutation in the factor V gene (factor V Leiden) and G20210A nucleotide substitution in the prothrombin gene. This double defect was also found in the patient's father, who had never experienced an episode of venous thromboembolism. Genetic and acquired thrombogenic risk factors are being detected increasingly in patients with BCS. With the discovery of new genetic defects leading to hypercoagulabiulity an increasing number of patients with serious thrombotic manifestations, such as BCS, will exhibit concurrence of hereditary and acquired risk factors for thrombosis.
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PMID:Budd-Chiari syndrome: combination of genetic defects and the use of oral contraceptives leading to hypercoagulability. 1102 10

Anagrelide hydrochloride (Agrylin, Roberts Pharmaceutical Corp.) is an oral imidazoquinazoline agent that has been shown to reduce elevated platelet counts and the risk of thrombosis in patients with thrombocythaemia in various myeloproliferative disorders (MPD). It is currently approved by the FDA as oral treatment for essential thrombocythaemia (ET) and thrombocythaemia associated with polycythaemia vera (PV). Anagrelide selectively suppresses bone marrow megakaryocytes by interfering with the maturation process and decreasing platelet production without affecting the erythroid and myeloid progenitor cells. Other medications indicated for the treatment of thrombocythaemia, including interferon alpha (IFN-alpha), alkylating agents and hydroxyurea, suppress all cell lines. Anagrelide is known to inhibit platelet cyclic adenosine monophosphate (cAMP) phosphodiesterase at concentrations that exceed those achieved at doses used to treat ET. Anagrelide is extensively metabolised in the liver and its metabolites are primarily excreted in the urine. Adverse effects associated with the use of anagrelide are primarily caused by the drugs' direct vasodilating and positive inotropic effects. These include headache, hypotension and diarrhoea. It has also been known to cause fluid retention, tachycardia, nausea, abdominal pain and arrhythmias. The starting dose of anagrelide ranges from 0.5 mg q.i.d. to 1 mg b.i.d. with a maximum dose of 2.5 mg q.i.d. Adequate responses have been maintained with a median dose of 2-2.5 mg/day. Platelet counts begin to decrease in 7-10 days, however, they return to pre-treatment levels within 4-8 days if therapy is stopped. Anagrelide 2 mg/day for one year costs approximately US$6439, and treatment must continue indefinitely [1].
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PMID:Anagrelide: a novel agent for the treatment of myeloproliferative disorders. 1124 36

Portal vein thrombosis, except in hepatocellular carcinoma and severe cirrhosis, is due to one or several prothrombotic disorders with or without a local precipitating factor. We report a case of a portal and splenic vein thrombosis, without cavernoma and varices which occurred in a 72-year-old man with abdominal pain and weakness. Three prothrombotic states including latent myeloproliferative disorder, antiphospholipid syndrome, and factor II G202101 mutation, were observed. Anticoagulant treatment resulted in complete repermeation of the portal and splenic veins without a hemorrhagic event. This illustrates that several prothrombotic states may occur in a single patient with portal vein thrombosis. Early anticoagulant therapy, in recent portal vein thrombosis, can result in repermeation.
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PMID:[Portal vein thrombosis associated with a myeloproliferative disorder, prothrombin G20210A mutation, antiphospholipid syndrome, with repermeation during anticoagulant therapy]. 1152 Nov 10

Essential thrombocythemia and polycythemia vera are both chronic progressive myeloproliferative disorders of insidious onset. If the excessive production of red cells and/or platelets is controlled, patients with these disorders may have prolonged survival. However, the clinical course of these patients can be complicated by a variety of events, including thrombotic episodes, bleeding episodes, arthropathies, pruritus, weakness, weight loss, neurologic impairment, erythromelalgia, fever, abdominal pain, and the life-threatening consequences of progression to myelofibrosis and/or acute leukemia. Effective control of hematopoiesis by phlebotomy or a variety of therapeutic agents has resulted in a reduction or elimination of many of these clinical events, but has not altered the evolution to myelofibrosis or acute leukemia. Use of each of these therapeutic strategies is also associated with a range of adverse events. Monitoring overall survival or a reduction in the frequency of clinical events has previously served as a means of assessing the results of these therapeutic interventions. Quality-of-life instruments have not been applied in a systematic fashion to the evaluation of outcomes in patients with these chronic myeloproliferative disorders. Quality-of-life assessments evaluate not only the state of well-being of a patient that results from an assessment of the individual's ability to perform everyday activities, which are reflective of physical, psychological, and social well-being, but also patient satisfaction with the control of disease and/or treatment-related symptoms. Quality-of-life instruments have been used to assess the clinical course of patients suffering from a variety of disorders, ranging from cancer to renal failure to chronic fatigue syndrome. Information about quality-of-life outcomes can contribute to the evaluation of variations in dose and timing of administration of therapeutic agents. It is possible that the side effects of a particular therapy may outweigh the disease regression achieved with a particular therapy. In the future, quality-of-life instruments may prove useful in prospectively evaluating therapeutic end points in patients with essential thrombocythemia and polycythemia vera.
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PMID:Quality of life issues in patients with essential thrombocythemia and polycythemia vera. 1209 51

