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Biomedical subjects

J A Cich

Publications and source records attributed to J A Cich.

5 recordsLinked to original sources
PubMed1988

Intrathoracic extravasation of sclerosing agents associated with central venous catheters.

Two children receiving continuous infusions of vesicant chemotherapy through central venous catheters (CVCs) developed venous thrombosis, and intrathoracic extravasations ensued. One child receiving a continuous vincristine infusion presented with signs of thoracic venous obstruction, fever, and respiratory distress and had pleural effusions and pulmonary infiltrates on his chest roentgenogram. The other child was receiving a continuous doxorubicin infusion and developed superior vena cava thrombosis and retrograde extravasation along the catheter tunnel site. Both children improved after chemotherapy was discontinued and the CVCs removed. Catheter placement and the continuous infusion of sclerosing agents are discussed.

Antineoplastic Agents↗
PubMed1983

Hemoglobin North Shore: a variant hemoglobin associated with the phenotype of beta-thalassemia.

Hemoglobin (Hb) North Shore (beta 134 val leads to glu) is a mutant hemoglobin that is associated with the phenotype of mild heterozygous beta-thalassemia. Heterozygotes are characterized low normal hemoglobin levels or mild anemia, microcytosis, increased HbA2, and 34%-38% Hb North Shore. The mechanism of the anemia and microcytosis associated with Hb North Shore was explored by studies of hemolysate thermal instability, peripheral blood globin biosynthesis, and whole blood oxygen affinity. Hb North Shore was mildly heat unstable in comparison to normal adult hemolysate. Pulse labeling of reticulocytes with 3H-leucine showed an alpha/beta ratio of 1.35 (normal 1.0). The beta North Shore/alpha ratio was 0.22-0.27, which was less than expected on the basis of gene dosage and less than that seen for most beta-chain variants. The beta A/alpha ratio was 0.50, as would be expected. The beta North Shore/alpha ratio was 0.26 after a 15-min pulse and did not decrease during 120 min of chase. These findings suggest that suboptimal synthesis rather than posttranslational degradation is responsible for the thalassemic phenotype associated with this variant hemoglobin. These observations parallel the findings in heterozygous HbE. It is not presently known whether the thalassemia phenotype is conferred by the structural mutation itself or by another mutation cis to the beta North Shore gene.

Amino Acids↗
PubMed1982

A syndrome of thrombosis and hemorrhage complicating L-asparaginase therapy for childhood acute lymphoblastic leukemia.

L-Asparaginase therapy for childhood acute lymphoblastic leukemia causes deficiencies of plasma hemostatic proteins, especially antithrombin, plasminogen, and fibrinogen. Severe thromboses and hemorrhages occurred in 18 children receiving vincristine, prednisone, and asparaginase therapy for ALL. Thirteen children had intracranial thrombosis or hemorrhage, four had extremity thrombosis, and one had both an intracranial hemorrhage and an extremity thrombosis. These events occur characteristically in the third and fourth weeks of therapy during or just after a three-week course of L-asparaginase. Symptoms of headache, obtundation, hemiparesis, and seizure were common for the intracranial events: local pain, swelling, and discoloration were common for the extremity thromboses. These complications have been recognized in 1 to 2% of children undergoing induction therapy which includes asparaginase.

Adolescent↗