Platelet Breakdown Research Articles

The Prevalence and Associated Risk Factors for Neonatal Thrombocytopenia Among Newborns Admitted to the Neonatal Intensive Care Unit.

Background Thrombocytopenia is the most prevalent hematological condition in neonates that develops in the neonatal intensive care unit (NICU). This set of illnesses is caused by either decreased platelet production due to placental insufficiency, increased platelet breakdown (consumption), or a combination of the two causes. Based on platelet count, it is defined as mild, moderate, or severe thrombocytopenia, with early and late onset. Purpose The purpose of this study is to determine the prevalence of thrombocytopenia and the factors that contribute to it in newborns hospitalized in the neonatal critical care unit at the Maternity and Children Hospital in Al Ahsa, Saudi Arabia. Methods This descriptive retrospective cross-sectional study was carried out at the NICU of the Maternity and Children Hospital in Al Ahsa, Saudi Arabia, over the span of one year (August 2022 to August 2023) among hospitalized neonates with thrombocytopenia. Thrombocytopenia is defined as a platelet count of 150,000 or less. These patients were monitored until they recovered or died. Results The inclusion criteria were met by a total of 242 newborns with thrombocytopenia. Half of the neonates (57%) were full-term, with Apgar scores greater than 5 at the first (84%) and fifth (93%) minutes, respectively. The great majority of individuals (84%) experienced early-onset thrombocytopenia of mild severity (62%) and were asymptomatic (93%). The majority of the cases resolved spontaneously, with only 21%requiring platelet transfusion. There was a significant relationship discovered between gestational age and the severity of thrombocytopenia, with very preterm infants having moderate to severe thrombocytopenia, as well as birth weight (p=0.001). Furthermore, neonates with severe thrombocytopenia had a considerably higher mortality rate (p=0.001). Conclusion The mortality and morbidity of newborns with perinatal risk for neonatal thrombocytopenia can be reduced with timely detection of the cause and development of thrombocytopenia, as well as adequate and early care.

Immune Thrombocytopenia (Itp) In Emergency Medicine

Immune Thrombocytopenia (ITP) is an autoimmune disorder characterised by a low platelet countless than 100? ×? 10^9/L, purpura, and hemorrhagic episodes induced by antiplatelet autoantibodies without anemia or leukopenia. Immune thrombocytopenia (ITP) occurs in 2 to 4/100? 000 adults. A wide range of signs and symptoms, from modest mucocutaneous petechiae to severe, life-threatening organ haemorrhage, are seen in ITP patients. they may present to the emergency department (ED) with life-threatening bleeding as a result of their thrombocytopenia. ITP has two distinct clinical syndromes, manifesting as an acute condition in children and a chronic condition in adults. IgG autoantibodies make circulating platelets more sensitive. It causes these cells to be removed more quickly by antigen-presenting cells (macrophages) of the spleen, and occasionally the liver or other components of the monocyte-macrophage system. Current evidence supports alternatives to splenectomy for second-line management of patients with persistently low platelet counts and bleeding. By increasing platelet production, bone marrow compensates for platelet breakdown. Immune Thrombocytopenia most commonly arises within a few weeks after a viral infection in healthy children and young adults. Immunosuppressive treatment is usually effective in treating ITP. Many patients with ITP require no emergent treatment. However, the emergency physician should start treatment with a platelet transfusion, corticosteroids, and intravenous immune globulin (IVIG) as soon as the patient with suspected ITP arrives at the ED with serious haemorrhage.The diagnosis is usually made by ruling out all known causes of thrombocytopenia. This review aims to summarize current evidences regarding prevalence, causes, diagnosis and management of immune thrombocytopenia. Keywords:,,,

The role of CXCR5+ CD4+T-follicular helper cells in idiopathic thrombocytopenic purpura

Background Primary immune thrombocytopenic purpura (ITP) is an autoimmune illness characterized by increased platelet breakdown in the peripheral blood as well as impaired platelet production and it is also characterized by platelet counts less than 100 × 109/L. T-follicular helper (TFH) cells have been linked to the pathogenesis of autoimmune conditions. Aim The study’s aim was to study the role of TFH cells and their function in ITP children. Patients and methods This research involved 25 ITP patients and 20 age-matched and sex-matched controls, with the frequency of circulating TFH cells measured by BD FACS Calibur Flowcytometer in both ITP patients and healthy controls. Results The results showed that the ratio of circulating CD4+ CXCR5+ PD1+ (TFH) in ITP (+) patients, that is, (ITP patients with antiplatelet antibody-positive results) was dramatically higher than those of ITP (−) patients, that is, (ITP patients with antiplatelet antibody-negative results) and it was discovered that the ratios of circulating CD4+ CXCR5+ PD1+ (TFH) were dramatically higher in ITP (+) patients than the control group. However, the ratio of circulating CD4+ CXCR5 +PD1+ (TFH) was not dramatically different between ITP (−) patients and the control group. Conclusion Patients with ITP have an increased number of TFH cells, which prove its critical role in B-cell proliferation, resulting in the development of autoantibodies that contribute to the pathophysiology of ITP.

