Hematological Findings In Patients Research Articles

Study of clinical profile of physiological and hematological findings in patients with chronic bronchitis and emphysema with cardiac complications

Introduction: Chronic bronchitis is a symptom of chronic obstructive pulmonary disease (COPD). Chronic bronchitis is one of a number of lung conditions included in this group. These conditions can obstruct lung airflow and lead to breathing issues. Chronicbronchitis and emphysema are the 2 most prevalent diseases associated with COPD. Method: The investigation was carried out at the Government Medical College in Jagdalpur, Chhattisgarh's Bastar district. Cross sectional study was the method used. 32 subjects in all were enrolled in this investigation. The participants in the study ranged in age from 35 to over 70. Each person who was a part of this study signed an informed consent form. In this study, people between the ages of 35 and beyond 70 were included. Result: In comparison to female individuals, male subjects were more. More than 50% of participants reported having trouble breathing, while 12(37.5%) of them also reported having chest pain. In addition, 15 of the subjects displayed indications of tachypnea, while 10 of them had tachycardia, and 7 of them had cyanosis. Twenty patients had neutrophilia, ten had lymphocytosis, two had eosinophilia, and just one had leucocytosis.

Clinical joints manifestations in patients with psoriatic arthritis on musculoskeletal ultrasound

To investigate the clinical joints manifestations under musculoskeletal ultrasound (MSUS) and hematological findings in patients with psoriatic arthritis (PsA), which may provide a basis for improving the early diagnosis of PsA. From September 2016 to February 2021, 328 patients with psoriasis visited the dermatological and rheumatic outpatient of the Beijing Friendship Hospital were enrolled in this retrospective study. Patients were enrolled according to a paired-design method. The PsA group included 164 patients diagnosed with PsA, and the control group included 164 patients diagnosed with psoriasis without PsA. Both groups of patients were evaluated by a rheumatoid immunologist, a dermatologist, and a sonographer. Demographic data, course of disease, severity of skin lesions, combined diseases, and previous treatment were all collected. All patients received MSUS and blood examinations. Lower extremity enthsis diseases were evaluated by Glasgow ultrasound enthesitis scoring system (GUESS). In the comparison of baseline clinical characteristics, the PsA group has longer course of psoriasis (P = 0.005), longer course of joints pain (P = 0.035), higher incidence of peripheral joints pain (P = 0.001), higher GUESS score (P < 0.001), and higher incidence of involved nails or toenails (P = 0.036) The most common joints involved were proximal interphalangeal joint (33.5%), knee (27.4%), and metacarpophalangeal joint (25.0%). Differences in clinical manifestations at different lower limb enthesitis on MSUS have also been proved. The positive incidences of rheumatoid factor (RF) (P = 0.002) and anti-cyclic citrullinated peptide (CCP) antibody (P < 0.001) in the PsA group were significantly higher than those in the control group. Binary Logistic regression showed that patients with anti-CCP antibody positive had a higher risk of active PsA compared to patients with negative antibodies in PsA group (OR: 0.626, 95%CI: 0.361-0.792, P < 0.05). In conclusion, the most common joints involved were proximal interphalangeal joint, knee, and metacarpophalangeal joint in patients with PsA, and the common types of diseased joints manifestations on MSUS were synovial thickening, fluid accumulation, bone destruction, increased blood flow signals, and attachment site inflammation. GUESS scoring systems can be used to identify PsA in patients with psoriasis. Psoriasis patients with RF and anti-CCP antibody positive were more likely to develop PsA, and anti-CCP antibody positive was a risk factor for active PsA. • GUESS scoring systems can be used to identify PsA in patients with psoriasis. • Psoriasis patients with RF and anti-CCP antibody positive were more likely to develop PsA, and anti-CCP antibody positive was a risk factor for active PsA.

Does Anemia Have a Potential Effect on Type 2 Hepatorenal Syndrome?

