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Recombinant glycosylated human interleukin-6 accelerates peripheral blood platelet count recovery in radiation-induced bone marrow depression in baboons.

This report was aimed at confirming the potential clinical use for a genetically engineered glycosylated human interleukin-6 (rhIL-6) in hematopoiesis. Its tolerance and efficacy were assessed on hematopoietic restoration after neutron radiation-induced bone marrow injury on baboons, which represent an adequate model of parallelism for studying hematology in the human. The particular neutron radiation absorption pattern in the body allows the preservation of underexposed bone marrow areas that mimics an autotransplantation-like situation. An initial dose finding study (1 microgram up to 20 micrograms/kg/d for 8 consecutive days) in normal baboons established a dose-dependent response regarding the peripheral platelet count (range of increase, 1.5- to 4-fold). A significant elevation in white blood cell (WBC) count, as well as a substantial reversible normochromic normocytic anemia, were observed for the highest doses only (10 and 20 micrograms/kg/d). All rhIL-6 administered doses were clinically well tolerated. In myelosuppressed baboons, a selected dose of 10 micrograms/kg/d of rhIL-6 for 13 consecutive days significantly lessened the degree of induced thrombocytopenia as compared with the control group (P = .01) and shortened the time to occurrence of the nadir, showing that the onset of recovery occurs much earlier, ie, an average of 5 days (P = .003), in the treated group. Moreover, this accelerated platelet recovery is evidenced by an 8-day shorter mean time back to baseline values (P = .03) in the rhIL-6--treated animals. At this dose no effect was observed on the WBC recovery pattern. Importantly rhIL-6 did not accentuate the radiation-induced anemia and was clinically well tolerated. All tested monkeys recovered from their induced pancytopenia and no animal loss was recorded. IL-6, tumor necrosis factor, and IL-1 blood measurements are reported. In conclusion, rhIL-6 is a potent thrombopoietic factor for the treatment of induced thrombocytopenia in nonhuman primates at a clinically well-tolerated dose.

Animals↗

The peripheral platelet count in response to intravenous infusion of isoprenaline.

5 healthy male volunteers received i.v. infusions of isoprenaline in doses of 0.03, 0.06 and 0.09 mug X kg-1 X min-1 over a period of 6 min. A statistically significant decrease in the peripheral platelet count was obtained, but no dose-response-curve for isoprenaline was observed. It is suggested that while an i.v. infusion of epinephrine causes a release of platelets from the exchangeable splenic platelet pool, isoprenaline might have the opposite effect on the spleen, thereby causing a decrease of platelets in the peripheral blood.

Adult↗

No correlation between site of breakpoint in the BCR gene and platelet counts in Philadelphia chromosome-positive CML.

In chronic myelogenous leukemia (CML) malignant cells are characterised by the Philadelphia chromosome (Ph), resulting from a translocation t(9;22). The position of the breakpoint within the major breakpoint cluster region (M-bcr) on chromosome 22 has been shown to correlate with the clinical course of the disease or, more recently, thrombopoietic activity. We have therefore determined the breakpoint localisation in 53 Ph-positive CML patients. Following the 5'/3'-region definition of Inokuchi et al. Leukemia Research 15, 1067 (1991) [1], 22 of our patients have 5' and 31 of our patients have 3' orientated breaks. No correlation was found between platelet counts and breakpoint localisation.

Chromosome Aberrations↗

[Correlation of serum IgA levels with serum IgG levels, erythrocyte sedimentation rate and platelet counts in 98 patients with rheumatoid arthritis].

Rheumatoid arthritis (RA) is an autoimmune disease with unknown etiology. Polyclonal B cell activation (PBA) is one of immunological abnormalities commonly found in RA patients. We examined serum IgG, IgA, IgM levels in 98 RA patients and compared 31 patients with high serum IgA levels (group B) with 67 patients with normal serum IgA levels (group A) in clinical background. Group B patients had significantly higher mean values of serum IgG levels, erythrocyte sedimentation rate (ESR), and platelet counts than group A. However, there was no correlation between serum IgA levels and X-ray stage, class of ADL or disease duration of RA. These results indicate that high serum IgA levels reflect for disease activity of RA. Serum IgA levels did not correlate with interleukin (IL)-6 levels in 53 RA patients studied. It is speculated that high serum IgA levels might be caused by the following evidences 1) that transforming growth factor (TGF) beta, a known cytokine to increase IgA production by human splenic B cells, gene expression is enhanced in mononuclear cells from synovial fluid and 2) that iron deposition is found in RA synovial and high serum IgA levels are found in iron overload like thalassemia intermedia.

