PubMed Health⌕ Search

PubMed · 1130192

Abnormal proteolysis in sick newborns.

Abstract

87 newborn infants were studied on their first day of life for defects in the coagulation and fibrinolytic systems. The infants were divided into two diagnostic groups, one with IRDS, the other with mixed neonatal disorders. Factor V, fibrinogen and fibrin/fibrinogen degradation products (FDP) were abnormal more often than any of the other factors examined. The presence or absence of "multiple defects" appeared to depend on the severity of the illness and its ultimate course. Thus 28% of the surviving infants or 85% of those who died had "multiple defects". The pattern of abnormalities did not differ between the infants with IRDS and those with mixed disorders. The "multiple defects" are ascribed to the following mechanisms: (1) impaired synthesis due to vitamin K deficiency and/or liver damage, (2) abnormal proteolytic activity stimulated by tissue damage and causing (a) an activation of the coagulation process (b) activation of the fibrinolytic system, or (c) of both the coagulation and the fibrinolytic systems. Differentiation between these pathways to defective haemostasis are important when deciding upon therapeutic measures in addition to the basic treatment.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P Henriksson, H Ekelund. 1975. Abnormal proteolysis in sick newborns.. https://doi.org/10.1111/j.1651-2227.1975.tb03843.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Hematological abnormalities during the first week of life among neonates with Down syndrome: data from a multihospital healthcare system.

Various hematological abnormalities have been reported among neonates with Down syndrome. Thrombocytosis, thrombocytopenia, polycythemia, neutrophilia, transient myeloproliferative disorder (TMD), and congenital leukemia have all been reported. The two largest case series previously reported involved 63 and 31 cases. To acquire hematological data from a larger case series, we obtained all CBCs done during the first week after birth on all neonates with Down syndrome cared for in an Intermountain Healthcare (IHC) hospital with a date of birth between January 1, 2001 and December 31, 2005. During this period, 145,522 live births were recorded at 18 hospitals. Down syndrome was recognized in 226 (1 in 644). One hundred fifty-eight (70%) of these had one or more CBCs obtained before the seventh day (144 hr). Neonates who did versus did not have a CBC in the first week had a similar gestational age, birth weight, percentage who were LGA and SGA, and length of stay. Neutrophilia was the most common hematological abnormality detected, with 80% of absolute neutrophil counts above the upper limit of normal for age. Six percent (9/158) had blasts identified on the blood film and three, where this was persistent, were referred to the pediatric hematology service for further evaluation. The next most commonly detected abnormality was thrombocytopenia, with 66% of platelet counts <150,000/microl, and with 6% of counts <50,000/microl. The mean platelet volume did not correlate with the platelet count, but tended to run slightly large (9.2 +/- 1.3 fl), with 24% of values above 10 fl. Only one had a platelet transfusion. Polycythemia was the next most common hematological abnormality detected, with 33% of hematocrit values above 65% or hemoglobin concentrations above 22 g/dl. Six had a reduction transfusion. One patient had significant anemia (hematocrit <15%) and received an erythrocyte transfusion. One had neutropenia associated with an infection after bowel surgery. Neutrophilia, thrombocytopenia, and polycythemia were the most common hematological abnormalities observed among neonates with Down syndrome. Anemia, thrombocytosis, and neutropenia were not more common than among neonates who do not have Down syndrome. Hematological abnormalities were so common in this group that it seems reasonable to recommend that one or more CBCs be obtained on all neonates with Down syndrome.

Blood Cell Count↗

Profound thrombocytopenia related to G-CSF.

Severe thrombocytopenia in association with G-CSF therapy is extremely rare. Here we report a case of profound thrombocytopenia in a 57-year-old male with refractory cardiac ischemia, who received G-CSF during an angiogenesis trial. After 5 days of G-CSF therapy (10 microg/kg/day) the platelet count fell progressively to a nadir of 5x10(9)/L. The patient received steroid, immunoglobulin and platelet support and recovered without sequelae. Subsequent investigations suggested an underlying immune-mediated thrombocytopenia, which we hypothesize was exacerbated by G-CSF therapy.

Blood Cell Count↗

In vivo effects of sequential granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin-2 (IL-2) on circulating dendritic cells (DC) in patients with surgically resected high risk cutaneous melanoma.

Dendritic cells were assayed repeatedly in the peripheral blood of consenting melanoma patients receiving adjuvant biotherapy for high risk (stages IIb-IV) melanoma. Postoperatively, adjuvant biotherapy consisted of granulocyte-macrophage colony-stimulating factor [125 microg/m2/day] for 14 consecutive days, followed by interleukin-2 [9 million IU/m2/day] for the next 4 days, and then no treatment for 10-12 days. This was repeated monthly for six cycles. Although white blood cell counts increased, there was no significant elevation in dendritic cell counts during therapy of eleven patients. Within the first cycle during granulocyte-macrophage colony-stimulating factor treatment of seven patients, the absolute DC count decreased (p < 0.04), the percentage of myeloid BDCA-1+ BDCA-2- dendritic cells was significantly lower than baseline (p < 0.003) and the percentage of plasmacytoid BDCA-1- BDCA-2+ dendritic cells was significantly higher than baseline (p < 0.009). Our data suggest mechanisms of potential anti-tumor responses in patients receiving systemic sequential granulocyte-macrophage colony-stimulating factor and interleukin-2 do not include a cumulative gain in peripheral dendritic cell counts or an increase in myeloid BDCA-1+ BDCA-2- dendritic cell subset in the peripheral blood.

Blood Cell Count↗