Marked Hemolysis Research Articles

Haemolysis and cholestasis following implantation of a transjugular intrahepatic portosystemic shunt

Objective: To report a case where a patient developed clinically overt haemolysis and cholestasis following implantation of a transjugular intrahepatic portosystemic shunt (TIPS). Patient: A 69-year-old man with posthepatic (B and C) cirrhosis and refractory ascites. Results: Immediate onset of marked cholestasis and haemolysis following TIPS implantation, with spontaneous gradual improvement. On follow-up 4 months later, however, evidence of mild haemolysis and cholestasis persisted. Conclusion: Haemolysis and cholestasis can complicate the insertion of a TIPS shunt. The cause of cholestasis observed in this patient is unclear. Haemolysis following TIPS implanation was probably caused by mechanical damage to the erythrocytes, related to local turbulent blood flow, and because the intravenous sections of the stent were not fully covered with endothelial cells.

Hemolytic interactions of Dermatophilus congolensis.

The strains of Dermatophilus congolensis grew on blood agar with washed sheep erythrocytes with marked total hemolysis. In testing for hemolytic interactions they gave a significant synergistic effect of a characteristic shape with Rhodococcus equi and Streptococcus agalactiae, whereas with Staphylococcus aureus producing beta hemolysin and with Staphylococcus aureus producing delta hemolysin a simultaneous synergistic as well as antagonistic effect were observed. First of all a conspicuous inhibition of in the beta hemolysin zone began and then the hemolytic effect of D. congolensis was enhanced. A similar double reaction was also observed with Listeria ivanovii. With delta hemolysin there was an inhibition of the hemolytic effect of D. congolensis and at the same time a synergistic effect could be observed. Also D. congolensis gave a weak synergistic effect with Micrococcus lylae and Listeria monocytogenes, and a further weak antagonistic effect with alpha hemolysin of Staphylococcus aureus, Staphylococcus hyicus, Staphylococcus chromogenes and Micrococcus luteus. No interaction of D. congolensis was established with Corynebacterium pseudotuberculosis.

Enhancement of ethanol-induced lipid peroxidation in rat liver by lowered carbohydrate intake

In order to investigate the effect of carbohydrate intake on ethanol-induced lipid peroxidation and cytotoxicity, rats were maintained on four different test diets, a medium-carbohydrate (carbohydrate intake, 8.4 g/day/rat on average), a low-carbohydrate (carbohydrate intake, 2.8 g/day/rat on average), an ethanol-containing medium-carbohydrate (carbohydrate and an ethanol intake, 8.4 and 2.9 g/day/ rat on average, respectively), and an ethanol-containing low-carbohydrate diet (2.8 and 2.9 g/day/rat on average, respectively). Ethanol and the low-carbohydrate diet each increased the liver malondialdehyde content, but the combined effect of both (ethanol-containing low-carbohydrate diet) was much more prominent than either alone. The degree of increase in malondialdehyde content almost paralleled the activity of the microsomal ethanol oxidizing system. Both the low-carbohydrate and the ethanol-containing low-carbohydrate diets decreased the liver glutathione content, but ethanol combined with the medium-carbohydrate diet had no effect on the content. Ethanol treatment increased the liver triglyceride content only when combined with the low-carbohydrate diet. The rate of NADPH-dependent microsomal malondialdehyde formation was much higher in microsomes from rats maintained on the ethanol-containing low-carbohydrate diet than in those from rats on the ethanol-containing medium-carbohydrate diet, indicating that lowered carbohydrate intake augments ethanol-induced malon-dialdehyde accumulation in the liver by enhancing the rate of lipid peroxidation. In addition, when incubated with red blood cells in the presence of NADPH, microsomes from rats fed the ethanol-containing low-carbohydrate diet caused marked hemolysis, which was prevented by the addition of 5mM glutathione to the incubation system. Furthermore, addition of 50 mM ethanol to the reaction system greatly accentuated the hemolysis. These results suggest that lowered carbohydrate intake at the time of ethanol consumption potentiates ethanol cytotoxicity by enhancing ethanol-induced lipid peroxidation.

