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PubMed1978

[Pathomorphology of radiation sickness in sheep following whole body roentgen irradiation].

Whole-body X-ray treatment was experimentally applied (380 median-line dosage) to eight Merino mutton sheep aged approximately one year. Five of the test animals were lost between 16 and 25 days after irradiation. A great diversity of pathomorphological changes was recorded from organs and tissues, and the most important pathological processes which occurred concomitantly with acute to subacute radiation syndrome of sheep were defective haematopoiesis, septico-toxic processes, haemorrhagic diathesis, and partial epilation. Severe damage to the organs involved in haematopoiesis was one of the primary pathological processes and reflected mainly in lymphopenia, agranulocytosis, and thrombocytopenia, in other words, with lymphopoieses, granulopoiesis, and thrombocytopoiesis particularly involved. Insufficiency of cellular (and humoral) defence would obviously cause germ flooding of the organism, starting from the intestine, and eventually lead to septic intoxication. Haemorrhagic diathesis was found to occur only short of death and is thought to result from thrombocytopenia due to damage to thrombopoiesis as well as from septico-toxic effects upon the blood coagulation and partitioning vascular system. Loss of wool (epilation) was recordable only from neck and shoulder regions, and even there it was on the decline.

Alopecia↗
PubMed1978

[Pathomorphology and pathogenesis of radiation sickness in calves and young cattle following whole body roentgen irradiation].

Here are the most important pathomorphological findings recorded from 14 calves or heads of young cattle following whole-body X-ray treatment (170 R and u50 R median-line dosage): 1. Damage was caused to the haematopoietic system, with the most severe effects on granulopoiesis, thrombocytopoiesis, and lymphopoiesis, but less conspicuous lesion of erythropoiesis. 2. Haemorrhagic diathesis developed together with pneumonia in 86 per cent of all cases, manifested in most of them as severe fibrinous pneumonia and pleuropneumonia (in 75 per cent of the cases) and progressing pericarditis. 3. Liver degeneration occurred to all animals, usually in the form of centrobular liver cell necrobiosis (86 per cent), with most of the cases accompanied by diffuse degenerative hepatoparenchymal damage (80 per cent) as well as by granular degeneration of the myocardium and acute fubulonephrosis, the latter two processes obviously developing only short time before death. 4. Catarrhal as well as fibrinous and circumscribed diphtheroid enteritis developed in 43 per cent of all animals, those which had received a median-line dosage of 170 R. 5. Deficiency in supply was recorded, too, with severe damage to the haematopoietic organs being in the focus of the pathological process. That damage actually was the cause of the haematologically established granulocytopenia or agranulocytosis, thrombocytopenia, and lymphopenia. That was the background against which radiation syndrome of calf could be accompanied by activation of latent or subclinical infection of respiratory organs and the development of severe pneumonia as well as by changes in the intestinal flora leading to the outbreak of enteritis. The collapse of cellular defence mechanisms obviously caused intestinal induction of resorption of bacterial toxins and decomposed tissue products, with the pneumonia-damaged lungs being involved. The results eventually were intoxication with haemodynamic disorders, increase in vascular permeability, and degenerative damage to the parenchyma. Haemorrhagic diathesis was the result of thrombocytopenia and, possibly, endotoxic or toxic damage to the coagulation and blood vessel system. Further pathogenetic aspects relating to the radiation syndrome in calf and young cattle are discussed.

Age Factors↗
PubMed1980

Conservative management of the Zollinger-Ellison syndrome. Ectopic gastrin production by an ovarian cystadenoma.

Techniques for evaluating ectopic gastrin production associated with the Zollinger-Ellison syndrome are described. The site of gastrin production in this example was a mucinous cystadenoma of the ovary confirmed by immunoperoxidase localization of gastrin within the ovarian tumor cells and by radioimmunoassay of the tumor's gastrin content. These methods, localizing the source of ectopic gastrin, permitted conservative management of the ulcer diathesis with surgical resection of the mucinous cystadenoma. After oophorectomy the patient's serum gastrin level returned to normal, and the ulcer diathesis ceased.

Cystadenoma↗
PubMed1980

Exchange transfusion for sickle cell intrahepatic cholestasis.