The behaviour of platelets in natural diamonds and the development of a new mantle thermometer

Platelets are one of the most common defects occurring in natural diamonds but their behaviour has not previously been well understood. Recent technical advances, and a much improved understanding of the correct interpretation of the main infrared (IR) feature associated with platelets (Speich et al. 2017), facilitated a systematic study of platelets in 40 natural diamonds. Three different types of platelet behaviour were identified here. Regular diamonds show linear correlations between both B-centre concentrations and platelet density and also between platelet size and platelet density. Irregular diamonds display reduced platelet density due to platelet breakdown, anomalously large or small platelets and a larger platelet size distribution. These features are indicative of high mantle storage temperatures. Finally, a previously unreported category of subregular diamonds is defined. These diamonds experienced low mantle residence temperatures and show smaller than expected platelets. Combining the systematic variation in platelet density with temperatures of mantle storage, determined by nitrogen aggregation, we can demonstrate that platelet degradation proceeds at a predictable rate. Thus, in platelet-bearing diamonds where N aggregation is complete, an estimate of annealing temperature can now be made for the first time.

Platelet Distribution Width (PDW) - A Rarely Studied Platelet Indice for Determining the Causes of Thrombocytopenia

Background: Thrombocytopenia (TCP) is low platelets count, which is either due to defective platelet production or due to increased platelet breakdown. The platelet number alone does not give a complete picture of platelet maturity and function, therefore, the platelet indices have been the subject of intensive study in recent years, but they have not been firmly established. Mean platelet volume (MPV) and platelet distribution width (PDW) are useful parameters in evaluating disorders of platelets. This study was undertaken to evaluate the effectiveness of PDW in diagnosing causes of thrombocytopenia. Methods: 510 cases of thrombocytopenia and 500 cases of Control group with normal platelet count were included in the study. TCP was defined as platelet counts below 1.5 lacs/cumm. Hematological analysis was done on Mindray BC-3000 plus automated hematology analyzer. All cases were reevaluated by peripheral smear examination. Only those cases were included in the study, which showed platelet count and platelet volume parameters with graph both in cases and in control group. Results: Hyper-destructive group constituted majority of the cases 352 (69%), while hypo-productive group and abnormal pooling constituted 30% and 1.42% cases respectively. The mean PDW was significantly higher in hyper-destructive group when compared with hypo-productive group, Abnormal pooling and control group. The difference was statistically significant. Conclusion: PDW provides plenty of clinical information about the causes and patho-mechanisms of thrombocytopenia and could be helpful to distinguish hyper-destructive thrombocytopenia from hypo-productive thrombocytopenia. More attention should be paid to PDW along with other platelet indices to differentiate between hyper-destructive TCP from hypo-productive and abnormal pooling TCP.

Nouvelle cuisine: platelets served with inflammation.

Platelets are small cellular fragments with the primary physiological role of maintaining hemostasis. In addition to this well-described classical function, it is becoming increasingly clear that platelets have an intimate connection with infection and inflammation. This stems from several platelet characteristics, including their ability to bind infectious agents and secrete many immunomodulatory cytokines and chemokines, as well as their expression of receptors for various immune effector and regulatory functions, such as TLRs, which allow them to sense pathogen-associated molecular patterns. Furthermore, platelets contain RNA that can be nascently translated under different environmental stresses, and they are able to release membrane microparticles that can transport inflammatory cargo to inflammatory cells. Interestingly, acute infections can also result in platelet breakdown and thrombocytopenia. This report highlights these relatively new aspects of platelets and, thus, their nonhemostatic nature in an inflammatory setting.

