Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A one-month-old male infant with spontaneous intracerebral and subdural hematomas due to vitamin K deficiency was described. He was breastfed. Loose stools continued and began to contain blood. He had fever, vomiting and convulsion, and became drowsy. The blood studies showed anemia and hypoprothrombinemia. Left carotid angiograms revealed intracerebral and subdural hematomas. He was treated successfully by immediate operation and administration of vitamin K. 2) Vitamin K deficient hemorrhage beyond the immediate newborn period was discussed with reference in the literature. Three etiologic factors included, decreased vitamin K intake, decreased intestinal absorption of vitamin K and decreased production of vitamin K by colon bacteria. The most important factor of the three seemed to be low vitamin K intake. Intracranial hemorrhage was recognized in about one third of the cases in the literature. It was emphasized that vitamin K deficiency occurring beyond the immediate newborn period was very important as a cause of intracranial hemorrhage in infancy.
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PMID:[Intracranial hemorrhage in an infant due to vitamin K deficiency --successful management of spontaneous intracerebral and subjural hematoma]. 103 36

The patient was a 76-year-old male with disturbance of consciousness due to cerebral infarction. He was found lying in his garden on July 30, 1990 and was immediately hospitalized. Central venous alimentation was started on the same day, because the patient was incapable of oral nutritional intake. Aspiration pneumonia developed on August 3. As Pseudomonas aeruginosa and Candida were detected by sputum cultures on August 20, antibiotics were changed to latamoxef (LMOX), 6 g/day, tobramycin, 180 mg/day, and fluconazole, 200 mg/day, from August 30. Macroscopic hematuria was noted after exchange of the urethral catheter. Hematuria gradually worsened, bladder tamponade occurred, and anemia had exacerbated with Hb decreasing from 13.4 to 8.7 g/dl and Hct from 39.1 to 26% on September 14, when the patient was referred to our department. Corresponding marked increases were observed in PT from 11.5 to 50.1 seconds and in APTT from 33.7 to 107.6 seconds. As the hematuria was suspected to be due to vitamin K deficiency hypoprothrombinemia induced by LMOX, its administration was discontinued on the day of the referral. Hematuria was alleviated from the next day, and PT normalized to 12.1 seconds and APTT to 36.6 seconds 3 days after discontinuation. The administration of vitamin K was started on this day, and hematuria disappeared 7 days after discontinuation of LMOX administration.
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PMID:[A case of hematuria associated with cefem group antibiotics]. 156 59

Elderly diabetics take more drugs than other groups of elderly patients. Their multiple drug use is largely explained by the drugs that they take for complications of their primary disease; these include cardiovascular drugs for macrovascular disease and antibiotics for secondary infections. They also take more drugs for control of other conditions that are etiologically associated with the development and progression of their diabetes, including antihypertensive agents, antilipemic agents and steroids, and nonsteroidal antiinflammatory drugs (NSAIDs), which are taken for relief of joint pain that is intensified by arthritic joints bearing excess weight. Drugs taken by elderly diabetics that contribute to the high prevalence of drug-nutrient interactions include those taken as antidiabetic agents, including both insulin and sulfonylureas as well as calcium channel blockers; they also include thiazides, loop diuretics, sulfa drugs, cephalosporin antibiotics, tetracyclines, antifungal agents, cholestyramine and colestipol, niacin, prednisone and other corticosteroids, and NSAIDs. These drugs and drug combinations contribute to the risk of hyperglycemia, which can cause nonketotic hyperglycemia in the elderly; to the risk of hypoglycemia, which in the elderly carries the risk of inducing pseudo-stroke; to the risk of drug-induced nutritional deficiencies from antilipemics and cephalosporins, which can induce vitamin K deficiency; to the risk of acute incompatibility reactions, including flush reactions from chlorpropamide, niacin, and calcium channel blockers; and to the risk of edema, anemia, and hyperkalemia from NSAIDs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Drug and nutrient interactions in the elderly diabetic. 307 52

A neonate who was not given prophylactic vitamin K injection was admitted with acute anemia and hemoperitoneum. The evolution was favorable with medical treatment only. Vitamin K deficiency appears to be the main cause of this hemorrhagic disease. There is a controversy on this subject, as hepatic deficiency seems to be involved in certain cases.
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PMID:[Acute anemia caused by hemoperitoneum disclosing hemorrhagic disease of the newborn]. 336 4

It is well known that vitamin K deficiency is an important cause of the spontaneous intracranial hemorrhage in infancy. A 60-day-old male infant with spontaneous intracerebral hematomas due to vitamin K deficiency was presented. He was breast-fed. He had been medicated oral antibiotic agent for diarrhea and fever. Three days later he developed petechien, vomiting and twitching, and became drowsy. The blood studies showed anemia, and advance of ESR. He was administered of vitamin K immediately. CT scan was showed four intracerebral hematomas with niveau, which were surrounded by high-density rings. The ring-like figures were unique for this case. The reason may be next, we think. Under the states in which blood can separate easily with advance of ESR, blood clot would adhere to the wall of the hematomas. So these hematomas showed ring-like figures and had niveau in them. CT scan of this case was also interesting because there was little deviation in spite of the big hematomas. The reason of this may be that the brain of infancy is incomplete in myelination and contains much water, and that the possibility of bleeding due to vitamin K occurs slowly. We examined 84 cases of intracranial hemorrhage due to vitamin K deficiency from literatures, and they were all identified for the hemorrhage sites by CT scan. Subarachnoidal hemorrhage was in 72 cases (85.7%), subdural hemorrhage was in 41 cases (48.8%), intracerebral hematomas was in 36 cases (42.9%) and intraventricular hemorrhage was in 9 cases (10.7%). In 52 cases the CT findings were described.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intracranial hemorrhage in infancy due to vitamin K deficiency: report of a case with multiple intracerebral hematomas with ring-like high density figures]. 382 41