DIAGNOSTIC CIRCUMSTANCES: Portal vein thrombosis is the second cause of portal hypertension after cirrhosis in Western countries. Diagnosis can be either made at the acute stage in the context of abdominal pain or after appearance of a porto-portal collateral venous circulation leading to the formation of a portal cavernoma, the diagnosis being made in the circumstance of rupture of oesophageal varicose veins or manifestations of hypersplenism. AETIOLOGICAL SURVEY: In the absence of hepatocellular carcinoma, causes that need to be investigated are cirrhosis, local factors (intra-abdominal sepsis, abdominal surgery, splenectomy or pancreatitis), and one or several prothrombotic affections (acquired or inherited prothrombotic states are present in 70% of cases, with myeloproliferative disease ranking first). REGARDING TREATMENT: Anticoagulant therapy generally allows recanalisation of the thombosed veins in recently constituted thrombosis. Some patients at the portal cavernoma stage can also benefit from anticoagulant therapy: patients with a prothrombotic state without large oesophageal-gastric varicose veins. In the case of large oesophageal-gastric varicose veins that have never bled, treatment to prevent haemorrhages due to portal hypertension according to the same modalities as in cirrhosis must be associated with the prescription of an anticoagulant. In the absence of prothrombotic affection or in patients having already suffered from haemorrhages due to portal hypertension, the benefit of anticoagulant therapy is less clearly established.
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PMID:[Portal vein thrombosis]. 1453 80

A 46-year-old man with myeloproliferative disorder received a stem cell transplant from an HLA-identical unrelated donor. Eight months status post transplantation, during the course of tacrolimus therapy, the patient developed severe epigastric pain and fever. FGS findings showed eruptions with blisters in the esophagus and ulcers in the stomach. Biopsy specimens revealed acidophilic inclusion bodies in the nuclei. Varicella zoster virus (VZV) DNA copies were detected in the serum. No skin lesions were observed prior to hospital admission. The diagnosis of visceral VZV infection was made and the gastric and esophageal lesions were successfully healed with acyclovir (ACV). Severe abdominal pain is one of the most important signs of VZV infection for recipients of stem cell transplantation.
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PMID:Involvement of the esophagus and stomach as a first manifestation of varicella zoster virus infection after allogeneic bone marrow transplantation. 1549 26

Portal vein thrombosis may complicate splenectomy in patients with hemolytic anemia and myeloproliferative disease, whereas the frequency of portal vein thrombosis in case of trauma is not defined. A case of right portal vein thrombosis after splenectomy for trauma is reported in this paper. Hematologic workup did not reveal an underlying platelet or coagulation disorder. The patient was promptly anti-coagulated with complete recanalization of the portal vein. We conclude that mild symptoms, like abdominal pain and fever, after splenectomy should be investigated with a color Doppler ultrasonography to confirm or rule out a diagnosis of portal thrombosis and to anti-coagulate the patient with thrombosis, thus preventing bowel infarction and secondary portal hypertension. Routine postoperative color Doppler might also be justified in all postsplenectomy patients (without hematologic diseases) for early detection of a portal vein thrombosis.
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PMID:Right portal vein thrombosis after splenectomy for trauma. 1586 58

Splenic abscess is a rare disease but with increasing frequency. The authors present 9 patients with splenic abscess treated at the Institute of Digestive System Diseases, Clinical Centre of Serbia, in a period from January 1, 1986 to May 15, 2004. Splenic abscess was the complication of septic endocarditis in 4, trauma in 2, dental infection in 1, while in 2 cases it was the complication of chemotherapy in myeloproliferative disorders. All 9 patients had fever, 7 - abdominal pain, 4 - left shoulder pain, and 1 patient had nausea and vomiting. Higher white blood count was found in 6 patients, pleural effusion in 4, elevated left hemidiaphragm in 1 and basal pneumonia in 1 patient as well. Ultrasonography and CT were the most reliable diagnostic procedures. CT was superior in diagnosis of multiple small abscesses. Culture of the pus recovered the Enterococcus in 3 cases, Streptococcus a hemolyticus in 1, Staphylococcus epidermidis and Candida albicans in 1, Staphylococcus aureus, E. Coil and Candida albicans in 1, Staphylococcus aureus i Salmonella enteritidis in 1 case. Eight patients underwent splenectomy and 1 was cured by combined antibiotics in high doses. One patient died postoperatively due to septic endocarditis that had been present before surgery. The authors believe that splenectomy and antibiotics administered according to drug susceptibility test as well as management of underlying disease are the method of choice for splenic abscess treatment. Conservative antibiotic treatment is indicated in selected cases only.
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PMID:[Abscess of the spleen]. 1605 75


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