Arthritis, Rheumatoid↗

Chronic myeloproliferative diseases with an elevated platelet count (in excess of 1,000,000/microliter): a clinicopathological study on 46 patients with special emphasis on primary (essential) thrombocythemia.

A clinicopathological study was performed on 46 patients with chronic myeloproliferative diseases (CMPD) showing a thrombocythemia in excess of 1,000 x 10(9)/liter. When applying rigid diagnostic criteria only 23 patients were compatible with the initially suspected diagnosis of primary thrombocythemia (PTH). Comparison of PTH with the other entities of CMPD (CGL, 10, AMM, 6, and polycythemia, 7 cases) revealed a sustained elevation of the platelet count observable over a period of 2 to 8 years, no marked leukocytosis or abnormalities of the differential blood count, and a normal score of the leukocyte alkaline phosphatase. Episodes of hemorrhage and thrombosis as well as neurological symptoms (paresthesias, dizziness, headache), were encountered frequently as clinical manifestations in PTH. Survival time in PTH was significantly longer than in CGL with accompanying thrombocythemia. In a consecutively biopsied population of patients with CMPD, incidence of PTH was about 8%. In PTH the characteristic histopathology of the bone marrow consisted of an isolated (monolinear) proliferation of the megakaryocytes (density 127 +/- 47/mm2) without gross abnormalities of this cell lineage or a conspicuous increase in neutrophilic granulo- or erythrocytopoiesis. These lesions are significantly different from the morphological findings in the other CMPD with extreme thrombocytosis.

Actuarial Analysis↗

Splenectomy for adult patients with idiopathic thrombocytopenic purpura: a systematic review to assess long-term platelet count responses, prediction of response, and surgical complications.

Splenectomy has been a standard treatment for adult patients with idiopathic thrombocytopenic purpura (ITP) for more than 50 years. However, the durability of responses, the ability to predict who will respond, and the frequency of surgical complications with splenectomy all remain uncertain. To better interpret current knowledge we systematically identified and reviewed all 135 case series, 1966 to 2004, that described 15 or more consecutive patients who had splenectomy for ITP and that had data for 1 of these 3 outcomes. Complete response was defined as a normal platelet count following splenectomy and for the duration of follow-up with no additional treatment. Forty-seven case series reported complete response in 1731 (66%) of 2623 adult patients with follow-up for 1 to 153 months; complete response rates did not correlate with duration of follow-up (r = -0.103, P = .49). None of 12 preoperative characteristics that have been reported consistently predicted response to splenectomy. Mortality was 1.0% (48 of 4955 patients) with laparotomy and 0.2% (3 of 1301 patients) with laparoscopy. Complication rates were 12.9% (318 of 2465) with laparotomy and 9.6% (88 of 921 patients) with laparoscopic splenectomy. Although the risk of surgery is an important consideration, splenectomy provides a high frequency of durable responses for adult patients with ITP.

Adult↗

Reticulated platelet counts in the assessment of thrombocytopenic disorders.

Reticulated platelets (RP) are the youngest platelets in the circulation and can be measured by analysing the RNA content of platelets from whole blood or platelet-rich plasma by flow cytometry. Increased RP are indicative of increased production of platelets. Despite the current lack of standardization for the measurement of RP, it is useful in the assessment of patients with ITP by aiding the distinction of these patients from those with decreased platelet production. RP counts also have a role in the assessment of the complicated patient with multiple possible aetiologies for thrombocytopenia. Measurement of the RP count may hold predictive value for marrow recovery following myelosuppressive or myeloablative chemotherapy, and may play a role in monitoring the administration of the various thrombopoietins currently under clinical trial.

Blood Platelets↗

Increased prothrombin time and platelet counts in living donor right hepatectomy: implications for epidural anesthesia.

