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Biomedical subjects

C S Kitchens

Publications and source records attributed to C S Kitchens.

15 recordsLinked to original sources
PubMed1992

Evolution of our understanding of the pathophysiology of primary mesenteric venous thrombosis.

Mesenteric venous thrombosis is a rare insidious event that is difficult to diagnose. Approximately half the cases in the past were deemed "primary" or "idiopathic." These cases were also frequently associated with a previous history of thromboembolism and a family history positive for thromboembolism. Inherited hypercoagulable disorders, such as deficiency of protein C, protein S, or antithrombin III, will probably explain many "primary" cases. Prompt diagnosis, especially with modern imaging techniques, and prompt anticoagulant therapy decrease mortality.

Humans↗
PubMed1992

Changes in coagulation and anticoagulation in women taking low-dose triphasic oral contraceptives: a controlled comparative 12-month clinical trial.

OBJECTIVE: The effects of two triphasic oral contraceptives on coagulation and anticoagulation factors were compared in a 12-month open-label study. STUDY DESIGN: Fifty-two women (mean age 26 years) were enrolled in and completed the study; 20 had been randomly assigned to receive levonorgestrel plus ethinyl estradiol, 24 had been randomly assigned to receive norethindrone plus ethinyl estradiol, and eight surgically sterile women acted as untreated controls. Coagulation and anticoagulation factors were measured at baseline and during the sixth and twelfth months. RESULTS: Both oral contraceptives produced significant decreases from baseline in prothrombin time and partial thromboplastin time; there were also significant changes in laboratory control times. Factor XII was significantly increased in both oral contraceptive groups after 6 and 12 months. Fibrinogen antigen was significantly increased for norethindrone plus ethinyl estradiol after 6 and 12 months and for levonorgestrel plus ethinyl estradiol after 12 months. Platelet counts were unchanged. There was a significant increase in antithrombin III activity with norethindrone plus ethinyl estradiol at 12 months. Antithrombin III antigen was unchanged with the oral contraceptives; however, significant increases existed for alpha 1-antitrypsin antigen and plasminogen antigen and activity after 6 and 12 months and for alpha 2-macroglobulin antigen after 12 months for both oral contraceptives. alpha 2-Antiplasmin antigen was significantly increased for norethindrone plus ethinyl estradiol at the 12-month evaluation. There were no significant differences between the oral contraceptives for any coagulation or anticoagulation factor, and mean values generally remained within reference ranges. CONCLUSIONS: Levonorgestrel plus ethinyl estradiol and norethindrone plus ethinyl estradiol had equivalent, minimal effects on hemostasis, and changes in coagulation factors appeared to be balanced by changes in anticoagulation factors.

Adult↗
PubMed1992

Hemostatic aspects of envenomation by North American snakes.

1. North American poisonous snakes have a wide spectrum of complex venoms. 2. Venom, especially that of the rattlesnakes, may cause a variety of hemostatic abnormalities by directly, yet only partially, cleaving fibrinogen, activating the fibrinolytic system, or activating and clearing platelets through the action of proteolytic enzymes. 3. Because these venoms do not result in the generation of thrombin, the syndrome is distinct from true DIC. Bleeding or thrombosis is rare. 4. As thrombin generation remains intact, hemostasis is largely preserved despite dramatic changes in hemostatic tests. 5. Therapy with heparin, blood, or blood products is rarely indicated. 6. Therapy with antivenin in selected cases is logical and efficacious.

Animals↗
PubMed1992

Approach to the bleeding patient.

A broad, open, inquisitive, and semiskeptical mind must be used when approaching the bleeding patient. As in most endeavors in medicine, the history and physical examination provide an important baseline. Key laboratory tests must be quickly ordered and interpreted. Using this data base, one can quickly determine whether the hemorrhagic disorder is congenital or acquired, severe or mild, and progressive or stable. Hemostasis may fail owing to deficiencies of platelets, the plasma coagulation protein system, or endothelial disturbances. A precise diagnosis and appreciation of the tempo of the disorder will guide specific therapy.

Blood Coagulation Factors↗
PubMed1979

Factor XIII.

