Progressive warfarin anticoagulation in protein C deficiency: a therapeutic strategy
Article Abstract:
Protein C is a vitamin K-dependent blood protein that prevents coagulation or blood clotting. A deficiency of protein C is a genetic disorder associated with recurrent thrombosis or blood clot formation in the veins. Although the anticoagulant warfarin (Coumadin) is used to prevent recurrent thrombosis, the initiation of warfarin therapy has been associated with skin necrosis or tissue death and a rapid decline in protein C levels, which may lead to conditions of increased blood clot formation. A case is described of a 34-year-old woman, who underwent successful anticoagulant treatment with warfarin without a rapid decline in protein C levels at the beginning of drug treatment. The patient developed a pulmonary embolus (PE), or clot in her lungs, possibly resulting from oral contraceptive use and smoking. She was treated with the anticoagulant heparin. When the PE recurred, the patient was given heparin and warfarin. After a third PE, she was diagnosed as having protein C deficiency, and treated with gradually increasing doses of oral warfarin over a period of 20 days. In this case, the onset of warfarin treatment was not associated with skin necrosis or recurrent thrombosis. This case shows that protein C levels can be decreased gradually by progressively increasing warfarin doses over an extended period. The gradual decline in protein C levels prevents the development of a hypercoagulable state, or conditions of increased clot formation, which may cause skin necrosis or recurrent thrombosis. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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Congenital methemoglobinemia due to methemoglobin reductase deficiency in two unrelated American black families
Article Abstract:
Methemoglobinemia is a condition in which hemoglobin, the oxygen-carrying protein in red blood cells, is oxidized (an aging process) and unable to transport oxygen. The principal sign of the disorder is cyanosis, a bluish to dark purple discoloration of the skin. Hereditary methemoglobinemia can be caused by the inheritance of a defective hemoglobin or a deficiency in one of two enzymes that are part of the reactions which reduce methemoglobin back to hemoglobin. Most patients with the disorder have asymptomatic cyanosis, but 10 percent of patients have severe neurological defects. It was expected that cyanosis would be masked in blacks due to their darker skin pigmentation. Two cases in unrelated American black women are described; both lacked a red blood cell enzyme. Neither patient had neurological deficits or abnormal symptoms. In one, cyanosis was noted during tonsillectomy at age four, while the other was observed to have cyanosis and chocolate brown blood while undergoing obstetric delivery. Neither woman had family members with the disorder. Both patients were in their twenties when studied for this report. Laboratory studies indicated the deficit was in methemoglobin reductase, which has not been reported previously in a black individual. The variance in the enzyme in each subject remains to be determined by further DNA study. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
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Chronic acetaminophen ingestion associated with (1;7)(pll;pll) translocation and immune deficiency syndrome
Article Abstract:
The effect of chronic ingestion of high doses of acetaminophen by humans is unknown. A case is described of a patient who abused acetaminophen and developed opportunistic infections, cancer of the tonsil, T cell defects, and a myelodysplastic (bone marrow dysfunction) syndrome resulting from chromosomal changes. For seven years the patient had been taking up to 18 grams of acetaminophen a day; he also abused codeine over the same time period. Symptoms noted on first examination included weight loss over three months, muscle aches, loss of appetite, jaundice, and fever. Recurrent yeast infections of the mouth and throat were also noted. Testing for human immunodeficiency virus, the agent responsible for AIDS, was negative. A bone marrow biopsy showed myelodysplastic features, and study of the chromosomes showed a translocation. A biopsy of a lymph node confirmed cancer of the tonsil, and radiation therapy was begun. A subsequent lung biopsy showed granuloma formation. Computerized tomography indicated progressive impairment of the neurologic system, and the patient died. It is concluded that chronic ingestion of acetaminophen may produce chromosomal changes and changes in the DNA. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1990
User Contributions:
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