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Biomedical subjects

J A Penner

Publications and source records attributed to J A Penner.

At least 37 records · Page 2Linked to original sources
PubMed1981

Management of abdominal hemophilic pseudotumor.

The abdominal hemophilic pseudotumor is a rare but frequently disabling and life-threatening complication in patients with severe hemophilia. Our patients were observed for a considerable period of time to document progressive enlargement of the pseudotumor and increasing disability from severe pain, nerve compression, or leg swelling. The decision to operate was made on the basis of incapacitating symptomatology or fear of impending rupture. Although the complications resulting from operation may be major, with the current availability of large amounts of factor VIII and activated prothrombin complex concentrate, excision of this lesion can be performed without concern for the hazard of uncontrollable hemorrhage. Late recurrence of the pseudotumor may necessitate further operative management.

Adult↗
PubMed1980

Hypercoagulation and thrombosis.

As knowledge of blood coagulation has advanced we have begun to examine not only the clinical entities associated with hemorrhage but also a group in which thrombosis represents the major problem. Thrombotic disorders believed to be associated with coagulation are recognized clinically but seldom investigated in the laboratory. The present approach to the problem is based on theoretical and experimental knowledge and a rapidly developing body of clinical information related to the role of platelets and antithrombin III in the initiation and control of thrombosis.

Arteries↗
PubMed1980

An improved clinical assay for antithrombin III (heparin cofactor).

A method for determining antithrombin-III heparin cofactor activity that requires no defibrinogenation of plasma, can be used with heparinized samples, and is specific for antithrombin-III heparin cofactor activity was developed. The procedure requires minimal pipetting, uses small amounts of sample over a single short incubation period, and is relatively inexpensive. The antithrombin-III assay appears to be superior to other commercially available procedures when employed in the diagnosis of deficiencies and in the identification of decreased levels of antithrombin III associated with liver disease and thrombotic disorders.

Antithrombin III↗
PubMed1980

Anti-inhibitor Coagulant Complex (Autoplex) for treatment of factor VIII inhibitors in hemophilia.

Fourteen individuals with severe hemophilia complicated by factor VIII inhibitors (1 to 132 Bethesda Units) were treated for 33 bleeding episodes with a new activated prothrombin complex concentrate, Anti-Inhibitor Coagulant Complex (Autoplex, Hyland, Glendale, Calif.). Excellent or good results were observed in 21 of 25 minor bleeding episodes treated, which included joint, soft tissue, and mucous membrane hemorrhages. Eight major bleeding problems (an epidural bleed, a puncture wound, 2 serious soft tissue hemorrhages, 2 lacerations, and 2 major surgical procedures) were treated with excellent (6) or good (2) results. No serious complications were encountered, but two children developed transient hypofibrinogenemia following Autoplex infusion. Although some shortening of the prothrombin time and activated partial thromboplastin time was noted after infusion of Autoplex, there is no useful laboratory test for monitoring therapy. Despite the unknown mechanism of action for bypassing factor VIII, Autoplex appears to be a useful and needed interim product and is safe and effective. In view of the possible potentiation of thrombosis concurrent use of fibrinolytic inhibitors should be avoided.

Adolescent↗
PubMed1980

Effect of complement on collagen-induced platelet aggregation.

Evidence that early members of the classic pathway of complement are involved in the interaction of collagen with the blood platelet is presented. C4 is required for platelet aggregation response to low concentrations of fibrous collagen but not for adhesion of collagen to platelets obtained from guinea pigs genetically lacking C4. The aggregation response is restored, however, by preincubation with either C4 or normal plasma. It is suggested that membrane-bound C1s is the receptor site for collagen, inasmuch as preincubation of normal platelets with antiserum to C1q specifically enhances the platelet-collagen interaction, demonstrating a potential competition between C1q and collagen for the platelet binding site. This concept is further supported by the fact that C1s inhibitors also enhance aggregation response to collagen. Under physiologic conditions, the role of complement in the platelet response to collagen should be highly significant.

Animals↗
PubMed1979

Gold-induced thrombocytopenia responsive to cyclophosphamide.

Thrombocytopenia and nephrotic syndrome developed in a 51-year-old patient receiving gold therapy for rheumatoid arthritis. Marrrow findings and platelet infusion studies were consistent with a pattern of increased platelet destruction, known to occur in gold-induced thrombocytopenia. Improvement in the platelet count after therapy with dimercaprol was transient, and although steroids and splenectomy were not effective, a response was achieved with cyclophosphamide. The use of immunosuppressive drugs can be considered in refractory cases of gold-induced thrombocytopenia in which a significant hemorrhagic risk is present.

Aurothioglucose↗
PubMed1979

Endotoxin-induced intravascular coagulation (DIC) and its therapy.

Anticoagulants in the form of heparin, dipyridimole, steroids, prostaglandin E1, Macrodex, and antithrombin III were administered in separate experiments prior to endotoxin infusion in the dog. The pattern of disseminated intravascular coagulation (DIC) developed consistently when endotoxin alone was administered. Heparin dosages from 1 to 10 mg/kg did not influence the appearance of thrombocytopenia but effectively eliminated the decrease in fibrinogen levels ordinarily found. Antithrombin III (AT III), obtained from the National Red Cross, administered in a dose designed to provide a doubling of the circulating AT III, reduced the fibrinogen utilization to a similar degree as heparin without affecting the platelet loss. Dipyridimole, as administered, was ineffective in this model, and did not alter the development of thrombocytopenia or the hypofibrinogenemia. Steroids, Macrodex, and prostaglandin E1 had minimal effect on the coagulopathy. Our finding would suggest that the endotoxin effect on dog platelets id direct, and not mediated by thrombin, and that the role of heparin in the clinical management of DIC should be considered only in instances in which renal complications exist.

Animals↗
PubMed1977

The effect of propranolol on hemolysis in patients with an aortic prosthetic valve.

Propranolol was given to five patients with severe hemolytic anemia from arotic prostheses. Red cell survival, lactic dehydrogenase, serum hemoglobin, and 24 hour urine iron values were used to evaluate the severity of hemolysis with and without propranolol treatment. Three patients had a clear decrease in the level of hemolysis with propranolol therapy. One patient developed congestive failure after 6 months on propranolol. The decrease in hemolysis is most likely related to a slower heart rate.

Anemia, Hemolytic↗
PubMed1977

Fatal colitis in a hemophilic patient with inhibitor.

A severe colitis developed in a hemophilic patient following an antibiotic regimen which included clindamycin. A surgical procedure, total hip replacement, had been complicated by the appearance of a powerful factor VIII inhibitor and a Bacteroides fragilis infection. The resulting bleeding diathesis was successfully managed with the use of an "activated prothrombin complex"; however, the occurrence of colitis following intravenous clindamycin therapy proved to be fatal. Clindamycin, like the related antibiotic lincomycin, appears to have significant intestinal toxicity and should be restricted to the treatment of life-threatening proven Bacteroides infections.

Adult↗