1. Activated factor XIII is the enzyme that covalently cross-links fibrin monomers into fibrin polymers and results in increased clot strength and resistance of the clot to fibrinolysis. 2. Small amounts (greater than 1% of normal) of factor XIII are necessary for normal in vitro and in vivo activity. 3. Factor XIII deficiency is a rare autosomal recessive illness in which a hemorrhagic diathesis is caused by the virtual absence of the active a subunit of factor XIII. Approximately 100 cases have been described. 4. The disease in homozygotes is characterized by umbilical stump bleeding, a high incidence of fetal wastage, delayed soft tissue hemorrhage, and a high incidence of intracranial bleeding. The heterozygote is asymptomatic. 5. This paper calls attention to the apparent high incidence of oligospermia and small testes seen in homozygote males. Otherwise secondary sex characterics are normal. 6. Because there is no abnormality in thrombin generation and conversion of fibrinogen to fibrin, route coagulation tests (prothrombin time, partial thromboplastin time, thrombin time, etc.) are normal. Platelet function tests are normal. 7. Clots made from recalcified plasma severely deficient in factor XIII are soluble in 5 M urea or 1% monochloroacetic acid. These screening tests are simple and nearly pathognomonic of the illness. 8. More sophisticated and quantitative tests (e.g., dansylcadaverine incorporation) are available for definitive diagnosis and heterozygote detection. 9. Replacement treatment of the illness is simple, effective, and relatively inexpensive. Due to the long half-life of infused factor XIII and the small amounts necessary for normal hemostasis, prophylaxis is feasible and encouraged.

Adult↗
PubMed1977

Clinical observations of human bone marrow macrophages.

Although human bone marrow is usually obtained to examine precursors of formed elements of blood, important diagnostic information can be gleaned from study of macrophages. These cells are usually unnoticed. Macrophages may be involved in a number of different pathophysiologic mechanisms which are pointed out in this clinical and pictorial study. Inherited enzymatic deficiencies usually result in "storage cells" as exemplified by Gaucher disease. Relative deficiencies may be acquired if phagocytic activity overcomes normal enzymatic mechanisms.

Adult↗
PubMed1977

Amelioration of endothelial abnormalities by prednisone in experimental thrombocytopenia in the rabbit.

Experimental thrombocytopenia results in endothelial alterations associated with bleeding. In this study prednisone was shown to prevent or reverse these changes, which supports the clinical inference that adrenocorticosteroids decrease capillary fragility in thrombocytopenia. Rabbits (3-4 kg), intraperitoneally injected with busulfan, developed 98-99% reductions in platelet count and hemorrhaged profusely. Orally administered prednisone (0.2 mg/kg or 1.0 mg/kg daily) reduced bleeding despite persistent thrombocytopenia. Tongue biopsies obtained after 3 days of prednisone treatment were examined by electron microscopy. Normal rabbits served as controls. 25 consecutive capillaries or venules from each of four animals in the control group and each of five experimental groups were examined for fenestrations, "thin spots" (<800 A thick), and mean wall thickness as determined by planimetry. Vessels from control animals had no thin spots or fenestrations, and the mean vessel wall thickness was 4,254+/-105 A SEM. The 100 vessels from the thrombocytopenic animals had a mean vessel wall thickness of 2,081+/-218 A (P < 0.001), and 42 had thin spots of fenestrations. After administration of the smaller dosage of prednisone, the mean vessel wall thickness increased to 3,556+/-40 A (P < 0.001), and only nine vessels had thin spots or fenestrations. With the larger dosage, only six vessels had thin spots or fenestrations and the mean vessel wall thickness of this group increased to 3,704+/-206 A (P < 0.005). All preparations demonstrated normal endothelial junctions. The data are consistent with the hypothesis that the bleeding of thrombocytopenia is caused by altered capillary and venule endothelium and that diminished bleeding observed with prednisone administration results from amelioration of these endothelial changes.

Animals↗
PubMed1977

Retropharyngeal hematoma in a hemophiliac.

A retropharyngeal hemorrhage, a rare but potentially fatal complication of hemophilia, is described. Its early manifestation may be a "sore throat", and the patient with this symptom must be closely observed. If there is any doubt about the clinical situation, or if hemorrhage in and around the throat occurs, appropriate replacement therapy with factor VIII should be started at once.

Adolescent↗
PubMed1976

Hemorrhagic diathesis in a carrier of hemophilia B.