Background/Aims. Hepatorenal syndrome (HRS) is a form of functional renal failure arising in advanced cirrhosis and is characterized by a poor survival rate. Anemia is frequently observed during the clinical course of cirrhosis. Our study aimed to investigate the hematologic findings in patients with cirrhosis to determine the effects of anemia on renal functions in type 2 HRS and if it was a potential aggravating factor. Materials and Methods. This prospective study, in which all consecutive patients with cirrhosis were enrolled, was performed at a tertiary-level hospital (Military Hospital of Tunis) from January 2019 to June 2019. A total of 9 patients with HRS fulfilled the type 2 HRS diagnostic criteria, and 41 patients with cirrhosis without HRS were included. All data regarding patients were obtained from the medical record. Demographic data, routine hemograms, biochemical, and urinary test results were collected. Models of end-stage liver disease (MELD) and Child–Turcotte–Pugh (CTP) scores were calculated. Results. The most common etiology of cirrhosis was viral hepatitis (66%). According to the CTP score, 23 patients were in the CTP-A stage, 13 in the CTP-B stage, and 14 patients were in the CTP-C stage. Patients with type 2 HRS had significantly lower hemoglobin levels compared with non-HRS stable cirrhosis patients. As hemoglobin levels decreased, renal function worsened on patients with type 2 HRS. Patients with lower hemoglobin levels had poor prognosis and survival compared with patients with higher hemoglobin levels. Logistic regression analysis showed that lower hemoglobin levels and higher MELD and CTP scores were statistically significant for an onset of type 2 HRS. Conclusion. Renal dysfunction is a frequent complication in patients with end-stage chronic liver disease. The role of anemia in aggravating HRS in patients with cirrhosis is explained by hypoxia that can lead to microcirculatory renal ischemia. Other studies are required to determine if anemia is a precipitant factor for HRS or not.

Hematological Findings in Patients with Acute Peripheral Facial Palsy.

This study aimed at evaluating the clinical significance of hematological findings in patients with acute peripheral facial palsy. For this retrospective case series review, 84 patients who visited our university hospital and were diagnosed with Bell's palsy (BP) or Ramsay Hunt syndrome (RHS) between March 2017 and March 2019 were enrolled. We documented their epidemiological details, final diagnoses, House-Brackmann (HB) palsy grades, and pretreatment and day 7 post-hospitalization complete blood counts. The outcome was considered favorable if the HB grade at weeks 10-16 was I or II. We analyzed the hematological findings in terms of diagnosis and the final treatment outcomes. A higher pretreatment neutrophil-to-lymphocyte ratio (NLR) and neutrophil count and a lower day-7 lymphocyte count were observed in patients with RHS with unfavorable outcomes. In such patients, moderate positive correlations were observed between the pretreatment white blood cell, neutrophil, and basophil counts; the NLR and basophil-to-lymphocyte ratio; and the initial HB grade. Only the latter was a significant risk factor for a poor treatment outcome. In patients with BP, both the initial HB grade and the pretreatment eosinophil count were included in a regression model predicting prognosis. Inflammation plays an important role in RHS pathogenesis. Initial RHS severity and the response to corticosteroids may determine the final treatment outcome. However, inflammatory markers do not predict all BP outcomes; BP may be etiologically heterogeneous.