Only one of eight previously described patients with sickle cell intrahepatic cholestasis (SCIH) survived. Death usually resulted from liver failure and/or a hemorrhagic diathesis. This report deals with the successful treatment of SCIH by partial blood-plasma exchange transfusion. This treatment led to regression of hepatic encephalopathy, impending bleeding diathesis, and noticeable clinical improvement withn 48 hours. Within six days, the serum bilirubin level decreased from 146 to 16 mg/dL. Partial blood-plasma exchange transfusion may be valuable for the treatment of SCIH.

Adult↗
PubMed1994

[Congenital blood coagulation factor X deficiency. Successful result of the use prothrombin concentrated complex in the control of ++cesarean section hemorrhage in 2 pregnancies].

There is little experience in the prevention of the severe hemorrhagic diathesis of factor X coagulation factor deficiency, before surgical procedures. A female with congenital deficiency of factor X that received prothrombin complex concentrates that contained 1.000 IU of factor X (16.7 U/l Kg BW) immediately prior to a cesarean section in two occasions, is reported. Factor X concentration rose from 1 to 25% in the first occasion and from 10 to 63% in the second. In both episodes, factor X decreased in the first 24 h of the postoperative period and required new infusions of prothrombin complex concentrates. No episodes of abnormal bleeding were observed. It is concluded that the infusion of prothrombin complex concentrates prevents the hemorrhagic diathesis of factor X deficiency, despite its modest increase in plasma. A initial infusion of 1.000 UI of factor X (16-20 IU/Kg BW), followed by 500 IU (8-10 IU/Kg) every 24 hours is suggested for an adequate management of this condition.

Adult↗
PubMed1995

[The hemorrhagic form of acute bovine virus diarrhea: literature review and case report].

Infection of cattle with certain strains of BVD-virus causes a severe thrombocytopenia. The most obvious clinical and pathological lesions are multiple hemorrhages. Until now, problems with the Hemorrhagic syndrome have been reported predominantly from veal calf operations in the U.S.A. This publication presents first a literature review about the Hemorrhagic syndrome. The current data are based upon retrospective studies of field cases and experimental infections. Afterwards clinical, pathological and virological findings from three herds of veal calves in Germany are reported in which hemorrhagic diathesis was observed in calves and BVD-virus was isolated from tissues of diseased calves. The findings in these herds closely resemble the ones described in the literature for the Hemorrhagic syndrome. Therefore, infection with BVD-virus should be considered as differential diagnoses in Germany too, when hemorrhagic diathesis is observed in cattle.

Animals↗
PubMed1995

[Dupuytren contracture--current status in research and clinical practice].

Dupuytren's contracture is a disease of the connective tissue, especially of the palmar side of the hand. Today, by means of electron microscopy and histochemistry, several alternations specific of pathology of the disease can be shown, providing a better understanding. However, a revolutionary change of treatment is far out of reach. Dupuytren's diathesis can be influenced by none of today's known methods, and therapy is still empirical. Operative therapy is only indicated in functional impairment. Treatment should be done by well-trained surgeons and in case of extensive diathesis by carefully planning and longtime follow-up to avoid complications and eruption of the disease.

Dupuytren Contracture↗
PubMed1994

[Retinoid receptors and hematologic diseases].

Acute promyelocytic leukemia is a rare disease combining a specific cell type, a bleeding diathesis and a translocation t(15;17). All trans retinoic acid is able to induce a maturation of malignant cells, up to terminal differentiation. After 2 months of treatment a complete remission is obtained without any aplastic anemia. The bleeding diathesis rapidly disappears. However relapses occur within few months due to the catabolism of retinoic acid induced by the treatment itself. A chemotherapy is generally proposed, in order to consolidate the complete remission. The combination of retinoic acid and chemotherapy has dramatically increased the probability of long term survival. The breakpoint of the translocation t(15;17) is located inside the retinoic acid receptor gene on chromosome 17. A new product is made, due to the fusion of the truncated retinoic acid receptor and a gene on chromosome 15. The hybrid product blocks the program normally performed by the retinoic acid receptor and consequently blocks the maturation of the granulocytes. Why pharmacological doses restore the impaired program is still an enigma.

Humans↗
PubMed1993

[Disseminated intravascular coagulation--pathophysiology].

The main cause of DIC (disseminated intravascular syndrome) is contact of tissue factor with circulating blood. The main symptoms of DIC are bleeding diathesis caused by consumption coagulopathy and organ dysfunction related to circulatory disturbances due to multiple thrombi. However, the symptoms of DIC differ according to degree of fibrinolysis which is characterized by causal disease of DIC. Usually, enhanced fibrinolysis does not cause organ failure but hemorrhagic diathesis, while impaired fibrinolysis does not cause severe bleeding but organ dysfunction. In almost all cases of acute leukemia and in some cases of solid cancer with DIC, hyperfibrinolysis is common. In cases of severe infection with DIC, impaired fibrinolysis due to abnormal elevation of plasminogen activator inhibitor-1 is frequently seen.

