ExtractStudies of platelet function were performed on venous blood specimens from 64 newborn infants within 0-48 h after birth. Fifty-two of the infants studied were normal, full-term average for gestational age (AGA) infants, three were normal, premature AGA infants, seven were premature AGA infants with the respiratory distress syndrome (RDS), and two were premature AGA infants who had repeated apneic periods. Although it was not possible to study all variables of platelet function in each of the groups, those studies that were performed showed no differences in the results based on the group to which an individual infant belonged.Compared with 24 normal adult controls, the infants showed impaired platelet aggregation in the presence of ADP, collagen, and thrombin. The mean time required for maximal platelet aggregation with ADP, collagen, and thrombin for the adults was 120, 230, and 74 sec, respectively, compared with values of 160, 443, and 158 sec for the infants (table II, figs. 2, 3, and 4). The percentage total platelet aggregation with ADP, collagen, and thrombin for the adults was 79, 91, and 74 % compared with 47, 73, and 47%, respectively, for the infants (table II, figs. 2, 3,.and 4). Infant whole blood and platelet-rich plasma clot retraction were markedly defective compared with normal adults (table I). In addition, platelet factor 3 release in 10 normal infants, as measured by the modified Stypven time, was decreased when compared with 10 values for normal adults ( fig. 5). Other variables of platelet function (bleeding times, native blood platelet adhesiveness, petechiometer tests) studied in newborn infants were normal (table I). Thrombelastograms were compatible with hypercoagulability of the blood (table I). None of the infants studied had clinical evidence of a bleeding tendency.In vitro mixing experiments suggested that the impaired ADP platelet aggregation was due neither to the presence of plasma ADP inhibitors, a refractory state due to increased circulating levels of ADP, anticoagulants, nor to a selected population of platelets. Physiologic alterations of infant platelets are similar to platelet functional changes observed in thrombasthenia.

In this seminar by a member of the house staff of the Department of Pediatrics of the University of Colorado, attention is called to several interesting new and important observations regarding the clinical use of tetracyclines. In addition to the possibility of producing discoloration of the teeth, it is pointed out that the tetracyclines may produce a number of other complications including the "bulging fontanel syndrome," a "reversible Fanconi syndrome," and alterations of skeletal mineralization and growth. This seminar also reviews other recent developments and new knowledge concerning these drugs which should be of particular interest to the physician in practice and in training.

Eleven of 19 sick newborn infants were shown to have either laboratory and/or pathologic evidence of disseminated intravascular coagulation (DIC) during an observation period of 8 months. Three of the affected infants had severe viral diseases (rubella, cytomegalic inclusion virus, and herpes simplex). Seven of the infants had severe idiopathic respiratory distress syndrome (IRDS), and one infant (the product of a severely toxemic mother) had transient respiratory distress. The remainder of the sick infants had mild IRDS without evidence of DIC. Diagnosis of DIC in the newborn is best made by reliance upon specific clotting factor assays (platelets, fibrinogen, and factors V and VIII) rather than nonspecific screening tests or presence of fibrin degradation products. DIC may be a more common complication of severely ill newborn infants than is generally realized.

A patient with classic hemophilia (AHF-deficiency) who demonstrated an acquired platelet functional and bleeding time defect concurrently with an AHF inhibitor is described. Possible etiologies for the platelet defect have been proposed and their role in this patient evaluated. Platelet function studies on six other patients with hemophilia A were normal with the exception of defective platelet adhesion to glass in a patient who had been recently transfused. The combined platelet functional defect and AHF inhibitor found in our patient may be more common than is generally realized. We suggest that any hemophiliac who fails to respond to conventional transfusion therapy should be investigated for both abnormalities.