Coexistence of B-Cell Dyscrasia with Large Granular Lymphocytic Leukemia

Large granular lymphocytic leukemia (LGLL) is an indolent disease and often associated with autoimmune disorders such as rheumatoid arthritis. The association of humoral immune disorders resulting from abnormal B cell activity, may affect original LGLL pathogenesis, clinical presentation and management through modifying disease presentation, progression and/ or resistance to standard care. Coexistence of T cell LGL leukemia with B cell abnormalities has previously been identified in the literature although described in sporadic case reports. However, no large case series or cohorts have been collected so far to study the frequency of the B-cell dyscrasia (BCD) associated with LGLL and describe clinical/ hematological findings in patients with this co-association. Here, we conducted a retrospective review of patients diagnosed with LGL leukemia at The Cleveland Clinic Foundation to search for any associated BCDs. We then classified our population into 2 groups: LGLL with BCD vs. LGLL without BCD, and comprehensively compared them for baseline, clinical and molecular characteristics. A total of 244 T-LGL patients were collected and studied. All cases were uniformly diagnosed with LGLL if 3 out of 4 following criteria were fulfilled, including: 1) LGL count &gt;500/µL in blood for more than 6 months; 2) presence of abnormal CTLs expressing CD3, CD8 and CD57 by flow cytometry; 3) preferential usage of a TCR Vβ family by flow cytometry; 4) TCR gene rearrangement by PCR. Molecular studies including targeted deep sequencing for STAT3mutations were performed. Bone marrow biopsy results were reviewed to exclude other conditions. Endpoints of the study were death or lost to follow up. In our cohort, we found a frequent manifestation of humoral immune system abnormalities. We identified coexisting BCD in 45% (109/ 244) of LGLL patients, of whom 28 (11.2%) had monoclonal gammopathy of unknown significance (MGUS), and 13 (5.2%) had chronic lymphocytic leukemia (CLL/SLL). Six LGLL patients had multiple myeloma (2.4%). Moreover, polyclonal hypergammaglobulinemia (n=28, 11.2%) or hypogammaglobulinemia (n=14, 5.6%) was reported in 42 LGLL-patients (16.8%). The frequency of other disorders of B-cell origin was also examined. The total incidence of B-cell abnormalities in our LGLL cohort was 45%. Indeed an heterogeneous appearance of other B-cell disorders was observed including mantle cell lymphoma (n=2), DLBCL (n=6), marginal zone lymphoma (n=3), Waldenstrom's macroglobulinemia (n=1), Burkitt's lymphoma (n=1), indolent lymphoma (n=1), Hodgkin's lymphoma (n=1), non-Hodgkin's lymphoma (n=3), neck lymphoma (n=1), and smoldering myeloma (n=2). Patient with LGLL-BCD were older as compared to the ones without (median age: 62 vs. 63 years; ≥60 years: 57% vs. 69%, respectively), although the difference was not statistically significant (P=0.07). Gender was equally distributed (male: 54%, n=132; female: 46%, n=112) in patients who developed BCD. Conventional cytogenetics showed that patients without BCD were more often associated with abnormal cytogenetics (24%, n=9) as compared to LGLL-BCD (9%, n=5). Interestingly, BCD was found in 55 men and 54 women in whom only 6 patients had NK-LGLL while the remaining (n=103 patients) had T-LGLL suggesting a higher association with LGLL of T- rather than of NK-cell origin. Leukopenia was observed in 25/109 patients, with average absolute lymphocytes of 4.18 k/µL and LGL count of 2333 k/µL. Blood count showed: neutropenia in 44, anemia in 65, and thrombocytopenia in 29 out of 109 LGLL patients with BCD. TCR rearrangements were seen in 74 while somatic STAT3 mutations were observed in 37 LGLL patients while more enriched (44%, n=52) in LGLL without BCD. The association of other autoimmune conditions e.g., rheumatoid arthritis, was not different between the two groups (15% vs. 16% in LGLL with BCD vs. without; P=0.8). In sum, our investigation shows that BCD were frequent in LGLL and coexisted in 45% of the patients, commonly in the form of MGUS, and/ or hypergamaglobulinemia. Perhaps, the co-association of B-cell pathology with LGLL suggests that the two diseases either share pathogenetic driving mechanisms to enhance both B cells and T cells clones or that immunological dysfunction in setting of B cell dyscrasia could trigger/potentiate LGL expansion and/or transformation in this context. Disclosures No relevant conflicts of interest to declare.