Disseminated Intravascular Coagulation↗
PubMed1993

[Progress in diagnosis of disseminated intravascular coagulation (DIC)--diagnostic criteria of DIC].

DIC is an acquired disorder in which intravascular coagulation may lead to microvascular fibrin formation and a hemorrhagic diathesis. If DIC is acute and severe, fibrin formation may lead to microvascular thrombosis, and consumption of coagulation factors and platelets may result in a hemorrhagic diathesis. Secondary to or simultaneously with coagulation, the fibrinolytic system may be activated, accentuating the bleeding tendency. All the systems involved in DIC, such as coagulation, fibrinolysis, kallikrein-kinin, complement, and possibly other systems are regulated. Coagulation is the central event of DIC. The different coagulation factor derivatives may be generated that can be determined and used as markers for the degree of DIC and for effective control of therapy. Some of the procoagulant and anticoagulant factors are converted in the course of coagulation to their active forms and activation peptides. The active factor is subsequently neutralized by forming a complex with an inhibitor. Hemostatic molecular markers, D-dimer of cross-linked fibrin degradation products (D-dimer), thrombin-antithrombin III complex (TAT), and plasmin-alpha 2-plasmin inhibitor complex (PIC) have all been used for the diagnosis of DIC.

Antifibrinolytic Agents↗
PubMed1993

Helicobacter pylori infection and duodenal ulcer disease.

H. pylori is undoubtedly the dominant factor in the multifactorial peptic ulcer diathesis. We should not ignore the other contributing factors but rather try to identify how they interact with the organism and initiate the ulcerative process. The interplay of acid attack and mucosal defence is modulated by genetics, gender, blood group, smoking, age, and various physiologic considerations, which include acid output. These and other considerations probably explain the discrepancy between the high frequency of H. pylori infection in the population and the comparatively small proportion of individuals who develop a DU. Most agents used in DU are aimed at reducing acid secretion and achieve healing by minimizing acid attack. Such treatments, however, have no effect on H. pylori status and do not remedy the underlying gastroduodenitis. The mucosa therefore remains ill and vulnerable. After cessation of acid suppressive therapy, ulcer relapse is likely. Goodwin has likened the inflamed mucosa to a leaking roof, in which temporary dryness (healing) is assured if the rain (acid) is removed but permanent protection can be achieved only by mending the roof through healing of the mucosa. Therefore, therapy that fails to address the role of H. pylori in the causation of the mucosal inflammation, which predisposes to ulceration, is likely to confer only short-term benefit. Eradication of the infection has been shown beyond doubt to markedly alter the natural history of the disease, a number of series showing no recurrence at the end of 1 year, compared with a natural recurrence of > 70%. The economic savings after not only eradication but even suppression of H. pylori in DU disease have been estimated to be enormous. Despite these striking findings indicating H. pylori inflammation as the dominant factor in the DU diathesis and the possibilities of cure after H. pylori eradication, a large proportion of the medical community is still not willing to accept the consequences. There are presumably several reasons for this skeptical attitude. First, it takes time before physicians are willing to accept such drastic changes in their conventional way of thinking about DU disease, because it has been stressed during decades that DU disease is dominated by excessive acid as the main culprit. Second, current acid-suppressive therapy is highly efficacious in healing DU and in keeping those ulcers healed with maintenance therapy. These drugs are well tolerated and have a low side effect profile.(ABSTRACT TRUNCATED AT 400 WORDS)

Drug Therapy, Combination↗
PubMedDate not supplied

Haemostatical and rheological aspects of dysfibrinogenemia.