Fatal thrombocytopenia associated with intracardiac mass

Platelets are anuclear blood cells whose function is to form blood clots when we injure ourselves, to prevent excessive blood loss. Thrombocytopenia is a relative low number of platelets in the blood. Thrombocytopenia has several possible causes, including the trapping of platelets in spleen, reduced production of platelets and increased breakdown of platelets. Some examples of an increase in platelet breakdown include pregnancy, idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome, infection, autoimmune diseases and medications (e.g., heparin). Thrombocytopenia may often be asymptomatic and can only be revealed by full blood cell count. Alternatively, it may cause excessive bruises and/or bleeding. In some cases, platelet count is so low that dangerous internal bleeding occurs.

Review article: blood platelet number and function in chronic liver disease and cirrhosis

The liver plays a central role in coagulation and fibrinolysis but is also closely intertwined with the function and number of blood platelets. To describe and integrate all literature concerning blood platelets and liver disease by performing a thorough literature research. A thorough literature research on 'blood platelets' and 'liver disease' was performed. Thrombocytopenia is a marked feature of chronic liver disease and cirrhosis. Traditionally, this thrombocytopenia was attributed to passive platelet sequestration in the spleen. More recent insights suggest an increased platelet breakdown and to a lesser extent decreased platelet production plays a more important role. Besides the reduction in number, other studies suggest functional platelet defects. This platelet dysfunction is probably both intrinsic to the platelets and secondary to soluble plasma factors. It reflects not only a decrease in aggregability, but also an activation of the intrinsic inhibitory pathways. The net effect, finally, is a decreased platelet function in the various types of chronic liver diseases and cirrhosis. Finally, recent data suggest that platelets are not only affected by but can also contribute to the liver disease process, as for instance, in viral hepatitis and cholestatic liver disease. Platelet research in liver disease is a growing area of investigation and could provide new pathophysiological insights.

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Inhibitory mechanisms of naloxone on human platelets.

1. In the present study, naloxone was tested for its antiplatelet activities in human platelet-rich plasma (PRP). In human PRP, naloxone (0.1-0.5 mmol/L) inhibited aggregation stimulated by a variety of agonists (i.e. collagen, adenosine diphosphate (ADP), U46619 and adrenaline). 2. Naloxone (0.1-0.5 mmol/L) did not significantly affect cyclic adenosine monophosphate and cGMP levels in human washed platelets, whereas naloxone (0.5 mmol/L) significantly inhibited thromboxane B2 formation stimulated by collagen (5 micrograms/mL) in human washed platelets. 3. Naloxone (0.5 mmol/L) significantly inhibited [3H]-inositol monophosphate formation of [3H]-myoinositol-loaded platelets stimulated by collagen and U46619. Moreover, naloxone did not influence the binding of 125I-triflavin to platelet membranes. Triflavin is an Arg-Gly-Asp-containing specific fibrinogen receptor antagonist. 4. Addition of naloxone (0.5 mmol/L) to platelet preparations tagged with diphenylhexatriene (DPH) resulted in a considerable decrease in relative fluorescence intensity. 5. It is suggested that the anti-platelet effects of naloxone may be caused, at least partly, by the induction of conformational changes in the platelet membrane initially, followed by the inhibition of thromboxane A2 formation and phosphoinositide breakdown of platelets stimulated by agonists.

Intervillous microthrombus and collagen

Because intravascular fibrin deposition is found in the glomerular capillaries of patients who have died of eclampsia, it was long assumed that a chronic form of intravascular clotting represents the decisive cause of the condition. Fibrin deposition is also typically observed in the uteroplacental bloodstream. The occurrence of high levels of soluble fibrin and fibrin(ogen) degradation products, which in severe cases can also include fibrin oligomers, in combination with thrombocytopenia and factor VIII consumption were interpreted as additional evidence for the significance of intravascular clotting in the pathogenesis of EPH gestosis. The hemolysis of the microangiopathologic type, which occurs in severe cases, was attributed to the resulting impairment in microcirculation. Doubts regarding this theory arose when it was noted that the course of EPH gestosis is not altered by the use of heparin, and that even in severe cases of eclampsia with hemolysis and thrombocytopenia the plasmatic clotting system is involved only to a small extent and probably only secondarily. More recent investigations have yielded the first evidence of reduced prostacyclin synthesis in maternal and fetal vessels in patients with EPH gestosis. Since prostacyclins lower arterial resistance yet at the same time are strong inhibitors of thrombocyte aggregation, this prostacyclin deficiency could account for the hypertension and the occurrence of platelet thrombi in the placental bloodstream associated with EPH gestosis. The observation of a reduction in the number of thrombocytes as a consequence of increased platelet breakdown, which precedes a rise in the level of fibrin(ogen) degradation products, also points to the significance of an abnormal interrelation between platelets and endothelium. In addition to the plasmatic and thrombocytic hypercoagulability and impaired prostacyclin synthesis, hemoconcentration with increased microvascular permeability is also observed. Early detection of disturbances of the vessel wall and vessel contents may provide a means of prophylaxis.