Metastasis of solid tumors into bone marrow – Single center experience

Introduction: Metastases of solid tumors to the bone marrow are rarely reported. Clinical manifestation and laboratory findings remain uncharacteristic and lead to misdiagnosis. Detection of bone marrow metastases may have an impact on therapeutic decisions and is usually associated with poor prognosis. Aim: To characterize clinical picture and hematological findings in patients with bone marrow metastasis. Material and methods: We retrospectively reviewed medical records of patients with bone marrow metastases who were primary misdiagnosed with hematological malignancies. Results: Ten patients at median age of 51 years at diagnosis were included. There were following findings on admission: duopenia (n=7), pancytopenia (n=1), anemia (n=1) and skeletal lytic lesions (n=1). The diagnosis of prior cancer was reported in 3 patients and included multiple myeloma, breast cancer and oligoastrocytoma. Clinical manifestations were hepatomegaly (n=4), lymphadenopathy (n=4), skin pallor (n=3), cachexia (n=2) and hemorrhagic diathesis (n=2). Imaging studies revealed diffuse bone lesions (n=5), pulmonary infiltrates (n=2) and liver masses (n=2). Leukoerythroblastosis was demonstrated in 4 cases. Bone marrow aspirate detected the presence of abnormal cell population in 4 patients. In all studied patients a final diagnosis was established by immunohistochemistry of bone marrow biopsy. The following malignancies were detected: prostate adenocarcinoma (n=2), anaplastic microcellular carcinoma of unknown origin (n=2), adenocarcinoma of unknown origin (n=2), Ewing's sarcoma (n=1), breast cancer (n=1), clarocellular renal cancer (n=1) and neuroendocrine tumor (n=1). Nine out of the 10 metastatic patients died shortly after chemotherapy. Conclusions: Unexplained hematological abnormalities should arise the suspicion of bone marrow metastases.

Clinical and Laboratory Hematologic Findings in Patients Receiving Repeated-Dose Injectable HPBCD-Diclofenac for Acute Postoperative Pain: Pooled Analysis of Two Randomized Controlled Phase III Clinical Trials

Objective: While the non-steroidal anti-inflammatory drugs (NSAIDs) represent an important option for the management of acute postoperative pain, their use can be limited due to potential safety concerns, including bleeding risks. This study examined the bleeding-related safety of injectable diclofenac formulated with hydroxypropyl-β-cyclodextrin (HPβCD-diclofenac) when used for postoperative pain management. Methods: Data from two randomized, double-blind, placebo- and active comparator-controlled phase III trials were pooled. Patients in both studies received HPβCD-diclofenac, placebo, or the active comparator ketorolac via intravenous injection every 6 hours for ≤ 5 days following abdominal/pelvic or orthopedic surgery. Bleeding adverse events (AEs) were evaluated through the treatment period and follow-up (≤ 37 days), and relative bleeding AE risks (RR) were estimated. Changes in hematology laboratory values were also assessed. Results: Overall, 608 surgical patients received ≥ 1 dose of study medication. Bleeding AEs occurred in n=9/318 (2.8%) patients receiving HPβCD-diclofenac, n=8/142 (5.6%) patients receiving ketorolac, and n=4/148 (2.7%) patients receiving placebo. Over the period examined, HPβCD-diclofenac was not associated with increased bleeding AE RR versus placebo (1.05 [0.33, 3.35]; p=0.93), nor was ketorolac (2.08 [0.64, 6.77]; p=0.22). Bleeding AEs were predominantly mild or moderate in severity. No treatment-related bleeding AEs occurred in the HPβCDdiclofenac group (1 in both the placebo and ketorolac groups). Among the subset of patients receiving concomitant anticoagulants, bleeding AEs occurred in n=3/60 (5.0%) patients receiving HPβCD-diclofenac, n=2/29 (6.9%) patients receiving ketorolac, and n=0/35 patients receiving placebo. In the HPβCD-diclofenac group, postsurgical shifts to low hematocrit and hemoglobin occurred in 35.7% and 28.3% of patients, respectively (versus 31.4% and 21.5%, respectively, with placebo). Postsurgical shifts in platelet count were uncommon (<3.0% across treatment groups). Conclusions: While follow-up studies in larger populations are warranted, this analysis suggests that HPβCDdiclofenac may not present a significant incremental bleeding AE risk versus placebo when used for acute postoperative pain management.