Congenital dysfibrinogenemia is based on different alterations in the structure of the fibrinogen molecule leading to a variety of disturbances in the clotting process. Clinical manifestations of the disorder are showing a wide range from asymptomatic states to mild bleeding diathesis as well as thrombotic complications. In this study two of the 14 patients with dysfibrinogenemia showed a history of mild bleeding while the others showed no clinical symptoms. As fibrinogen is also an important factor of the blood fluidity not only haemostatic but also rheological parameters were measured. Included in the study were 14 patients with ascertained dysfibrinogenemia in comparison to 11 non-affected relatives and a control group of 297 apparently healthy subjects. Plasma viscosity (p < 0.0001) and erythrocyte aggregation index (p < 0.00001) were significantly higher in the patients than in their healthy relatives and the control group. A pathologically increased erythrocyte aggregation was found in 10 of the 14 patients but only in 1 of the 10 relatives. The dysfunction of the fibrinogen molecule thus influences the aggregation process of the red blood cells to a greater extent than normal fibrinogen. Moreover, there seems to be a stronger influence of the dysfunctional fibrinogen molecule on the aggregation process than on plasma viscosity. To date the question if the enhanced erythrocyte aggregation in dysfibrinogenemic patients may be of any diagnostic interest and if there are significant differences between patients with bleeding diathesis and thrombophilia cannot be answered and remains to be cleared in further investigations.

Analysis of Variance↗
PubMed1997

[Genetically engineered mice for study of human hypertension].

Human essential hypertension is generally recognized as a multifactorial disease based on genetic diathesis. Despite the usefulness of SHR and Dahl rats as laboratory tools, the genetic diathesis including the development of hypertension in these rats remains unclear. Rapid advances in embryonic engineering and molecular biological techniques may make it possible to develop transgenic mice and gene-targeted mice and open new avenues for the molecular investigation of human disease. This report introduces genetically engineered mice with hypertension and hypotension.

Animals↗
PubMed1997

[Acquired haemophilia A].

A 74-year-old man developed a severe bleeding disorder on the basis of acquired Factor VIII (F VIII) inhibitor. Coagulation assays showed a prolonged activated partial thromboplastin time (APTT) with a normal prothrombin time (PT);F VIII level was 0.07 IU and F VIII inhibitor level 8.8 Bethesda units (BU). At least half the cases of acquired haemophilia A are associated with pregnancy, the postpartum period or an underlying malignancy or autoimmune disease. Haemorrhagic diathesis can be severe and life-threatening. Treatment of acute haemorrhages consists of human or porcine factor VIII concentrate, activated prothrombin complex concentrate (FEIBA) or recombinant factor VIIa, depending on the antibody titre. Immunosuppressive therapy is successful in at least 60% of the patients in making the inhibitor disappear. In patients with a spontaneous haemorrhagic diathesis, a thorough medical history should be taken, coagulation assays should be performed and a specialist should be consulted.

Aged↗
PubMed1998

Natural history of severe duodenal ulcer disease.

BACKGROUND: A subset of patients with chronic duodenal ulcer has severe ulcer diathesis in the form of frequent relapses and complications like perforation and hemorrhage. We observed the effect of drug treatment on the natural history of this subset. METHODS: Of 526 patients diagnosed to have chronic duodenal ulcer by endoscopy, 23 patients with severe diathesis were available for long follow-up (mean period 36 months). Each patient was assessed clinically and endoscopically every 2 months for at least 12 months and then every 3 months or when symptomatic. Helicobacter pylori status was assessed during endoscopy. The effect of antisecretory drugs and anti-H. pylori therapy on natural history was determined. RESULTS: Thirteen of 23 patients (56%) had refractory ulcers; six responded to double dose of H2-receptor antagonists (H2RA) for 8 weeks and six to omeprazole 40 mg daily for 4-8 weeks. Of 20 patients (87%) who were H. pylori-positive, 15 completed triple-drug therapy; of these, 10 patients eradicated H. pylori. These 10 patients were followed up for 24 months; there were no ulcer relapses within the first 12 months but 8 of them relapsed between 12 and 24 months (total number of relapses 8). Reinfection with H. pylori occurred in 3 patients. In the other 10 patients who remained H. pylori-positive, there were 19 episodes of ulcer relapse in 7 patients over 24 months, in spite of maintenance therapy with H2RA (p < 0.05). CONCLUSIONS: Refractoriness in patients with severe ulcer disease is usually episodic and amenable to larger doses of omeprazole or H2RA. Anti-H. pylori therapy improves the natural history but its effect in preventing ulcer relapse is short lasting (less than 12 months). Recurrence of infection is a problem in our population.

Adult↗
PubMed1976

Ultrastructural changes in skeletal muscle of selenium-vitamin E-deficient chicks.

