Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human hookworm infection is a major cause of gastrointestinal blood loss and iron deficiency anemia, affecting up to one billion people in the developing world. These soil-transmitted helminths cause blood loss during attachment to the intestinal mucosa by lacerating capillaries and ingesting extravasated blood. We have isolated the major anticoagulant used by adult worms to facilitate feeding and exacerbate intestinal blood loss. This 8.7-kDa peptide, named the Ancylostoma caninum anticoagulant peptide (AcAP), was purified by using a combination of ion-exchange chromatography, gel-filtration chromatography, and reverse-phase HPLC. N-terminal sequencing of AcAP reveals no homology to any previously identified anticoagulant or protease inhibitor. Single-stage chromogenic assays reveal that AcAP is a highly potent and specific inhibitor of human coagulation, with an intrinsic K*i for the inhibition of free factor Xa of 323.5 pM. In plasma-based clotting time assays, AcAP was more effective at prolonging the prothrombin time than both recombinant hirudin and tick anticoagulant peptide. These data suggest that AcAP, a specific inhibitor of factor Xa, is one of the most potent naturally occurring anticoagulants described to date.
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PMID:Ancylostoma caninum anticoagulant peptide: a hookworm-derived inhibitor of human coagulation factor Xa. 759 95

We wanted to describe the hematologic manifestations of celiac disease (CD) in childhood. This study included 22 children with CD in whom the disease remained undiagnosed until they had presented with hematological abnormalities, such as anemia, thrombocytopenia, leukopenia or prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT). Anemia was present alone in 19 (86.3%) patients, and leukopenia coexisted with anemia in 2 (9%) patients. Thrombocytopenia was found alone in 1 (4.5%) patient. Twelve patients had an iron deficiency anemia. Iron deficiency coexisted with zinc and vitamin B(12) deficiency in 3 patients, copper and vitamin B(12) deficiency in two, vitamin B(12) deficiency in two, zinc deficiency in two and one patient had combined iron, zinc, and copper deficiency. Males had significantly lower values of hemoglobin (p < 0.05) and MCV (p < 0.05) compared to the females. In conclusion CD should be included in the differential diagnosis in children who present with anemia, leukopenia, thrombocytopenia or prolonged PT and APTT, especially in geographical areas where the prevalence of the CD is high.
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PMID:Hematologic manifestation of childhood celiac disease. 1515 13

A case is presented of a 26-year-old woman who was referred to the hematology clinic because of her report of a family history of plasminogen activator inhibitor-1 (PAI-1) deficiency. Since menarche, she had suffered from severe menorrhagia, but she had assumed that this was unrelated to her mother's history of repeated life-threatening bleeding. Her menorraghia was evident by using greater than 100 pads per period, bleeding as long as 4 continuous months, and even bleeding through her clothes despite using both tampons and pads. Evaluation with pelvic examination, endometrial biopsy, and pelvic ultrasound was unremarkable. Medroxyprogesterone acetate treatment for her dysfunctional uterine bleeding was unsuccessful. Laboratory evaluation revealed iron deficiency anemia but otherwise normal platelets, bleeding time, prothrombin time, activated partial thromboplastin time, and vonWillebrand's studies. Despite any preconceptions, examination for a fibrinolytic defect ultimately demonstrated a PAI-1 antigen level of 11.4 ng/mL (4.0-43 ng/mL) and PAI-1 activity less than 5 AU/mL (5-37 AU/mL) and clinically supported a diagnosis of a hereditary, qualitative PAI-1 defect. She was treated with aminocaproic acid with return to relatively normal menses. Future treatment should also prevent excessive bleeding during trauma, surgery, or childbirth. Further evaluation of this patient and her family is planned and may help elucidate the important role of PAI-1 in the complicated balance between hemostasis and hemorrhage.
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PMID:Menorrhagia due to a qualitative deficiency of plasminogen activator inhibitor-1: case report and literature review. 1524 91

Background: Plummer-Vinson syndrome (PVS), a rare disorder characterized by dysphagia, iron deficiency anemia, and esophageal webs, has principally been described in middle-aged women. This disorder is uncommon in the 21st century because of the abundance of iron-fortified foods. Clotting factor deficiencies are also rare. Factor VII deficiency is a bleeding disorder characterized by the absence of a critical protein in the coagulation cascade. Case Report: We present a case of PVS associated with factor VII deficiency in a 26-year-old African American female. The patient had a history of anemia that was repeatedly attributed to menstrual bleeding and dysphagia for 10 years. She presented with symptomatic anemia requiring transfusion. She reported a history of food getting stuck in her chest, and workup revealed esophageal webs with no evidence of overt luminal gastrointestinal bleeding. Coagulation laboratory tests revealed the incidental finding of a borderline increased prothrombin time. Hematologic studies confirmed the presence of factor VII deficiency. Conclusion: To our knowledge, no case has been published about a patient diagnosed with PVS and concomitant factor VII deficiency. Our case illustrates several learning points: (1) PVS is an uncommon disorder that may still be diagnosed in a developed country in the 21st century; (2) PVS requires close follow-up and esophageal surveillance because of the increased risk of esophageal cancer; (3) factor VII exhibits a high degree of phenotypic variability; (4) phenotype in factor VII deficiency does not always correlate with factor VII activity, although life-threatening spontaneous bleeding is not expected with levels >2%.
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PMID:Plummer-Vinson Syndrome With Concomitant Factor VII Deficiency. 3152 44

This case involves a 73-year-old man who visited a clinic because he was experiencing dyspnea on exertion and acid reflux. He was diagnosed with anemia and referred for a medical check-up and treatment by his primary care physician. Iron deficiency anemia and prolonged prothrombin time were confirmed with a blood test and an abdominal enhanced CT revealed marked expansion of the afferent loop after a gastrectomy. The medical check-up revealed abnormal blood coagulation due to afferent loop obstruction, which resulted in vitamin K deficiency. He was supplemented with vitamin K, and surgery was performed for the afferent loop obstruction. Postoperatively, his anemia, nutritional status, serum vitamin K levels, and prothrombin time improved steadily. In conclusion, nutrient malabsorption may occur in cases of afferent loop obstruction and abnormal blood coagulation due to vitamin K deficiency.
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PMID:[Vitamin K deficiency caused by nutritional malabsorption accompanying afferent loop obstruction:a case report]. 3182 42