Comment on: the relationship between splenomegaly and hematologic findings in patients with hepatosplenic schistosomiasis

The aim of the authors of the paper 'Relationship between splenomegaly and hematologic findings in patients with hepatosplenic schistosomiasis' published in this edition of the Revista Brasileira de Hematologia e Hemoterapia was to evaluate hematological and hemostatic abnormalities in patients with the severe form of schistosomiasis and its possible association with splenomegaly and portal hypertension(1). For this purpose a prospective study was performed of 55 compensated hepatosplenic schistosomiasis patients previously treated with praziquantel. All patients were outpatients of the Gastrointestinal Service of the Hospital das Clinicas of the Universidade Federal de Pernambuco (UFPE), Recife, Brazil, during the period 2010-2012. Thirty healthy individuals were selected as a control group. An abdominal ultrasound was performed in all patients and the Niamey protocols were used to measure the longitudinal diameter of the spleen and to classify the pattern of fibrosis. Moreover, routine liver tests were performed including albumin, aminotransferases (AST, ALT), alkaline phosphatase (ALP) and gamma glutamyl-transferase (γ-GT). A complete blood count and hemostatic tests such as prothrombin time/international normalization ratio (PT/INR), partial thromboplastin time (PTT), fibrinogen and D-dimer were carried out. The authors observed that patients showed predominance of advanced pattern fibrosis. Furthermore, the routine liver and hemostatic tests had increased values compared to the control group with the exception of the level of fibrinogen. There were also high frequencies of upper gastrointestinal bleeding in patients (34%) and thrombocytopenia (83%); 36.5% had anemia and 47% presented leukopenia. An inverse correlation was found between the longitudinal diameter of the spleen and the platelet count. The development of gastro-esophageal varices is a common complication of portal hypertension and bleeding from varices is a frequent cause of mortality and morbidity(2,3). As the platelet count is a commonly available parameter and measurement of the spleen bipolar diameter has a high reproducibility in abdominal ultrasound studies(4,5), their use might be of help in the clinical management of patients with Schistosoma mansoni infection and suspected esophageal varices in endemic areas. According to some authors(6,7), increases in the ALT and AST levels occur with liver cell damage, but in S. mansoni infections this type of injury is not commonly observed. On the other hand, the most important cause of increases in γ-GT is the chronic stimulation of the microsomal fraction of hepatocytes and the presence of cholestasis(8). According to Martins & Borges, chronic stimulation of the microsomal fraction of hepatocytes occurs only in patients with the hepatosplenic form of schistosomiasis. Some authors(8,9) proposed that changes in the biliary tree, due to fibrosis of the portal space, may be the anatomical substrate for the increases in the ALP and γ-GT levels in patients with the hepatosplenic form of schistosomiasis. In the literature, there is a tendency to explain hematologic changes related to portal hypertension as being due to hypersplenism just through observing hematological laboratory values(10,11). It is noteworthy that pancytopenia in portal hypertension due to schistosomiasis is caused by intra-splenic blood stasis related to difficult venous drainage to the liver. Symmers fibrosis in hepatosplenic schistosomiasis does not interfere in the function of these organs. Therefore, there is doubt regarding the term hypersplenism which is perhaps confused with the term storage. In the case of splenomegaly schistosomiasis, cytopenia may be caused by the increase in splenic storage and not by a mononuclear phagocytic system disorder(11,12). Apart from these considerations, there is the difficulty of explaining why the very low platelet and leukocyte counts found in patients with portal hypertension and schistosomiasis are not accompanied by clinical symptoms(11,13). On the other hand, coagulation disorders are frequently observed in patients with schistosomiasis even though the pathophysiology for this has not yet been established. In patients with advanced hepatosplenic schistosomiasis, high levels of the pro-inflammatory cytokines, interleukin-1 alpha (IL-1α) and tumor necrosis factor alpha (TNF-α) and lipopolysaccharide (LPS) have been detected in the sera(14). It is therefore assumed that a tissue factor procoagulant expressed by endothelial cells because of stimulation by these agents may participate in the activation of the extrinsic coagulation cascade(14). Accordingly, it may be possible that host immune responses to schistosome eggs participate in not only granuloma formation and tissue fibrosis, but also in the development of hemostatic abnormalities in schistosomiasis mansoni(14).