The risks and benefits of adult-to-adult living donor liver transplantation need to be carefully evaluated. Anesthetic management includes postoperative epidural pain relief; however, even patients with a normal preoperative coagulation profile may suffer transient postoperative coagulation derangement. This study explores the possible causes of postoperative coagulation derangement after donor hepatectomy and the possible implications on epidural analgesia. Thirty donors, American Society of Anesthesiology I, with no history of liver disease were considered suitable for the study. A thoracic epidural catheter was inserted before induction and removed when laboratory values were as follows: prothrombin time (PT) > 60%, activated partial thromboplastin time < 1.24 (sec), and platelet count > 100,000 mmf pound sterling (mm3). Standard blood tests were evaluated before surgery, on admission to the recovery room, and daily until postoperative day (POD) 5. The volumes of blood loss and of intraoperative fluids administered were recorded. Coagulation abnormalities observed immediately after surgery may be related mostly to blood loss and to the diluting effect of the intraoperative infused fluids, although the extent of the resection appears to be the most important factor in the extension of the PT observed from POD 1. In conclusion, significant alterations in PT and platelet values were observed in our patients who underwent uncomplicated major liver resection for living donor liver transplantation. Because the potential benefits of epidural analgesia for liver resection are undefined according to available data, additional prospective randomized studies comparing the effectiveness and safety of intravenous versus epidural analgesia in this patient population should be performed.

Adult↗

B-cell subsets and platelet counts in HIV-1 seropositive subjects.

A subset of B lymphocytes positive for the CD5 antigen have been implicated in several autoimmune disorders. To investigate their role in human immunodeficiency virus type 1 (HIV-1) infection, we studied peripheral-blood B and T lymphocytes from HIV-1-positive patients with (n = 13) and without (n = 18) thrombocytopenia, 8 patients with classic autoimmune thrombocytopenia, and 16 healthy controls. The proportion of CD5-positive B cells was significantly higher in the HIV-1-positive thrombocytopenic patients than in the healthy controls, as a result of both higher numbers of CD5-positive B cells and lower numbers of CD5-negative B cells. Platelet count was positively correlated with CD5-negative B-cell count (r = 0.6, p less than 0.001) and negatively correlated with proportion of B cells that were CD5 positive (r = -0.5, p less than 0.01) among the HIV-1-positive patients. The high concentrations of IgM-containing immune complexes in HIV-1-positive patients with autoimmune disorders may be due to changes in the CD5-positive B-cell subset.

Adult↗

On-site prothrombin time, activated partial thromboplastin time, and platelet count. A comparison between whole blood and laboratory assays with coagulation factor analysis in patients presenting for cardiac surgery.

BACKGROUND: Although available hemostasis assays from institutional laboratories permit an analytical approach to diagnosis and treatment of coagulation disorders following cardiopulmonary bypass, their clinical utility has been limited by delays in obtaining results. The development of instrumentation for on-site testing allows rapid return of results. This study was designed to compare whole blood (WB) results obtained from on-site coagulation assays with values provided by our institutional laboratory (LAB). METHODS: After Institutional Human Studies Committee approval, 362 patients presenting for cardiac surgery requiring cardiopulmonary bypass were enrolled in this study. Prothrombin time (PT), activated partial thromboplastin time (aPTT), and platelet count (PLT) assays were performed in both WB and LAB systems. PT, aPTT, and PLT measurements were compared between WB and LAB assays using blood specimens obtained from at least two time points for each patient. Normal range values for both PT and aPTT methods were determined by using measurements from a normal reference population. Coagulation factor levels were measured in a subset of patients to characterize the response of PT and aPTT assays to individual and multiple factor levels. To employ Bayes' theorem and calculate predictive indexes (e.g., sensitivity, specificity), the disease or factor deficiency was determined using factor levels. Predictive indexes were used to evaluate the ability of PT and aPTT assays to identify factor deficiency. RESULTS: PLT counts were similar between systems. Linear regression and bias analysis demonstrated similar results for WB and LAB PT and discordant results for aPTT measurements. Both PT assays had a similar normal range, whereas a wider distribution of results was evident for the WB aPTT normal range. Although statistically greater slopes for factor:aPTT regressions were observed for the WB system, WB aPTT correlated better with factor V and with factor V, VIII, and XII levels (multivariate linear regression). Diagnostic performance for factor levels less than 0.3 and 0.4 U/ml was similar for both WB and laboratory PT and aPTT assays. WB and LAB PT and aPTT assays performed similarly in detecting factor deficiency in the period after cardiopulmonary bypass. CONCLUSIONS: WB PT and PLT values correlate well with those obtained from the LAB. The discrepancy between measurement systems in aPTT values is probably a reflection of both different normal ranges and responsiveness to factor deficiency. These WB assays provide coagulation results that can accurately identify patients with quantitative deficiencies in platelets and coagulation factors.