“Haemorrhagic” carotid plaque does not contain haemorrhage

The presence of haemorrhage in carotid bifurcation atheromatous plaques is widely believed to be associated with the production of ischaemic neurological events. This study set out to characterise plaque composition in symptomatic (SYM) and asymptomatic (ASYM) patients and to identify, if possible, the origin of intra-plaque haemorrhage. Fifty-nine plaques (50 SYM and 9 ASYM) were serially sectioned and examined for haemorrhage, haemosiderin, fibrin, cholesterol and collagen. Immunoperoxidase and electron microscopy studies were carried out on sections from five plaques in order to identify blood breakdown products. Intra-plaque haemorrhage was identified in 40 (68%) plaques and was similar in SYM and ASYM plaques. In only one did it constitute more than 15% of plaque content, and in the remainder it consisted of small collections of erythrocytes constituting greater than 1% of plaque content in only 21 (35%) plaques. The predominant non-fibrous component was a pink amorphous material mixed with cholesterol. Apart from traces of platelet breakdown products there was no evidence of haemorrhage in this pink material. Plaque roof rupture or ulceration was seen in 39 (66%) and in almost all cases overlay the amorphous/cholesterol material. Blood vessels were identified in 51 87%) plaques but were in close proximity to haemorrhage in only nine (15%).

Recent aspects of hemostasis, hematology and hemorheology in preeclampsia-eclampsia

Because intravascular fibrin deposition is found in the glomerular capillaries of patients who have died of eclampsia, it was long assumed that a chronic form of intravascular clotting represents the decisive cause of the condition. Fibrin deposition is also typically observed in the uteroplacental bloodstream. The occurrence of high levels of soluble fibrin and fibrin(ogen) degradation products, which in severe cases can also include fibrin oligomers, in combination with thrombocytopenia and factor VIII consumption were interpreted as additional evidence for the significance of intravascular clotting in the pathogenesis of EPH gestosis. The hemolysis of the microangiopathologic type, which occurs in severe cases, was attributed to the resulting impairment in microcirculation. Doubts regarding this theory arose when it was noted that the course of EPH gestosis is not altered by the use of heparin, and that even in severe cases of eclampsia with hemolysis and thrombocytopenia the plasmatic clotting system is involved only to a small extent and probably only secondarily. More recent investigations have yielded the first evidence of reduced prostacyclin synthesis in maternal and fetal vessels in patients with EPH gestosis. Since prostacyclins lower arterial resistance yet at the same time are strong inhibitors of thrombocyte aggregation, this prostacyclin deficiency could account for the hypertension and the occurrence of platelet thrombi in the placental bloodstream associated with EPH gestosis. The observation of a reduction in the number of thrombocytes as a consequence of increased platelet breakdown, which precedes a rise in the level of fibrin(ogen) degradation products, also points to the significance of an abnormal interrelation between platelets and endothelium. In addition to the plasmatic and thrombocytic hypercoagulability and impaired prostacyclin synthesis, hemoconcentration with increased microvascular permeability is also observed. Early detection of disturbances of the vessel wall and vessel contents may provide a means of prophylaxis.

Platelet phagocytosis in the spleen of patients with idiopathic thrombocytopenic purpura (ITP)

The ultrastructure of spleen from four patients with idiopathic thrombocytopenic purpura (ITP) is studied. Platelets, with no evidence of degranulation and aggregation, leave the circulation by passing through gaps in the sinus wall in the marginal zones and the red pulp. They are then trapped by pseudopods of macrophages and are phagocytosed as whole elements. The endothelial cells lining the sinuses do not phagocytose platelets or other circulating blood cells. The degradation of these platelets in the phagolysosomes of macrophages is incomplete and results in the formation of myelinic‐like figures which accumulate in large numbers in these cells. This incomplete platelet breakdown may be due to a deficiency of specific lysosomal enzymes. Erythroleucophagocytosis in ITP is normal. The results are consistent with the concept that ‘self’ constituents are normally and readily destroyed by autolytic enzymes. In the case of enzyme deficiency or the presence of ‘foreign’ antigens, including altered ‘self’ antigens, these enzymes become ineffective for rapid and complete degradation of the substrate. Through macrophage‐lymphocyte interaction, antibody‐forming cells are activated against these residual substances. These antibodies, in turn, facilitate the phagocytosis of the specific ‘antigens’ by macrophages. The massive platelet phagocytosis and the presence of large numbers of germinal centres in the white pulp and plasma cells in the marginal zone and red pulp suggest that the spleen is the major site of platelet destruction, as well as the site of antiplatelet antibody synthesis.