Relationship between splenomegaly and hematologic findings in patients with hepatosplenic schistosomiasis

BackgroundSchistosomiasis is a tropical disease. Patients who develop hepatosplenic schistosomiasis have clinical findings including periportal fibrosis, portal hypertension, cytopenia, splenomegaly and gastrointestinal hemorrhage. ObjectiveThe aim of this study was to analyze the hemostatic and hematologic findings of patients with schistosomiasis and correlate these to the size of the spleen. MethodsFifty-five adults with hepatosplenic schistosomiasis and 30 healthy subjects were selected through a history of contact with contaminated water, physical examination and ultrasound characteristics such as periportal fibrosis and splenomegaly in the Gastroenterology Service of the Universidade Federal de Pernambuco. Blood samples were collected to determine liver function, blood counts, prothrombin (international normalized ratio), partial thromboplastin time and fibrinogen and D-Dimer levels using the Pentra 120 hematological analyzer (HORIBA/ABX), Density Plus (test photo-optical Trinity Biotech, Ireland) and COBAS analyzer 6000 (Roche). Furthermore, the longitudinal size of the spleen was measured by ultrasound (Acuson X analyzer 150, Siemens). The Student t-test, the Fisher test and Pearson's correlation were used to analyze the results with statistical significance being set for a p-value < 0.05. ResultsThe mean age was higher for the Study Group than for the Control Group (54 ± 13.9 vs. 38 ± 12.7 years). The average longitudinal diameter of the spleen was 16.9 cm (Range: 12.3-26.3 cm). Anemia is a common finding in patients with schistosomiasis (36.3%). The mean platelet and leukocyte counts of patients were lower than for the Control Group (p-value < 0.001). Moreover, the international normalized ratio (1.42 vs. 1.04), partial thromboplastin time (37.9 vs. 30.5 seconds) and D-Dimer concentration (393 vs. 86.5 ng/mL) were higher for the Study Group compared to the Control Group. ConclusionThis study suggests that hematological and hemostatic abnormalities are associated with splenomegaly, hypersplenism and portal hypertension.

Comment on: Relationship between splenomegaly and hematologic findings in patients with hepatosplenic schistosomiasis