Hemodynamic and Morphological Changes in the Dog Kidney after Injection of 5% Ethanolamine Oleate into the Superior Vena cava

The effect of the sclerosant 5% ethanolamine oleate (EO) on renal circulation was evaluated in 20 mongrel dogs into which we injected 5% EO (0.5 ml/kg) into the superior vena cava. There was a marked hemolysis and a significant decrease in creatinine clearance from 104.4 +/- 17.1 (mean +/- SD) to 40.7 +/- 5.0 ml/min (p less than 0.01) at 120 min. The renal arterial blood flow (RAF) decreased biphasically; from 75.3 +/- 13.1 to 9.8 +/- 9.3 ml/min during an average of 2.3 min, immediately after the injection (p less than 0.01) and gradually decreased after reaching the pretreatment level to 43.2 +/- 8.6 ml/min at 120 min (p less than 0.01). Cardiac output significantly decreased from 1.86 +/- 0.08 to 1.54 +/- 0.08 l/min (p less than 0.01). Tubular necrosis was histologically evidenced in the tissues examined at 6 h after the injection of EO. Biphasic decrease in renal arterial blood flow can be explained by the possible occurrence of spasm of the peripheral renal arteries in the acute phase and tubular necrosis in the late phase. This study suggests to us that the tubular necrosis induced by decreases in RAF as well as hemolytic nephropathy play a significant role in cases of renal dysfunction following the endoscopic injection of 5% EO to sclerose esophageal varices.

THE CIRCULATING PLATELET IN ACUTE MALARIA INFECTION

Professor Essien suggests in his hypothesis on thrombocytopenia associated with malaria (Essien, 1989) that release of ADP from damaged red cells plays a key role in platelet activation and subsequent removal from the circulation. Thus, one would expect that those patients with the most marked haemolysis would be the most likely to exhibit thrombocytopenia

Paroxysmal nocturnal haemoglobinuria with coexisting deficiency of the ninth component of complement: lack of massive haemolytic attack

A 47-year-old woman with paroxysmal nocturnal haemoglobinuria (PNH) was found to have an inherited deficiency in the ninth complement component (C9). In complement-sensitivity lysis tests, 80% of her erythrocytes were markedly complement-sensitive (PNH-III). Laser cytofluorimetry with a monoclonal antibody against decay-accelerating factor (DAF) revealed that 95% of her erythrocytes were DAF-negative. Surprisingly, she has suffered only mild haemolysis and has never experienced massive spontaneous haemolysis. Gross haemoglobinuria and jaundice occurred only after receiving postoperative transfusion of whole blood. In her serum, C9 was not detectable either by immunological or by functional assays. Both the Ham test and the sugar water test using normal human serum or plasma yielded marked haemolysis of the patient's erythrocytes. When the patient's serum or plasma was used, only a trace of lysis was detected. Addition of purified human C9 to her plasma fully restored haemolysis. These observations indicated that C9 may play a critical role in haemolytic attacks in patients with PNH and that characteristic haemolysis in PNH may be tempered by coexisting C9 deficiency.

Alpha-Interferon for Severe Cold Agglutinin Disease

Brief Reports1 August 1989Alpha-Interferon for Severe Cold Agglutinin DiseaseBrian M. O'Connor, MD, Jacqueline S. Clifford, BS, William D. Lawrence, MD, Gerald L. Logue, MDBrian M. O'Connor, MDSearch for more papers by this author, Jacqueline S. Clifford, BSSearch for more papers by this author, William D. Lawrence, MDSearch for more papers by this author, Gerald L. Logue, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-111-3-255 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptCold agglutinin disease may be classified as primary or secondary. Monoclonal IgM (occasionally IgG or IgA) proteins with the ability to bind to erythrocytes below body core temperature are found in the sera of patients with the primary (idiopathic) and secondary forms associated with lymphoproliferative disorders (1). In these disorders mild to moderate hemolytic anemia results from the deposition of complement as the cold agglutinin binds to the erythrocyte in the acral circulation. On exposure to cold, episodes of hemoglobinuria related to marked intravascular hemolysis may occur. Exposure to cold may also produce painful acrocyanosis caused by sludging and deoxygenation...

