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1. The reported cases of idiopathic hypoprothrombinemia are reviewed briefly, and a case observed for over three years is presented. Particular attention is called to the similar clinical pattern presented by the chronic cases. 2. Studies are presented indicating that in this patient the delay in prothrombin time was due, at least in part, to a deficiency of a factor necessary for rapid conversion of prothrombin. This factor, or factors, which we have called Ac-globulin, is contained in a highly active state in fresh normal serum. 3. After the in vitro demonstration of a deficiency of Ac-globulin in the patient’s blood, it was possible to bring about a marked reduction in the patient’s prothrombin time by the intravenous administration of relatively small amounts (15 to 45 cc.) of fresh normal (thrombin-free) serum. A further reduction of the prothrombin time to near normal values was brought about by combined whole blood and serum administration. The evidence suggests that partial correction of both prothrombin and Ac-globulin deficiency respectively resulted from such therapy. 4. The possible effects of serum and whole blood upon the delayed prothrombin conversion rate of dicoumarolization and liver disease are discussed and preliminary observations in the former type suggest that such therapy may be useful.

TUBERCULOSIS has been associated with a variety of hematological abnormalities. These include hypoplasia of the bone marrow,1,2 myelofibrosis,3-5 and polycythemia.6 Tuberculosis is sometimes associated with a leukemoid reaction which must be differentiated from leukemia. In 1911 Coley and Ewing,7 from postmortem studies, first drew attention to the leukemoid response which may be evoked by tuberculosis. The association was first made antemortem by Mills and Townsend 8 in 1937. We have found only 38 reports of patients who had leukemoid reactions to tuberculosis which fulfilled the following criteria: (1) tubercle bacilli had to be demonstrated and (2) an excessive leukocytosis or an abnormal shift towards immaturity in the peripheral blood or in the bone marrow. A diagnosis of leukemia was considered to be excluded if a lasting hematologic recovery occurred or if visceral infiltration with leukocytes could not be demonstrated at autopsy.It is the purpose of this paper to discuss

INTRODUCTION Polycythemia vera was first described by Vaquez in 1892.1 Osler, in 1903, collected 6 cases and proposed that this syndrome constituted a new clinical entity.2 At the present time polycythemia vera is usually classified as one of the myeloproliferative syndromes,3,4 because apparent transformations among polycythemia vera, acute leukemia, chronic myelocytic leukemia, myelofibrosis, and Digulielmo's syndrome have been observed; however, the cause of all these syndromes remains obscure. Polycythemia vera has been the subject of some excellent reviews.5-7The purpose of this paper is to review the clinical course, complications, and prognosis of polycythemia vera as exemplified by a group of 50 patients, with particular reference to the problem of surgical risk in this disorder. MATERIALS AND METHODS The records of 50 patients with polycythemia vera seen at the University of Virginia Hospital between the years of 1940 and 1958 have been reviewed. Information about these patients has been obtained

SICKLE cell anemia was described first by Herrick in 1910.1 Since then, surveys of Negroes in the United States have revealed the incidence of the symptomless sickle cell trait to be about 9% and incidence of sickle cell anemia to be about 2.25 per thousand.2 In the past decade sickle cell anemia has been the subject of many studies, which have contributed greatly to our understanding of many of the abnormalities that occur in the disease. Conclusions drawn from these studies form the basis for our current ideas of the pathogenesis of the disease. Since our present therapy is directed toward this aspect of the disease, the pathogenesis of sickle cell anemia will be reviewed briefly before treatment is discussed.It now seems well established that the sickling phenomenon is due to a gene which produces sickle cell anemia when it is present in the homozygous state and

1. Two Negro brothers with homozygous hemoglobin C disease are reported. In one splenectomy was performed. 2. Intraerythrocytic crystals in smears of peripheral blood were demonstrated only in the patient who had splenectomy. The crystals could not be found in re-examination of bone marrow preparations of this patient that were made prior to splenectomy. 3. Absence of the spleen may be a necessary factor for the formation of these crystals. 4. The presence of homozygous C disease is compatible with a normal life span.

Long-term response to corticosteroid therapy and splenectomy was evaluated in 66 adults with idiopathic thrombocytopenic purpura (ITP). In 75% of 57 patients, a rise in platelet count was observed during administration of corticosteroids. In 49% of the 57, platelet counts of greater than 50,000/cu mm were documented four months after cessation of treatment, and in 37% a sustained remission throughout follow-up periods of 1 to 18 years was seen. Splenectomy produced good or excellent responses in 83% of 35 patients evaluated four months after operation and in all but two patients remission has been sustained during follow-up periods of 1 to 25 years. Prognosis based upon response to the initial course of corticosteroid treatment appears to be more reliable than that based upon duration of symptoms prior to treatment.

We have previously demonstrated in a pilot study that phospho-soda is equivalent to PEG lavage in colon cleansing effectiveness (Am J Gastro 1998;93:A1684). PURPOSE: To compare the colon cleansing effectiveness, ease of consumption, and metabolic effects of phospho-soda (PS) and PEG lavage given as colonoscopic preparation. METHODS: Outpatients undergoing elective colonoscopy were randomized to receive either a phospho-soda prep kit (PS 45cc at 6pm + bisacodyl 3 P.O. hs + bisacodyl enema am) or PEG lavage (4L at 4pm) prior to colonoscopy. Subjects with creatinine >2.0, cardiac disease, cirrhosis, or pregnancy were excluded. Subjects completed a questionnaire rating prep tolerability. A side effect score was calculated for each subject (range 0-21, 0 = best). Chemistry profiles were performed before the prep and on the morning of the procedure. The endoscopist was blinded to the prep used. A global prep assessment was recorded for each subject based on the amount and consistency of residual stool {range = 1 (poor) to 5 (excellent)}. RESULTS: 167 subjects (74M, 93F, mean age 59.9 yr.) were enrolled. The two groups were similar in age, sex distribution, and indications for colonoscopy. 64/82 (78%) phospho-soda preps were ranked very good or excellent vs. 63/85 (74%) PEG preps (p=NS). Among 42 PS subjects who had taken PEG during a previous colonoscopy, 38 (90%) ranked PS as more tolerable than PEG. Data shown [see table below] are mean ± SE. CONCLUSIONS: Phospho-soda preps are equally effective and better tolerated when compared to PEG lavage for pre-endoscopic colon cleansing. Increases in serum phosphorous with phospho-soda are small and are likely to be clinically insignificant. Phospho-soda is an appropriate alternative to PEG lavage for the preparation of healthy patients undergoing colonoscopy.