Rapid inactivation of cyclooxygenase activity after stimulation of intact platelets

Trypsin, thrombin, and ionophore A23187 activate phospholipid breakdown of platelets that have been labeled with [(14)C]arachidonate, releasing their cyclooxygenase and lipoxygenase products. Intact platelets can also very effectively directly degrade low concentrations of exogenous, free [(14)C]arachidonate. Pretreatment of platelets with trypsin, thrombin, or ionophore A23187 for a minimum time of 30 sec leads to complete inactivation of cyclooxygenase activity, as demonstrated by subsequent exposure to [(14)C]arachidonate. Lipoxygenase activity is lost after 5 min. The thrombin-induced inactivation of cyclooxygenase and lipoxygenase is prevented by cyclic AMP (which inhibits the stimulated activity of phospholipase A(2)), although cyclic AMP does not affect the degradation of exogenous [(14)C]arachidonate. Exposure of platelets labeled with [(14)C]arachidonate to unlabeled arachidonate under conditions that lead to use of the latter also results in a similarly rapid inhibition of cyclooxygenase activity, as determined by subsequent challenge with thrombin. Under these conditions lipoxygenase activity is much less markedly inactivated. The arachidonate-induced inhibition of cyclooxygenase activity is not prevented by cyclic AMP. Trypsin does not induce platelet aggregation, and platelets whose cyclooxygenase activity has been inactivated are intact insofar as they are still able to undergo aggregation. These studies demonstrate that operation in intact platelets of the cyclooxygenase pathway, through use of endogenous or exogenous substrate, leads to a very rapid, irreversible inactivation of this enzyme. The lipoxygenase pathway is also progressively impaired, but much less rapidly than the cyclooxygenase enzyme and much less markedly on use of exogenous compared to endogenous substrate. The possible consequences of these physiological processes of spontaneous inactivation are considered.

Platelet Abnormalities in Cirrhosis of the Liver

Platelet abnormality in cirrhosis of the liver has been studied in our laboratory from biochemical, functional and morphological standpoint.In this paper we studied the causes of shortening of platelet life-span in cirrhosis of the liver in relation to the splenomegaly, protein, sialic acid and glycoprotein contents of platelet and platelet plasma membrane.[Result]1) The volume of the spleen in cirrhosis of the liver measured from 99mTcscinti gram increased to 648cm3 against 307cm3 of normal control.There was no significant correlation between the platelet counts and the spleen volume (r=0.02).2) The protein content of the platelet increased to 2.0mg/109 plat. against 1.2mg/109 plat. of normal control.3) The sialic acid content of the platelet decreased to 7.2μg/mg prot. against 9.6μg/mg prot. of normal control. And there was a good correlation between the platelet count and the platelet sialic acid content (r=0.65).4) On 7.5% SDS polyacrylamide gel electrophoresis (SDS-PAGE) of the solubilized platelet protein, in cirrhosis of the liver, a new band of MW 46, 000 appeared, while a band of MW 41, 000 almost disappeared.5) On SDS-PAGE of the solubilized platelet plasma membrane protein, the band of MW 156, 000 disappeared in both cirrhosis of the liver and normal control pretreated with neuraminidase.6) On 5.6% SDS-PAGE of the solubilized platelet plasma membrane glycoprotein, three major peaks (I, II, III) were observed in both normal and hepatic cirrhosis, but in the latter, peak III of MW 88, 000 was smaller than that of the former. The simillar change was observed in normal platelet plasma membrane glycoprotein pretreated with neuraminidase.From these findings, it may be suggested that in cirrhosis of the liver, the reduced platelet sialic acid or sialoglycoprotein may promote platelet break-down in reti culoendothelial system and shorten platelet life-span.