赤血球の保存に及ぼす撹はんの効果

To evaluate the effects of agitation on preservation of red blood cells, the cells were stored in citrate-phosphate-dextrose solution at 4 to 6°C for 35 days under two types of continuous agitation, reciprocal flat-bed and circular agitation. The pH, 2, 3-diphosphoglycerate (2, 3-DPG) level, adenosine triphosphate (ATP) level, morphology score and hemolysis were measured at weekly intervals. When 200ml polyvinyichloride (PVC) bags were used, both types of agitation showed better preservation of red cells as evaluated by morphology score than non-agitation, but there was no significant improvement in the pH and levels of 2, 3-DPG and ATP with either type of agitation. On the other hand, when stored in 600ml PVC bags, agitation maintained much higher 2, 3-DPG levels and morphology scores throughout storage. Flat-bed agitation did not increase hemolysis during 28 days of storage compared with non-agitation, but circular agitation caused marked hemolysis from 7 days on. These data indicate that a gentle mode of agitation and large bag size are important to preservation of red cells. Continuous flat-bed agitation seems to be effective in better maintenance of both oxygen-carrying capacity and viability of red cells during storage without causing mechanical injury to the cells.

Effects of mechanical trauma of blood cells on dynamic viscoelasticity of blood during clotting

Effects of mechanical trauma of platelets and red blood cells on dynamic viscoelasticity of blood during clotting were examined. Two different methods were attempted to give the mechanical damage to blood cells. In one method, a flow apparatus consisting of a thin teflon tube and two sample reservoirs connecting to both ends of the tube was employed. After a blood sample repeated the shuttle flow many times through the tube, the dynamic rigidity modulus (G') and loss modulus (G') of the blood sample during clotting were measured. The mechanical trauma of platelets brought about the increase of G' and G' for clots of PRP and whole blood, in addition to shorter clotting time. Slight hemolysis of red blood cells (less than 0.5 % of total hemolysis) only yielded shorter clotting time for whole blood. In other method, packed red blood cells were hemolyzed by exposing the ultrasonic wave (the amount of hemolysis was about 5 % of total hemolysis). Addition of supernatant of hemolyzed red blood cells to PRP caused the platelet aggregation. Furthermore, a marked hemolysis brought about higher values of G' and G″ for blood clot, in addition to shorter clotting time. These results suggest that the release of constituents from damaged red blood cells and alteration of cell surface due to mechanical damage would accelerate the coagulation sequence.

Hemolysis and Hyperkalemia Complicate Malignant Hyperpyrexia During Anesthetic Death

A healthy, 15-year-old male received a thiopental, nitrous oxide, oxygen, enflurane anesthetic for appendectomy. Cardiac arrest, following succinylcholine administration, was associated with marked hyperkalemia (potassium levels 8.7 to 11.6 meq), hemolysis (hematocrit fall from 41.7 to 26.6%, plasma hemoglobin 27 mg/dL), and creatine phosphokinase (CPK) elevation (8900 units). Vigorous resuscitative therapy including dantrolene was unsuccessful. The diagnosis of malignant hyperthermia was made by the marked CPK elevation on blood samples drawn during resuscitation and analyzed by the Medical Examiner's Office.

Blood flow heterogeneity in the renal cortex during burn shock in dogs.

Blood flow distribution and occurrence of intermittent, patchy ischaemia in the renal cortex were investigated in anaesthetized dogs before and during burn shock. Severe or moderate thermal injury was induced by scalding 30% of body surface by 90 degrees C or 70 degrees C hot water. Local blood flow in outer and inner cortex was measured by microspheres and by electrodes recording hydrogen gas washout rates. The haematocrit rose much more in the moderately than in the severely scalded dogs, due to marked haemolysis in the latter group. Cortical blood flow was reduced more after severe than after moderate thermal injury. A significant redistribution of blood flow from outer to inner cortex was not demonstrated. Abrupt shifts in local washout rates were observed in most dogs during shock, but was consistently more frequent in the moderately scalded dogs. Such episodes of patchy intermittent ischaemia were not seen after inhibition of prostaglandin synthesis by indomethacin. Thus, prostaglandins may mediate focal vasoconstriction in the renal cortex during burn shock in dogs.