A carrier of hemophilia B was found to have an unusually low factor IX level of 13 per cent. Her history of previous bleeding and the hospital course following elective dental extractions were consistent with a mild hemorrhagic diathesis. The patient is a member of a rare kindred of hemophiliacs. The mean level of factor IX in 12 carriers in this kindred was 42 per cent, with a range of 13 to 100 per cent. This patient represents the sixth reported case in which a female carrier of factor IX deficiency was symptomatic.

Adult↗
PubMed1976

Chronic painless hematuria and urethral bleeding as the presenting manifestations of Osler-Weber-Rendu disease.

A case of a young man with profound iron deficiency anemia, chronic painless hematuria and urethral bleeding is presented. He had the typical cutaneous findings of Osler-Weber-Rendu disease (hereditary hemorrhagic telangiectasia). Appropriate urological studies demonstrated bladder and urethral telangiectases, with no other explanation for the bleeding. Osler-Weber-Rendu disease should be considered in the differential diagnosis of chronic painless hematuria.

Adult↗
PubMed1976

Fatal Neisseria (Branhamella) catarrhalis pneumonia in an immunodeficient host.

A 64-year-old man with far-advanced IgA multiple myeloma presented with fulminant and rapidly fatal bronchopneumonia. Gram stains of expectorated sputum and of transtracheal aspirate revealed gram-negative intracellular and extracellular diplococci. Cultures of these specimens yielded Neisseria catarrhalis. Subsequent histologic examination of the lung confirmed the presence of numerous gram-negative diplococci in the alveolar spaces. The pathogenic potential of this nasopharyngeal commensal is discussed in both the normal and the immunosuppressed host.

Bacteriological Techniques↗
PubMed1976

Phenacetin-induced sulfhemoglobinemia: report of a case and review of the literature.

Phenacetin-induced sulfhemoglobinemia was diagnosed in a middle-aged woman with a 6-month history of cyanosis and a 10-year history of ingestion of analgesics. The laboratory and clincial diagnosis of sulfhemoglobinemia and methemoglobinemia are discussed. The reviewed medical literature suggests that the cyanosis of chronic phenacetin or acetanilid use is generally due to sulfhemoglobinemia rather than methemoglobinemia.

Adult↗
PubMed1975

Ultrastructural changes of endothelium associated with thrombocytopenia.

In a study of the relationship between thrombocytopenia and increased vascular fragility, changes in the endothelium of capillaries and postcapillary venules of the tongue were examined by electron microscopy. Adult male albino rabbits (4 kg) were maintained thrombocytopenic (platelets less than 20,000/cu mm) up to 24 hr by one to three injections of guinea pig antirabbit platelet serum. Within 6 hr the normal projections and folds of the lumenal surface of the endothelial surface were largely effaced. In addition, the endothelium became thinner. In places, pores and membranous diaphragms were observed. Endothelial junctions appeared normal. Identical findings were observed if rabbits were made thrombocytopenic by administration of intraperitoneal busulfan. Intravenously administered Thorotrast was observed in endothelial cells and in the extravascular spaces within 3 min after injection into thrombocytopenic animals, while it was seen only intravascularly in control rabbits. With the spontaneous restoration of circulating platelets, the endothelium reverted to normal.

Animals↗
PubMedDate not supplied

The syndrome of post-splenectomy fulminant sepsis. Case report and review of the literature.

Three years after splenectomy, a middle-aged woman had two separate episodes of fulminant bacterial sepsis. She recovered each time with prompt and appropriate treatment. Her immunologic system was examined and found to be normal with respect to antibody formation against diphtheria and tetanus toxoid, granulocyte killing of staphylococci and serum opsonizing activity. Granulocytes, bursa-equivalent (B) and thymus-dependent (T) lymphocytes and serum immunoglobulins were quantitatively normal. She produced antibody against subcutaneously injected polyvalent pneumococcal vaccine. She demonstrated cutaneous anergy. The literature on this syndrome was reviewed in an attempt to ascertain why hyposplenic patients are subject of fulminant bacterial, chiefly pneumococcal, sepsis. The probably explanation is the delayed production of antibodies against the phagocytic-resistant capsule of certain bacteria which the host had not previously encountered. The incidence of this syndrome appears to be on the order of 0.5 to 1.0%/year for splenectomized older children and adults. As the syndrome is seen chiefly in splenectomized or othewise hyposplenic patients, a causal relationship seems to exist.

Animals↗