Adult↗

A possible correlation between the type of bcr-abl hybrid messenger RNA and platelet count in Philadelphia-positive chronic myelogenous leukemia.

The Philadelphia (Ph1) chromosome, in which the hybrid bcr-abl gene is formed, is thought to be the initial event in chronic myelogenous leukemia (CML). The position of the breakpoint within the breakpoint cluster region (bcr) on Ph1 chromosome and the splicing pattern determine the species of the fused bcr-abl messenger RNA (mRNA). We tried to detect the two types of fused mRNAs in 57 chronic-phase cases of Ph1-positive CML using the polymerase chain reaction procedure (RT-PCR). The bcr exon 2/abl exon 2 fused mRNA (b2-a2) was detected in 17 patients, the bcr exon 3/abl exon 2 fused mRNA (b3-a2) was detected in 34 patients, and both types of mRNA were detected in six patients. The platelet counts of patients who expressed b3-a2 mRNA or both types were significantly higher than those of patients who expressed only b2-a2 (841.5 v 373.5 x 10(9)/L; P less than .015), although there was no significant difference in the white blood cell counts or hemoglobin. This finding suggests a possibility that the type of bcr-abl mRNA may affect the thrombopoietic activity in CML.

Base Sequence↗

Effects of melagatran, an inhibitor of thrombin, on fibrin deposits, haemodynamics, and platelet count in endotoxaemic pigs.

BACKGROUND: Thrombin plays a pivotal role in the development of septic shock. Porcine endotoxaemia can replicate this condition. We wanted to evaluate whether melagatran, a novel inhibitor of thrombin, would counteract some of the endotoxin-induced changes in this model. METHODS: Fifteen pigs were anaesthetised, monitored (circulatory and respiratory variables) and subjected to an infusion of E. coli endotoxin at 10 microg x kg(-1) x h(-1). Six pigs were given melagatran during the first 3 h of the 6-h endotoxaemic period. Nine controls were given the corresponding volume of saline instead of melagatran. Specimens from the liver and the left lung were taken for light microscopy post mortem. RESULTS: The endotoxin-induced increase in pulmonary capillary wedge pressure and drop in platelet count were significantly less pronounced in the melagatran-treated pigs. Deposits of pulmonary fibrin were significantly reduced in the melagatran group, without improving oxygenation. Light microscopy revealed no hepatic fibrin in the pigs treated with melagatran in contrast to the endotoxaemic controls. Hepatic neutrophil accumulation was reduced in the melagatran group as compared to controls. Hepatocellular degeneration and plasma levels of tumour necrosis factor alpha (TNF alpha) and bilirubin were of the same magnitude in both groups. CONCLUSION: Melagatran reduced pulmonary capillary wedge pressure, a retrograde reflection of the left ventricular end-diastolic filling pressure, and also pulmonary stasis in pigs subjected to endotoxaemic challenge. Pulmonary and hepatic fibrin depositions were reduced, but PaO2 levels or liver function markers were not affected by melagatran during the early phase of endotoxaemia. Obstruction of the intrahepatic bile ducts, by fibrin depositions, is not responsible for reduced excretion of conjugated bilirubin during endotoxaemia. The beneficial effects of melagatran during endotoxaemia were not due to any reduction of plasma TNF alpha.

Animals↗

Recombinant human leukemia inhibitory factor induces acute phase proteins and raises the blood platelet counts in nonhuman primates.

Recombinant human leukemia inhibitory factor (rhLIF) produced by Escherichia coli was administered subcutaneously (sc) to rhesus monkeys at doses of 2, 10, and 50 micrograms/kg body weight/d for 14 days to assess its biologic activities in vivo. Serum levels of positively regulated acute phase proteins (APP) (C-reactive protein, alpha 1-antitrypsin, haptoglobin, and ceruloplasmin) were increased, whereas the negatively regulated APP prealbumin decreased in response to rhLIF treatment. During the second week of treatment, blood platelet counts began to increase, resulting in a maximum of a twofold increase above normal levels a week after termination of the rhLIF treatment. No changes were seen in total and differential white blood cell counts in blood progenitor levels and in red blood cell numbers. The low- and medium-dose rhLIF treatments were tolerated without significant side effects. The animals treated with the high dose showed a reduction in body weight of approximately 10%. In conclusion, rhLIF was shown to stimulate APP and to increase the number of platelets in circulation in nonhuman primates.