Coagulation and fibrinolysis in hepatic cirrhosis

In order to clarify coagulation and fibrinolysis in hepatic cirrhosis following items were examined.1) Counts of megakaryocyte and its classification. 2) Lifespan of 5Cr-labeled platelet. 3) Platelet volume and its distribution (Coulter Counter ZB). 4) Platelet spreading test (Breddin's method). 5) Platelet aggregation (Evans Aggregometer). 6) Platelet Factor-3 (Kaolin). 7) Serum phospholipids and its fractionation. 8) Hepaplastin test (Eisai pharmaceutical Co, test for II, Vll, X factors) 9) Plasma fibrinogen (Tyrosine). 10) FDP (HIT). 11) Protamine sulfate test (Lipinski's). 12) Total plasmin (fibrin plate). 13) Plasminogen and antiplasmin (lysine sepharose affinity chromatography) 14) Factor XIII (Urayama's). from these examinations following facts were clarified.1) Reduction of platelet counts is due to disturbance of platelet formation and enhanced breakdown of platelets and may either due to pooling in the spleen.The remarkable reduction and its characteristic asthenic pattern of platelet aggregation may suggest hypofunction of the platelet cell. It may be supported with the facts of the large spreading tendency of the platelet and reduction of PF-3 availability.2) Hepaplastin test clearly shows reduction of extrinsic factor in cirrhosis of the liver.3) In regard to f ibrinolysis, in case of the hepatic cirrhosis, plasma fibrinogen tends to decrease, on the other hand protamind sulfate test tend to show higher value.Total plasma plasmin increased remarkably, on the other hand, plasminogen and antiplasmin slightly decreased. Factor XIII decreased either in case of cirrhosis.Whether the enhanced fibrinolysis may occur primary or secondary must be examined more in detail.

A note on the mathematical theory of the effect of nervous stress on coronary thrombosis.

The “classical” view of formation of blood clots is that the disintegration of platelets releases thrombokinase which activates prothrombin into thrombin. The latter combining with fibrinogen produces fibrin, the substance of the clot. There is, however, ample evidence of hormonal and other biochemical factors as playing a role in the process of clotting. Through the necessity of a breakdown of platelets has been challenged, yet theirpresence is considered as necessary for clotting. Thefirst part of this paper is based on the assumption that either a breakdown or even an injury of a platelet produces thrombokinase. An injury is likely to occur due to collisions between platelets, between platelets and erythrocytes or between platelets and leukocytes. A probability is ascribed to the production of thrombokinase by a collision. Thus not every collision is effective. The frequency of those collisions is calculated according to classical physics. Inasmuch as mental stress usually causes vasoconstriction and therefore an increase of concentration of the formed elements of blood, the frequency of collisions and therefore the production of small amounts of thrombokinase increases with stress. If thrombokinase formed by the collision remains preserved and therefore accumulates in the blood, we arrive at an expression which gives us the necessary total duration of stress to produce thrombosis. According to that equation, even in the absence of stress, any individual if he lives long enough should eventually develop a thrombosis. If, however the thrombokinase is destroyed, then it is necessary that during a sufficiently short time enough effective collisions occur to increase the amount of thrombokinase to a danger level. With this picture we find only theprobability of a formation of a thrombus as a function of the intensity of stress and its duration. The probability remains finite event for zero stress, showing that even individuals who are always relaxed may develop thrombi. In the second part of the paper an outline of a biochemical approach is given. Inasmuch as we know very little about the biochemical mechanism involved, it is simply assumed that during a stress of intensityS and duration Δ there is a probability of a thrombosis occurring. Then by applying the theory of probabilities, an expression is derived giving the probability of occurrence of a thrombus after a given number of stress incidences. The expressions are different from those obtained from the first approach but lead basically to the same results. A comparison of both or of their combination, with available data may give indications as to which of the factors plays a preponderant part.

Splenic Macrophages in Thrombocytopenia

Abstract Electron microscopic examination of splenic tissue obtained from patients with a variety of hematologic disorders has shown ultrastructural evidence for platelet breakdown within splenic histiocytes in seven out of eight patients with idiopathic thrombocytopenic purpura (I. T. P.). The morphologic characteristics of this intracellular digestion have been described.

Relation between platelet integrity and sulfhydryl groups.

Summary1. Incubation of freshly prepared human platelets with a variety of sulfhydryl inhibitors results in increased rate of platelet breakdown. 2. In all cases studied the effects of inhibitors can be decreased in extent by suitable concentrations of SH-containing substances such as cysteine or reduced glutathione. 3. Results obtained suggest a direct relationship between platelet sulfhydryl groups and platelet structure. The possible link of this relationship to platelet metabolism is briefly discussed.