The authors describe two cases of delayed haemorrhagic disease by vitamin K deficiency, occurring at 28 days and 2 months 1/2 of age. The first case was revealed by an hematoma in the thoracic wall and anemia, and the second by convulsions caused by meningeal hemorrhage. The study of hemostasis and the correction of prothrombin rate after vitamin K injection show that it is a delayed haemorrhagic disease caused by vitamin K deficiency. Etiologic factors of this affection are discussed. The authors insist on the preventive role of the vitamin K injection in infants fed exclusively at breast and presenting diarrhea.
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PMID:[Delayed hemorrhagic syndrome caused by hypovitaminosis K]. 383 6

Thymic hemorrhage related to coagulopathy by vitamin K deficiency is a rare condition. We report a case in a 4-week-old boy presenting with acute onset of respiratory distress and anemia. Ultrasound examination of a compressive anterior mediastinal mass established the diagnosis of thymic hemorrhage and allowed us to follow resolution under medical treatment.
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PMID:Ultrasound diagnosis of thymic hemorrhage in an infant with late-onset hemorrhagic disease. 807 31

Haemorrhagic diathesis with secondary anaemia was diagnosed in a 5-week-old infant. The reason for the haemorrhagic diathesis was vitamin K deficiency caused by intrasecretory pancreatic insufficiency.
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PMID:[Hemorrhagic diathesis in a 5-week-old infant with cystic fibrosis]. 896

A two-year mechanistic bioassay in male Crl:CD BR rats was initiated with 50 ppm Wyeth-14,643 (WY) to investigate the relationship between peroxisome proliferating compounds and Leydig cell adenoma formation. After 154 days, the survival rate in the WY group decreased below control levels. After 300 days, the dose was lowered to 25 ppm for the remainder of the study. Gross examination of WY-treated rats either found dead or euthanized in extremis revealed hemorrhages at several sites. To investigate this observation, blood was then collected on test day 281 from 10 randomly selected control and WY-treated rats and a clinical pathological examination was performed. The WY-treated rats had significantly decreased red blood cell count, hemoglobin, and hematocrit, and elevated platelet counts. In the WY-treated rats, prothrombin times in undiluted plasma were similar to the controls, but were markedly prolonged in 2 of 10 rats when the plasma samples were diluted to 25%. Subsequently, blood was collected prior to sacrificing WY-treated rats which were exhibiting clinical signs of anemia. These rats had prolonged prothrombin times, activated partial thromboplastin time, and thrombin clot time when compared to laboratory historical control data (116.7 vs 13.3, 116.4 vs 13.7, and 42.4 vs 25.7 seconds, respectively). In a subsequent, ongoing study, Vitamin K was added to control and WY-treated diets (100 ppm). No survival differences between control and WY-treated rats occurred through 260 days in this second study. These new data suggest that deaths in the WY-treated group in our initial study were due to a vitamin K deficiency. The role of increased serum estradiol, its effects on blood coagulation, and enhanced hepatic cell proliferation in the vitamin K-dependent coagulation processes warrant further investigation.
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PMID:Induction of coagulation effects by Wyeth-14,643 in Crl:CD BR rats. 918 58

The common bile duct-ligated (CBDL) rat, which is widely used as a model of human cirrhosis, rapidly develops secondary biliary cirrhosis (SBC) within 4 weeks. The CBDL rat shows poor viability, however, a detailed examination of the causes of its death has not been made. In this study, we investigated the outcome of bile duct ligation in detail and attempted to extend the life span of this model by feeding the animals a diet supplemented with nutrients. Survival rate, blood chemistry, blood cell counts, plasma levels of K vitamins and liver histology were compared among CBDL rats fed a standard diet and an enriched diet. Sham-operated rats were used as a control. Six out of 18 CBDL rats fed the standard diet died within 32 days of operation. The cause of death was massive internal hemorrhage in various organs or body cavities. All CBDL rats fed the enriched diet survived more than 31 days, but the viability of CBDL rats was not significant between those fed the standard diet and the enriched diet. The degree of anemia correlated significantly with the prolongation of prothrombin time. Plasma vitamin K1 levels in CBDL rats were significantly lower than those in sham-operated rats, but vitamin K2 levels were similar. We suggest that massive hemorrhage, which was the direct cause of death, is caused by the impairment of hemostasis resulting from vitamin K deficiency. The enriched diet with vitamin K nutritional supplements seemed to contribute to the prolongation of the life span of CBDL rats.
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PMID:Viability and plasma vitamin K levels in the common bile duct-ligated rats. 1589 25


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