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Biomedical subjects

M Karpatkin

Publications and source records attributed to M Karpatkin.

At least 37 records · Page 2Linked to original sources
PubMed1986

Low protein C in the neonatal period.

Protein C was measured by electroimmunoassay in 47 infants within 24 h of delivery. Gestational age ranged from 28 to 43 weeks. The mean level was 27% (range less than 10-67%) of the normal adult mean. In the 22 infants who had no clinical problems, protein C levels correlated significantly with gestational age. In the 25 who were sick there was no correlation, and the mean level was significantly lower than that of the healthy infants. Postnatal rise was slow; on day 7 the mean was 32% and on day 28, 31%. Levels of protein C correlated significantly with prothrombin in both the healthy and sick infants. Crossed immunoelectrophoresis in the presence of calcium ions gave one protein C peak of the same electrophoretic mobility as is seen in plasma of healthy adults, indicating that the infants' protein C is gamma carboxylated. It is concluded that: (1) Protein C in neonates is in or below the range associated with thromboembolism in patients congenitally deficient in this protein; (2) protein C levels correlate with gestational age; and (3) the low levels during the neonatal period are not due to decreased gamma carboxylation but may reflect decreased synthesis when compared to the older child or the adult.

Gestational Age↗
PubMed1984

Studies of the origin of platelet-associated fibrinogen.

Platelet membranes and whole platelet preparations were examined by crossed immunoelectrophoresis in normal individuals, in a patient with congenital afibrinogenemia, and in two unrelated patients with Glanzmann's thrombasthenia (types I and II) to study the origin of platelet-associated fibrinogen. Results indicate: (1) platelet and plasma fibrinogen are probably derived from the same gene product, (2) platelet fibrinogen is not derived from the surrounding plasma milieu, (3) under basal conditions, platelet fibrinogen is located only within the alpha-granules and not on the platelet surface, (4) addition of trypsin to fibrinogen uncovers either a neoantigen or a hidden pool of platelet fibrinogen in the alpha-granules, (5) platelets from two patients with Glanzmann's thrombasthenia contain near-normal quantities of fibrinogen.

Afibrinogenemia↗
PubMed1983

Effect of coumadin-induced coagulopoietin plasma on vitamin K-dependent carboxylation of liver microsomes.

Coumadin-treated rabbits have a humoral substance(s) (coagulopoietin) which is capable of elevating vitamin K-dependent coagulation factors when injected into recipient rabbits (Karpatkin & Karpatkin, 1973). Biologic levels of coagulation factors II, V, VII and X; immunologic levels of factors II and X; and vitamin K-dependent liver microsomal carboxylase activity were measured in recipient rabbits receiving coumadin-induced coagulopoietin plasma. Factor II biologic activity increased 3.5-fold compared to the increase in immunologic activity. Factor X biologic activity increased 1.7-fold compared to the increase in immunologic activity. This indicates an increase in specific activity of factors II and X. Coumadin-induced coagulopoietin plasma had no effect on vitamin K-dependent liver microsomal carboxylase activity in vitro. However, livers obtained from recipient animals treated with coumadin-induced coagulopoietin plasma enhanced their carboxylase activity (compared to control animals) 2.4-fold employing endogenous microsomal precursor for carboxylation, and 6.2-fold employing synthetic substrate, phe-leu-glu-glu-val. Thus, coumadin-induced coagulopoietin plasma enhances the biologic activity of vitamin K-dependent coagulation factors II, VII, and X as well as the ex vivo vitamin K-dependent carboxylase activity of liver microsomes.

Animals↗
PubMed1983

Plasma protease inhibitors in premature infants: influence of gestational age, postnatal age, and health status.

In newborn infants, the influence of gestational age (GA), postnatal age (PA), and health status on the plasma protease inhibitors alpha 2-macroglobulin (alpha 2-M), alpha 1-antitrypsin (alpha 1-AT), C1 esterase inhibitor (C1E-INH), alpha 2-antiplasmin (alpha 2-AP), and antithrombin III (AT-III) was investigated. Inhibitor levels were measured by radial-immunodiffusion and expressed as a percentage of pooled plasma from adults (mean +/- SEM). In total, 54 premature infants (28-36 weeks gestation) were classified at birth as healthy (N = 22) (IV fluids, antibiotics only) or sick (N = 32) (all other support, but excluding infants with disseminated intravascular coagulation (DIC] and studied on Days 1 and/or 7 of life. Healthy term infants (N = 18) and infants with DIC (N = 10) were studied on Day 1 only. All inhibitors except C1E-INH increased with increasing gestational age (P less than 0.01). In healthy premature infants all inhibitor levels reached the normal adult range by 1 week of age. In contrast, at 1 week of age, sick infants had lower levels of alpha 2-M and alpha 2-AP, and higher levels of alpha 1-AT compared to healthy infants (P less than 0.01). The presence of DIC depressed all of the inhibitors on Day 1 except alpha 1-AT when compared to healthy controls (P less than 0.01). Thus, gestational age, postnatal age, and health status all significantly influenced the levels of these plasma protease inhibitors.

Antithrombin III↗
PubMed1983

Demonstration of kallikrein-like protease activity in nonactivated plasma of patients with Cooley's anemia.