Uterine rupture with the use of vaginal prostaglandin E2 for induction of labor

that have been associated with fetal immune hemolytic anemia have been collectively referred to as “irregular antigens.“’ More than 40 such antigens have been identified.’ Anti-Kp”, a member of the subgroup of Kell antigen, has been reported to produce only mild hemolysis and to require only expectant management.’ Others, however, have noted that the Kpb antigen must be taken seriously. since marked hemolysis may occur.z Our experience with the patient presently described would support the latter conclusion. Information concerning the many different antigens that have been associated with immune hydrops is incomplete. Until our knowledge of the course of immune response for a particular antigen is more thoroughly established, it would seem prudent to manage such sensitization in the manner described for antiRh(D), including serial amniocenteses when prior obstetric historv and antibodv titers are significant.

Prostaglandin cytoprotection. Prostaglandin does not protect against aspirin- or alcohol-induced red blood cell hemolysis.

The hypothesis that prostaglandin cytoprotection involves cell membrane stabilization was tested in vitro using rat erythrocytes. Low concentrations of sodium acetylsalicylate, 0.02, 0.2, 2.0, and 20 mM, inhibited hypotonic hemolysis of red blood cell suspensions. While 35, 140, and 280 mM sodium acetylsalicylate had no hemolytic effect, 560 mM caused marked hemolysis. The prostaglandin E2 analog, 16,16-dimethyl prostaglandin E2, 0.4 X 10(-3), 10(-4), and 10(-5) M concentrations, did not alter this hemolysis. Fourteen percent ethanol caused red cell hemolysis, and this was unaffected by the prostaglandin. The findings do not support the hypothesis.

Hematologic effects of cis-platinum-bleomycin therapy.

A prospective study of the hematologic findings in 19 patients receiving cis-platinum (C-P) bleomycin (B) for squamous cell carcinoma of the head and neck was performed. CP 3 mg/kg was given on day 1, B 15 mg/m2 on day 3 and then by continuous infusison from day 3 to 10. Hematocrits declined in all patients from a mean of 41.6 +/- 3.9 to 36.6 +/- 4.9 (p less than 0.001) with the nadir seen by 10 days, reticulocyte count was unchanged. In 1 patient marked hemolysis occurred over 10-day period associated with the appearance of irregular spherocytes on smear, a situation similar to the index case which initiated this study. 5 other patients had spherocytes. A significant lymphopenia in the absence of neutropenia and thrombocytopenia was also observed.

Evaluation of the DuPont aca amylase method.

The dilution/activity curve for the DuPont aca kinetic amylase (EC 3.2.1.1) method is linear to approximately six times the upper limit of the expected range. Total reaction time on the aca is 4.3 min; however, there is a nonlinear rate of change in absorbance for at least the first 8 min, which is consistent with a lag phase. The within-run and day-to-day coefficients of variation were 2.4% at 100 U/L and 3.6% at 114 U/L, respectively. There was no interference by marked hemolysis (hemoglobin 4 g/L) or by glucose concentrations of 10--50 g/L. Comparisons by the split-sample method between the Amylochrome procedure and the aca procedure gave correlation coefficients of 0.992 for serum and 0.989 for urine. A second comparison, between the AutoAnalyzer I method and the aca, gave correlation coefficients of 0.998 for serum and 0.909 for urine. The expected range for serum was 18--106 U/L and for urine 2--33 U/2 h.

New continuous-flow analysis for simultaneous determination of creatinine and uric acid in 200 microliters of serum without use of a dialyzer.

We present a new method for direct continuous-flow (AutoAnalyzer II) measurement of serum creatinine and uric acid. The manifold is simple, inexpensive, and can be constructed in the laboratory. Only 200 microliters of serum is needed; analysis rate is 60 samples per hour. The incorporation of sodium dodecyl sulfate and the simultaneous provision of blank subtraction make it possible to omit the dialysis step. Our method does not require the linearizer, since instrument response and concentration of creatinine and uric acid are linearly related to 200 and 120 mg/liter, respectively. The percentages of steady state, interaction, and recovery are acceptable, Precision is excellent and the results obtained from the new method correlate well with those obtained by the comparison methods. Interferences are few and, when encountered, are generally smaller than in the modified Technicon method. Marked hemolysis interferes only with the uric acid assay; marked turbidity has no effect on results for creatinine. Icteric serum with total bilirubin of 50 and 100 mg/liter interferes significantly with results for creatinine and uric acid, respectively, by the new method.