Acute-Phase Proteins↗

Association of increased serum heat shock protein 70 and C-reactive protein concentrations and decreased serum alpha(2)-HS glycoprotein concentration with the syndrome of hemolysis, elevated liver enzymes, and low platelet count.

The primary aim of this study was to determine serum Hsp70 concentrations in HELLP syndrome. We measured also the serum concentrations of three acute phase proteins: C-reactive protein (CRP), alpha(2)-macroglobulin (AMG) and alpha(2)-HS glycoprotein (AHSG). Ten severe preeclamptic patients with HELLP syndrome, 20 severe preeclamptic patients without HELLP syndrome and 20 normotensive, healthy pregnant women were included in this case-control study. Serum concentrations of Hsp70, CRP, AMG and AHSG were measured using an enzyme-linked immunosorbent assay (Hsp70), particle-enhanced immunoturbidimetric assay (CRP) and radial immunodiffusion (AMG, AHSG). The serum Hsp70 and CRP concentrations were significantly higher, whereas the serum AHSG concentration was significantly lower in the HELLP group (H) than the severe preeclamptic (P) and control (C) groups (median (25-75 percentile); Hsp70: 2.02 ng/ml (0.76-2.23) (H) versus 0.54 ng/ml (0.47-0.79) (P), p<0.01, and 0.30 ng/ml (0.27-0.33) (C), p<0.001; CRP: 43.9 mg/l (27.1-84.5) (H) versus 6.5 mg/l (2.7-10.7) (P), p<0.001, and 2.5 mg/l (1.1-6.7) (C), p<0.001; AHSG: 588 microg/ml (492-660) (H) versus 654 microg/ml (576-768) (P), p<0.05, and 738 microg/ml (666-804) (C), p<0.01, respectively). The serum AMG concentration did not differ between the study groups. In the HELLP group, there was a statistically significant negative correlation between serum Hsp70 concentration and platelet count (Spearman R=-0.69, p=0.026). In conclusion, serum Hsp70 and CRP concentrations are increased, whereas serum AHSG concentration is decreased, in HELLP syndrome. The maternal systemic inflammation seems to be more pronounced in HELLP syndrome than preeclampsia without HELLP syndrome, as suggested by the alterations in serum CRP and AHSG levels. However, it requires further investigation to determine whether these changes are causes or consequences of the disease.

Adult↗

Severe ADAMTS13 deficiency in adult idiopathic thrombotic microangiopathies defines a subset of patients characterized by various autoimmune manifestations, lower platelet count, and mild renal involvement.

