Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Etiology of deep vein thrombosis in ambulant patients (DVTA = TVPA in text) varies: cancer, blood disease, infectious focus, dysimmunity syndrome, dysglobulinemia, extrinsic compression, metabolic disorder, anomaly of hemostasis. A prospective study was carried out between June 1988 and September 1989 by angiologists in 5 regions of France to evaluate the diagnostic rentability of an epidemiologic survey and to determine possible distinctive characters of DVTA. The survey was comprised of a questionnaire, a full clinical examination and screening tests: chest x-ray, abdominopelvic ultrasound imaging, a-uro/gynecologic examination, full blood count, serum iron, ferritin, uric acid, triglycerides, cholesterol, protein electrophoresis, antinuclear antibodies, circulating anticoagulant, hemostasis factors and liver function tests. The study included 128 patients, mean age 60 +/- 16 years with a DVTA developing without a previous immobilization. The usual predominance in the left leg was not observed. The etiology was identified in 33 cases, including 20 (15.6%) as a result of the screening tests: anomalies of hemostasis (8), blood diseases (3), dysimmunity syndromes (4), extrinsic compression (3), cancer metastasis (1) and hypertriglyceridemia in a diabetic (1). The screening procedure was of no greater value in the absence of a triggering or predisposing factor, on the contrary. An anomaly of hemostasis was detected more frequently in the presence of local or regional triggering factors in the men (4 out of 4) and in the women on the pill (4 out of 4). The number of cancers discovered following screening (2%) was smaller than that expected according to the literature (10%).(ABSTRACT TRUNCATED AT 250 WORDS)
J Mal Vasc 1992
PMID:[Prospective etiologic study of 128 patients with ambulatory dep vein thrombosis]. 149 55

The authors evaluate the positivity of the tumor markers CEA, AFP, TPA and ferritin among an homogeneous group of 500 patients suffering from a chronic hepatopathy and positive for HBsAg. The obtained results show a significant increase of TPA, AFP and Ferritin (70.4%, 20% and 24% respectively of the examined patients), while CEA is increased only in the 3.2%. The correlation between the positivity of these markers and possible evolution of the chronic hepatopathy is at present under investigation.
Arch Monaldi Mal Torace
PMID:[A retrospective study of the serum CEA, AFP, TPA and ferritin values in 500 patients with chronic liver diseases]. 172 99

Severe congestive cardiac failure developed in a few weeks in a 44 year old man who had undergone porto-caval anastamosis for post-hepatitis cirrhosis one year previously and then treated for anaemia by repeated blood transfusion and chronic daily oral iron therapy. Infiltrative, congestive and restrictive cardiomyopathy was diagnosed in the presence of global cardiomegaly, electrocardiographic changes (microvoltage, diffuse ST-T wave changes), echocardiographic appearances (dilatation of the left ventricle, with hypertrophic and hypokinetic walls), and hemodynamic signs of adiastole with equalisation of filling pressures at 15 mmHg and a cardiac index of 1,88 l/min/m2. Cardiac haemochromatosis was confirmed by the laboratory (serum iron: 35 mumol/l; siderophilin saturation: 100 p. 100; serum ferritin: 1854 ng/ml; induced siderouria: 51 mg/24 hours) and histological findings (endomyocardial biopsy showing pigment overload). The absence of a family history, of homozygote A3 antigen, of diabetes, of iron overload on hepatic biopsy one year previously, excluded the diagnosis of familial idiopathic haemochromatosis. A secondary form of the disease was diagnosed on a possible genetic predisposition (heterozygote A3 antigen) and on environmental factors (blood transfusions, iron therapy, cirrhosis, alcoholism and perhaps the porto-caval anastamosis. Cardiac haemochromatosis was cured in this case by iron chelating therapy comprising daily subcutaneous infusions of 2 g of desferrioxamine for 2 months. The cure was confirmed by regression of the signs of clinical cardiac failure and of cardiomegaly, the increase in QRS voltages and the near normalisation of the hemodynamic and laboratory findings.
Arch Mal Coeur Vaiss 1983 Oct
PMID:[Adiastole caused by a secondary cardiac hemochromatosis. Successful treatment with an iron chelating agent]. 641 3