Routine evaluation of 12 children with Cooley's anemia revealed that each one had a prolonged partial thromboplastin time. However, prothrombin time and thrombin time were within the normal range. Specific assays demonstrated low levels of the four contact factors: factors XI, XII, prekallikrein, and high molecular weight kininogen. Further investigation revealed activity against para-nitroanilide peptide substrates in unactivated plasma from all 12 patients. Following gel filtration on Sephadex G200, the activity emerged in one peak in the void volume, indicating a molecular weight of greater the 500,000. Activity was greatest against H-D-Pro-Phe-Arg-pNA, the substrate for plasma kallikrein, and was inhibited by diisopropyl fluorophosphate and trasolyl. It was unaffected by hirudin, soy bean trypsin inhibitor, and lima bean trypsin inhibitor. It was destroyed by heating at 56 degrees C. Specific antisera against human prekallikrein and human alpha-macroglobulin did not reduce the activity. It is concluded that a high molecular weight kallikrein-like protease, is present in the plasma of these patients. It is postulated that it is released into the circulation from tissue as a result of damage due to iron overload. It is further postulated that this protease brings about in vivo activation of the contrast factors, resulting in a fall in their circulating levels.

Adolescent↗
PubMed1981

Chelation therapy in beta-thalassemia major. III. The role of splenectomy in achieving iron balance.

Transfusion requirements for 1978 were compiled for 79 patients with thalassemia major (ages 1 to 29 years) who were maintained at hemoglobin concentrations of greater than 10 gm/dl. In 46 patients with intact spleens, the mean transfusion requirement was 258 ml/kg/year, and there was a clear increase with age. The transfusion history prior to 1978 had no influence on the increase of transfusion requirement with age. In contrast, in 33 splenectomized patients, the mean transfusion requirement was 203 ml/kg/year and it did not increase with age. Urinary iron excretion in response to deferoxamine increased with age, with no obvious difference between splenectomized and nonsplenectomized patients. The ability to achieve iron balance with a daily dose of 20 mg/kg of deferoxamine was a function of the transfusion requirement splenectomized patients with lower blood requirements generally achieved negative iron balance, whereas nonsplenectomized patients did not. We conclude that the spleen should be removed when the transfusion requirement exceeds 250 ml/kg/year, which usually occurs between 6 and 8 years of age. In young patients with intact spleens, a higher dose of deferoxamine may be use in order to prevent hemosiderosis.

Adolescent↗
PubMed1981

Immune thrombocytopenia in children.

Idiopathic thrombocytopenic purpura in the adult has a clearly established autoimmune etiology; IgG antiplatelet antibody is demonstrable on the patient's platelets and is frequently present in the serum. Platelet IgG is correlated inversely with the platelet count. In the acute childhood form of the disease, serum antibody is usually absent but increased IgG is present on the platelets, thus suggesting the immune nature of the childhood disease. The spleen acts as a significant source of antiplatelet antibody as well as the major reticulo-endothelial site for destruction of antibody-coated platelets. The majority of children with idiopathic (autoimmune) thrombocytopenia recover completely and have normal platelet counts within 6 months of diagnosis. Some patients recover after a longer period of time. Ten to 15 percent have a chronic form of the disease which is indistinguishable from the adult disease; splenectomy benefits approximately 70% of these patients.

Adrenal Cortex Hormones↗
PubMed1981

CT in B-thalassemia: iron deposition in the liver, spleen, and lymph nodes.

The authors report the striking increase in lymph node density due to hemochromatosis observed with computed tomography (CT) in nine patients with Cooley anemia treated with multiple blood transfusions. The CT appearance and pathologic findings of hemochromatosis of the liver and spleen in three of these patients were also observed and correlated with pathologic specimens. CT density of the liver seemed to relate to the degree of hepatic fibrosis or cirrhosis, rather than the amount of iron. Previous reports have not emphasized dense ferritinized lymph nodes in treated Cooley anemia patients.

Adolescent↗
PubMed1980

Thrombocytopenia in the high-risk infant.

One-hundred twenty-nine high-risk infants with thrombocytopenia and 238 control infants without thrombocytopenia were evaluated. Mothers of thrombocytopenic babies had similar history to those of nonthrombocytopenic babies, although fewer chronic narcotic abusers were found among mothers of thrombocytopenic babies. Thrombocytopenia was more common in babies less than 37 weeks' gestation and in sick babies compared to healthy babies. Sixty percent of infants had no recognizable cause of thrombocytopenia. Features associated with thrombocytopenia included umbilical line placement, respiratory assistance, hyperbilirubinemia, phototherapy, prematurity, respiratory distress syndrome, low Apgar score, sepsis, meconium aspiration, and necrotizing entercolitis. Thrombocytopenic babies had Apgar score, sepsis, meconium aspiration, and necrotizing entercolitis. Thrombocytopenic babies had more complications, more hemorrhage, and greater mortality than nonthrombocytopenic babies. Platelet size was increased in two babies with immune thrombocytopenia and in none of the others. This study shows that neonatal thrombocytopenia is often associated with high-risk factors and with increased hemorrhage, morbidity, and mortality. This relationship suggests an important prognostic value to platelet size was increased in two babies with immune thrombocytopenia and in none of the others. This study shows that neonatal thrombocytopenia is often associated with high-risk factors and with increased hemorrhage, morbidity, and mortality. This relationship suggests an important prognostic value to platelet counts, although the extent to which the thrombocytopenia contributed directly to morbidity and mortality is not clear.

Catheterization↗