The significance of ADAMTS13 deficiency in adult thrombotic microangiopathy (TMA) remains controversial. In an attempt to define the characteristics of adult TMA with severe ADAMTS13 deficiency, we determined 2 groups of patients on the basis of ADAMTS13 activity (undetectable or detectable). Clinical presentation, laboratory values, autoimmune manifestations, and outcome were compared between the groups. Patients were included retrospectively from 12 centers. All fulfilled the diagnosis criteria of TMA. Patients with a history of transplantation, cancer and chemotherapy, and Centers for Disease Control and Prevention (CDC) stage C human immunodeficiency virus (HIV) infection were not included. Forty-six patients were included. Thirty-one patients had an undetectable ADAMTS13 activity (<5%), and the remaining 15 patients had ADAMTS13 activity of >25%. Severe ADAMTS13 deficiency was associated with a plasmatic inhibitor in 17 cases (55%), suggesting an immune-mediated mechanism. Patients with undetectable ADAMTS13 were more frequently of Afro-Caribbean origin than patients with detectable ADAMTS13 activity (48.4% vs 13.3%, respectively; p = 0.03). As opposed to patients with detectable ADAMTS13 activity, patients with severe ADAMTS13 deficiency displayed various autoimmune manifestations that consisted of nondestructive polyarthritis (4 cases) associated in 1 case with malar rash and extramembranous glomerulonephritis, discoid lupus (3 cases), and autoimmune endocrinopathies, Raynaud phenomenon, and sarcoidosis-like disease (1 case each). In patients with severe ADAMTS13 deficiency, antinuclear antibodies, anti-double-stranded DNA antibodies, and anticardiolipin antibodies were positive in 22 (71%) cases, 3 (9.7%) cases, and 1 (3.2%) case, respectively. One patient fulfilled the criteria for the diagnosis of systemic lupus erythematosus. During follow-up, 1 patient with severe ADAMTS13 deficiency developed antinuclear antibodies, and 3 others developed anti-double-stranded DNA antibodies, in association with neurologic manifestations and anticardiolipin antibodies in 1 case. Patients with severe ADAMTS13 deficiency also had a lower platelet count (12 x 10(9)/L; range, 2-69 x 10(9)/L) and less severe renal failure (estimated glomerular filtration rate: 78 mL/min; range, 9-157 mL/min) than patients with detectable ADAMTS13 activity (49.5 x 10(9)/L; range, 6-103 x 10(9)/L; p = 0.0004, and 15.8 mL/min; range, 5.6-80 mL/min; p < 0.0001, respectively). End-stage renal failure occurred in 1 patient with severe ADAMTS13 deficiency and in 3 patients with detectable ADAMTS13 activity (3.2% vs 21.4%, respectively; p = 0.08). Flare-up and relapse episodes and survival were comparable between the groups. Taken together, these data indicate that adult idiopathic thrombotic thrombocytopenic purpura, as defined by severe ADAMTS13 deficiency, may occur preferentially in a particular ethnic group, and is characterized by severe thrombocytopenia, mild renal involvement, and a wide spectrum of autoimmune manifestations that may be completed during follow-up. Indeed, apparently idiopathic thrombotic thrombocytopenic purpura may be considered a specific autoimmune disease.

ADAM Proteins↗

Curasan PRP kit vs. PCCS PRP system. Collection efficiency and platelet counts of two different methods for the preparation of platelet-rich plasma.

An important reason to improve methods of isolating platelet-rich plasma (PRP) is the potential use of autologous thrombocyte growth factors. In addition to discontinuous cell separation, two methods for extracting PRP that can be performed directly by the surgeon are now available. This study compared the suitability of these two methods for the preparation of PRP. Whole blood was drawn from 47 healthy donors (18 men, 29 women) aged 20-59 years (mean 29.9, SD 7.7). For each donor, PRP was separated by the PCCS method (PCCS Kit, 3i Implant Innovations, Palm Beach Gardens, FL, USA) and by the Curasan method (analogous to the PRP kit, Curasan, Kleinostheim, Germany). Thrombocyte counts differed significantly (sign test P = 0.001) between the donor blood (mean 290,000/ micro l, SD 86,000/ microl), the PCCS PRP preparation (mean 2,209,000/ microl, SD 901,000/ microl), and the Curasan PRP (mean 1,075,000/ micro l, SD 636,000/ microl). The correlation between the thrombocyte count in the PRP and the thrombocyte count in the donor whole blood was greater for the PCCS PRP (Spearman's correlation coefficient rS = 0.60) than for the Curasan PRP (r(S) = 0.34). A slight, clinically irrelevant, influence of gender on thrombocyte concentration in whole blood was found, but no influence of age was detected.

Adult↗

Hepatic histopathologic condition does not correlate with laboratory abnormalities in HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count)

OBJECTIVE: Our objective was to categorize the histologic findings in the liver in patients with HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count) and to correlate these findings with the severity of clinical laboratory abnormalities. STUDY DESIGN: Eleven patients with laboratory criteria for HELLP syndrome who required cesarean delivery underwent needle biopsy of the liver under direct visualization. RESULTS: Eight patients had periportal hemorrhage, and six had fibrin deposition. Fatty infiltration was seen in four, one with large-droplet fat, three with microvesicular fat. There was no statistically significant correlation between the severity of the histologic findings of periportal hemorrhage and fibrin deposition and the clinical laboratory findings. Fatty infiltration did not correlate with the severity of the HELLP syndrome's histologic condition, but, in contrast, did correlate with thrombocytopenia and aminotransferase elevations. CONCLUSIONS: Laboratory abnormalities do not accurately reflect the severity of the underlying histopathologic condition in HELLP syndrome. We propose that all patients with HELLP syndrome, regardless of the degree of their laboratory abnormalities, be treated aggressively, primarily with delivery.

Adolescent↗