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Most midtrimester abortions are still being performed with hypertonic saline and hysterotomy, but the morbidity and mortality rates are too high. The efficacy of a single intra-amniotic injection of prostaglandin F2αand hyperosmolar urea without oxytocin augmentation was demonstrated and results were compared with those obtained by current methods.

Seventy-four patients, from I6 to 20 weeks pregnant, received intra-amniotic urea (80 Gm.) and intravenous oxytocin for the purpose of inducing abortion. Seventy-one of the 74 patients were successfully aborted by the primary method with a mean injection-to-abortion interval of 18.33 hours. There were no serious side effects, and the mean hospital stay was 32 hours. Following urea injection, the mean serum urea nitrogen rose to 33 mg. per cent at 4 hours. Maximum changes in serum electrolytes occurred at 8 to I2 hours after injection and included a decrease in the mean concentrations of sodium, chloride, and carbon dioxide and an increase in serum potassium. An increase in the urinary excretion of urea began within 4 hours, but significant diuresis did not occur in the presence of intravenous oxytocin administration. There was a significant increase in the leukocyte concentration while hematocrit values remained unchanged. Beginning approximately 8 hours following urea injection, the mean plasma fibrinogen concentration decreased by approximately 15 per cent and the mean platelet count showed a drop of approximately 18 per cent. Fibrinogen-fibrin degradation products were significantly increased in 36 per cent of the patients studied.

Serum lactic acid dehydrogenase (LDH) and fibrinogen-fibrin degradation product (FDP-fdp) levels were measured in 35 patients, and LDH isozyme distributions in 11 patients with arteriographically proved pulmonary emboli. Levels of LDH tended to be maximal during the 48 hours following embolization; 30% of those measured during this interval were elevated. Distribution of serum LDH levels in these patients was similar to that in patients with congestive heart failure or pneumonia with effusion. The LDH isozyme patterns of our patients were characterized by increased LDH 3. However, they were not sufficiently characteristic to differentiate pulmonary embolization from congestive heart failure or pneumonia. The FDP-fdp levels were elevated or borderline in 20%. Single measurements of LDH, LDH isozyme, and FDP-fdp levels, performed when the diagnosis is suspected with these methods, are not reliable tests for pulmonary emboli.

The cytogenetic and morphologic abnormalities arising in the bone marrow following therapy with 1-β-D-arabinofuranosylcytosine hydrochloride (cytosine arabinoside) were studied with 10 patients with various neoplasms. A 5-day course of daily, rapid administration of the drug was employed at a dose of 150-200 mg./m2 body surface area. Within 24 hours there was a high incidence of chromosomal aberrations in both granulocytic and erythroid marrow cells. These aberrations consisted of chromatid breaks, erosions, despiralization, precocious separation of the chromatids at the centromeric region, and extensive fragmentation. Prominent morphologic abnormalities were seen in nondividing cells of the erythroid series, but were absent from the granulocytic precursors. Following cessation of cytosine arabinoside therapy, the morphologic and cytogenetic abnormalities rapidly returned to normal. These features were discussed in relation to the known pharmacology of cytosine arabinoside.

Feinstone1 in 1940 called attention to the fact that following the oral administration of sulfonamides in lipid emulsion more sustained blood levels of free sulfonamide were obtained. Peterson and Finland2 in 1942 observed that patients given oral sulfonamides after meals had consistently higher blood levels than when the same dose was given in a fasting state. In 1945 Reinhold3 confirmed Peterson's observations and suggested the clinical use of lipid emulsions as vehicles for sulfonamide administration. No practical application of these observations was made until recently, when lipid emulsions of acetyl sulfisoxazole, sulfadiazine, and a triple sulfonamide were prepared.The present report is a comparative evaluation of the blood level of free sulfonamide obtained after the oral administration to fasting subjects of three sulfonamide preparations: (1) standard aqueous suspension, (2) a lipid emulsion base, and (3) in a limited number of patients the standard aqueous suspension followed by