Chicks fed a semisynthetic basal diet deficient in selenium and vitamin E for 14 to 22 days developed skeletal myodegeneration and exudative diathesis. Chicks fed the basal diet supplemented with either 0.2 ppm of selenium (as selenite) or 100 IU alpha-tocopherol acetate/kg were protected from deficiency disease, but chicks fed the basal diet plus 0.4% L-cystine were not protected. Pectoral muscles of deficient chicks were red and edematous. Light and electron microscopic study of affected muscles revealed fibers with hyaline and granular degeneration. In hyalinized fibers, the initial ultrastructural alterations were increased density of the sarcoplasm and myofibrils, dilatation of sarcoplasmic reticulum, formation of subsarcolemmal vacuoles, and disruption of mitochondrial membranes. In later stages, alterations in these fibers included myofibrillar disruption and lysis, nuclear pyknosis and lysis, disruption of the plasma membrane with persistence of basal lamina and scattered adhering satellite cells, and eventual invasion by macrophages. In fibers with granular degeneration, the ultrastructural observations included decreased density of the sarcoplasm, prominent mitochondrial swelling and distortion, and multiple foci of myofibrillar lysis that eventually coalesced to produce generalized lysis. Prominent vascular lesions associated with exudative diathesis were present in degenerated muscle but were not considered to precede development of fiber alterations. Affected blood vessels had endothelial cells with mitochondrial damage and accumulations of cytoplasmic dense bodies and areas of endothelial disruption with adhering fibrin thrombi.

Animals↗
PubMed1997

[Factor VIII inhibitor appearing in women during delivery].

Factor VIII inhibitor is rare, but very serious postpartum complication. Bleeding diathesis caused by this inhibitor is called acquired haemophilia. Three women with postpartum inhibitor to factor VIII and life threatening bleeding were described. In two patients bleeding was controlled by treatment with high doses of human and porcine factor VIII concentrates. One patient died presenting uncontrolled haemorrhagic diathesis. This work presents the problems of the diagnosis, treatment and also the elimination of the factor VIII inhibitor.

Adult↗
PubMed1998

[Selected parameters of blood platelet function in patients with myeloproliferative syndrome].

Symptoms of hemorrhagic diathesis and/or thrombotic complications are observed in patients with myeloproliferative syndrome (m-p.s.). It is emphasized that there is a meaningful direct and indirect share of blood platelets in the mentioned disturbances of hemostasis. Therefore in own investigations an attempt was made to evaluate the morphology and function of blood platelets in patients with various forms of m-p.s., as well as to find an answer to the question: do any differences in morphology and function (activation) of blood platelets appear in patients with m-p.s.?, and is activation of blood platelets always accompanied by the symptom of hemorrhagic diathesis or past thrombotic episodes (the second ones evidenced in the patients anamneses)?, do the blood platelets in idiopathic thrombocytopenia (one of the forms of m-p.s.), differ morphologically and functionally from platelets in other forms of m-p.s. The investigation comprised 45 patients, in whom m-p.s. was diagnosed at Department of Hematology PAM (28 women, 17 men) aged from 36 to 82 years (mean age 58.10 + 10.61). The diagnosis of m-p.s. in each patient was established on the basis of clinical picture and laboratory examinations (blood morphology, hematocrit, FAG score, histopathological examination of bone marrow). In patients the accomplished determination concerned blood platelets count, mean blood platelet volume, platelocrit, volume range of blood platelets, coagulation time by Duke's method. The function of platelets was estimated with the help of the following studies: aggregation of blood platelets under the influence of ADP according to Born's method, concentration of beta-thromboglobulin (beta-TG) and platelet factor--4 (PF-4) in plasma by ELISA method. In order to pay due consideration to the effect of blood platelets count exerted on the concentration of beta-TG and PF-4, a supplementary parameter was introduced, the so-called beta-TG and PF-4 standardized. That allowed for studying the platelets in all patients under the same conditions. The results of own investigations have shown that most of the patients with m-p.s. had disturbances involving the morphology of blood platelets (Tab. 2) and increased activity of platelets, being expressed by a rise in concentrations of beta-TG and PF-4 in plasma (Fig. 1, 2) and by abnormal aggregation of platelets due to ADP influence. Moreover, the determination of beta-TG and PF-4 concentration in plasma in thrombocytopenia states, particularly in patients with idiopathic thrombocytopenia ought to be performed after the standardization of platelets count, the finding being also supported by the results of own investigations (Tab. 3). There may be compliance with the viewpoint expressed in the literature that the results of studying the morphological parameters of blood platelets and their function (activation) in m-p.s. are not a prognostic factor for the appearance of thrombotic complications and/or hemorrhages.

Adult↗