Effect of Cerastes vipera snake venom on blood and bone marrow cells

A. H. Mohamed, A. M. Saleh, S. Ahmed and M. El-Maghraby. Effect of Cerastes vipera snake venom on blood and bone marrow cells. Toxicon 15, 35–40, 1977.— In vivo experiments Lethal doses of Cerastes vipera venom injected intraperitoneally in rabbits produced a significant initial rise of the erythrocyte count 15 min after venom injection, followed by a progressive drop. Total leucocyte and platelet counts gradually dropped. The bone marrow picture showed erythroid hyperplasia 3–4 hr after venom injection. Sublethal doses produced a small insignificant initial rise of red cell count followed by a progressive drop during the first hr. In the second hr the counts rose and gradually reached the pre-injection levels after 24 hr. An initial leucopenia and thrombocytopenia was followed by fluctuations in both counts with significant leucocytosis and increased percentage of neutrophil after 24 hr. The platelet counts reached the pre-injection values in 24 hr. The bone marrow picture revealed erythroid hyperplasia 5–6 hr after venom injection. Reticulocyte counts were above normal levels. In vitro studies Incubation of 1 ml blood with 0·5 mg venom for 1 hr resulted in marked haemolysis as evidenced by reddish coloration of plasma, decreased rouleaux formation, microspherocytosis, disruption of leucocytes and drop of all cell counts.

Heparin versus citrate anticoagulation in autotransfusion

Autotransfusion from controlled hemorrhage into a pelvic extraperitoneal pocket was performed in 19 baboons using a commercial autotransfusion apparatus. Nine heparinized animals (H) were compared to ten in which extracorporeal citrate plus cell-washing (CW) was employed. Serum hemoglobin levels were elevated in the H group but not in the CW group during autotransfusion. Elevated PT and PTT developed in both groups during autotransfusion with return to normal at 24 hr. Serum fibrinogen levels remained normal in the H group but were depressed in the CW group. Fibrin split products were more elevated in the H group than in the CW group. Interestingly, in the CW group total proteins were depressed with a disproportionate loss in the non-albumin fraction. The groups never differed from each other with respect to hematocrit, platelet aggregability, and serum total hemolytic complement levels. Both techniques provided adequate hypocoagulability for autotransfusion. The elevated PT, PTT, fibrin split products ( FSP) and decreased fibrinogen represent a clear picture of disseminated intravascular coagulopathy in the H group. The lesser changes in the CW group suggest that the combination of citrate plus plasmaphoresis kept any intravascular coagulopathy at a more tolerable level in the CW group. The lower plasma hemoglobin levels in the CW group decreased the threat to renal function in the presence of marked hemolysis. These findings suggest that extracorporeal citrate plus cell-washing is an attractive alternative to heparinization of patients for autotransfusion.

Platelet aggregation and haemolysis induced in rats by intravenous infusion of ADP - effect of potentially antithrombotic drugs.

This paper describes a simple experimental model to quantitate the in vivo aggregation of rat platelets induced by ADP and the in vivo effectiveness of compounds with potential anti‐aggregating activity; only drugs known to inhibit in vitro the first phases of platelet aggregation (PGE1, pyrimido‐pyrimidine compounds) were inhibitory in this model; in contrast, acetylsalicylic acid, known to inhibit in vitro the last phases of platelet aggregation, was ineffective; no interaction between pyrimido‐pyrimidine compounds and acetylsalicylic acid was observed. Besides platelet aggregation, ADP also induced a marked haemolysis; the latter was not inhibited by any of the drugs tested.

Experience with mitral heterografts. A clinical study with one-year follow-up.

Thirteen cases with mitral valve disease were operated upon with implantation of aortic pig hetero-grafts, mounted on a stainless steel ring covered with Da-cron. There were 3 early deaths, due to myocardial failure, aortic dissection, and myocardial haemorrhage, respectively. There were 3 late deaths, one due to an embolus, probably from the left atrium, one to graft failure with severe mitral regurgitation and marked haemolysis, and one to sepsis. The cause of the graft failure is unknown. There was no endocarditis in the case with sepsis. The remaining 7 cases were re-investigated with heart cathete-rization and left ventricular angiography. All cases were improved and there was no diastolic gradient over the grafts. In four there were physical or angiographical signs of minimal mitral regurgitation. Among the seven survivors only one presented laboratory findings suggestive of haemolysis.Since the time of re-investigation, an additional four heterograft valve failures have occurred among ths survivors.