1. Three adults with CML, 2 Ph1 chromosomes, and marked peripheral lymphadenopathy are described. 2. In each instance node enlargement was thought to be due to leukemic infiltration rather than a supervenient lymphomatous process. 3. Marked adenopathy is an unfavorable prognostic sign in CML, particularly if caused by myeloblastic infiltration. Such infiltration can precede myeloblastic involvement of the peripheral blood and bone marrow. 4. Karyotype analysis and touch preparations of extramedullary tumor tissue in CML will aid in accurate diagnosis and may help to answer more basic questions regarding the pathogenesis of this malignancy.

Spuriously low electronic platelet counts were obtained on blood collected in EDTA from six patients. Platelet numbers on blood smears and electronic counts performed on blood collected in other anticoagulants were normal. Plasma or sera from these patients agglutinated homologous, as well as autologous platelets, in the presence of EDTA or DTPA, but agglutination did not occur in blood or platelet-rich plasma anticoagulated with heparin, oxalate, or citrate. Agglutination in the presence of EDTA was not inhibited by heparin, α-tocopherol, or N-ethylmaleimide, but was inhibitied by excess EDTA or divalent cation. The agglutinin was temperature independent in five of the six patients and had the physical and immunologic characteristics of a gamma globulin. The clinical significance and mechanism of EDTA-dependent agglutination of platelets is unknown.

The effect of hypofibrinogenemia on production of the generalized Shwartzman reaction (GSR) by the administration of Thorotrast (3 ml/kg) and Escherichia coliendotoxin (50 µg) to rabbits was determined. Severe hypofibrinogenemia (fibrinogen less than 15 mg/ 100 ml) was produced by Arvin, a proteolytic coagulant from the venom of the Malayan pit viper, Agkistrodon rhodostoma. Development of the GSR was inhibited significantly only when hypofibrinogenemia was produced 30 hr before the preparatory injection of Thorotrast and maintained for the duration of the experiment. Severe hypofibrinogenemia of 2-20-hr duration before administration of endotoxin did not block the production of the GSR. Elevated levels of fibrinogen degradation products were demonstrated in the serum of all animals that received Arvin. The concentration of fibrinogen degradation products decreased markedly prior to death only in those animals that developed the GSR. The GSA was not observed in rabbits that received only Thorotrast and Arvin, although these animals had the highest levels of fibrinogen degradation products. The data suggest an essential role for fibrinogen or fibrinogen degradation products and endotoxin in the production of the GSR.

The widespread use of heparin in heart surgery has introduced the need for accurate tests to evaluate the blood clotting mechanism. In this study we compared three such methods: the Lee-White clotting time, the activated plasma partial thromboplastin time (APTT), and the blood activated recalcification time (BART). We found the BART to be a valuable adjunct in the management of heparinized patients. With this test, it is possible to control more accurately the degree of heparinization and to determine more precisely the amount of protamine that will be required. Furthermore, results of the BART can be obtained quickly and are reproducible.

Diabetic ketoacidosis may be the first manifestation of diabetes, particularly in the young patient. In most instances, a careful history will disclose the presence of diabetic symptoms for several days or months. Whereas a relative resistance to insulin is a well-recognized feature of diabetic acidosis, such resistance is usually of moderate intensity and only transient.We report an unusual case of diabetic ketoacidosis because it occurred in a previously unknown diabetic with documented absence of glycosuria on the preceding day that required 9,200 units of insulin to achieve metabolic control. Most important, it was associated with a fatal brain-stem infarction. PATIENT SUMMARY A 26-year-old, gravida 2, para 0, married woman was admitted for threatened abortion. Review of systems did not suggest any evidence of diabetes. Repeated urine testing for sugar was negative. There was no family history of diabetes mellitus. Physical examination was unremarkable except for scant bleeding through a