Schistosomiasis remains an important public health problem worldwide. It is a parasitic disease endemic in over 70 countries and is estimated that the infection is responsible for more than 200,000 deaths annually(1,2). For Gryseels et al.(3) inflammatory hepatic schistosomiasis is the main cause of hepatomegaly and severe splenomegaly in children and adolescents. The severity of disease is related to the intensity of the egg infestation. The most severe form of the disease, hepatosplenic schistosomiasis, is an important cause of morbidity and mortality (30% and 10% of those infected, respectively)(4). Dunn & Kamel(1) showed that Schistosomiasis is one of the most common causes of noncirrhotic portal hypertension in the world Schistosomiasis is associated to significant morbidity including anemia, chronic pain, diarrhea, exercise intolerance, malnutrition, bladder cancer, portal hypertension and central nervous system complications(5). Although most infections occur in residents of endemic areas, it has been clearly documented that brief freshwater exposure is sufficient to establish infection; thus, travelers may also be infected. From the standpoint of laboratory exams, these patients have leukopenia and significant thrombocytopenia. Sometimes patients have pancytopenia, iron deficiency anemia, leukopenia and thrombocytopenia secondary to great hepatosplenic schistosomiasis(6-8). We know that both leukopenia and thrombocytopenia are correlated to size of the spleen(9), but there are nostudies that directly or precisely correlate splenomegaly and hematologic findings. It is still controversial whether the thrombocytopenia observed in patients with chronic liver disease is more associated to splenomegaly or to very high portal blood pressure. In the early stages the portal resistance, hypertension is principally presinusoidal. However, due to progressive fibrotic changes in the portal tracts, lobular distortion occurs at the sinusoidal level. This results in increases in resistance to portal venous flow, as evidenced by increased wedged hepatic venous pressure in advanced cases(10). This may explain possible hematological abnormalities in these patients. Martins et al.(11) revisited 141 medical records of patients with hepatosplenic schistosomiasis mansoni submitted to the surgical treatment of portal hypertension. The variations in the serum levels of platelets in both the pre- and postoperative periods of these patients were directly correlated to changes in weight and volume of the spleen. Splenomegaly was directly responsible for the variation in the number of platelets. In this study, patients who underwent surgical treatment showed increased serum levels of platelets in the immediate postoperative compared to the preoperative period. Santos et al.(12) showed that this result refers to the splenic sequestration that occursin schistosomiasis. The results of this study suggest that ultrasound can be reliably usedin the classification of periportal fibrosis using the criteria of Niamey in patients withthe advanced form of schistosomiasis. Ultrasound scans in patients with schistosomiasishave been restricted to study the caliber of the portal and splenic veins, and organometricinvestigations of the portal vein(13). Some studies reported results relevant to the understanding of the importance of the correlation between splenomegaly and thrombocytopenia in hepatosplenic schistosomiasis. Martins et al.(11), analyzing the serum level of platelets in respect to pre and postoperative weight, tried to correlate this with volume of the spleen in patients with hepatosplenic schistosomiasis with indication for the surgical treatment of portal hypertension. He found that the number of platelets in the immediate postoperative period was inversely correlated with the weight of the spleen removed. Splenomegaly was directly responsible for the variation in the number of platelets. Thus, the study of Leite et al. is highly relevant since it suggests that the hematological abnormalities are associated with splenomegaly, hypersplenism and hypertension(14). Further studies are necessary to verify that the platelet count may be a non-invasive tool for portal hypertension.

First Observation of Hb Taybe [Codons 38/39 (−Acc) Thr→0 (α1)] In Greece: Clinical and Hematological Findings in Patients With Co-Inherited α+-Thalassemia Mutations

This report describes four unrelated Greek patients (one child and three adults) who all had an atypical thalassemia intermedia phenotype, characterized by chronic moderate anemia with mild hemolysis in some cases, and the absence of abnormal hemoglobin (Hb) fractions. DNA analysis identified the inheritance of common α+-thalassemia (α+-thal) mutations in trans to an in-frame 3 bp deletion at codons 38/39 (−ACC) on the α1-globin gene, previously described as Hb Taybe. Hematological findings in the parents of three of the Hb Taybe carrier cases, together with a fourth unrelated carrier, are also presented. These cases represent the first observation of Hb Taybe in the Greek population, as to date, it has only been observed in Israeli-Arab families. With the exception of one patient and his mother who both originate from Corfu, all our cases come from the Greek island of Crete.

Hematological presentation in systemic lupus erythematosus and its relationship with disease activity

Abnormalities of hematological system are very common in systemic lupus erythematosus (SLE). The aim of the study is to evaluate hematological findings in patients with SLE at the time of referral and their relationship with disease activity and organ involvement.The study was carried consecutive 115 patients, including 20 males and 85 females. Most of the cases had anemia at the time of presentation due to various etiologies. Anemia of chronic disease was seen in 46% and it was the most common encountered picture. The rate of hemolytic anemia was 28%, and Coombs' positivity rate was 22% among our patients. Leukopenia <4.0 × 109/l), neutropenia <1.8 × 109/l), and lymphopenia <1.5 × 109/l) rates were 57, 20, and 82%, respectively. Thrombocytopenia was seen in 40% for <150 × 109/l, 26% for <100 × 109/l, and 8% for <50 × 109/l. Of our patients, 10% had antiphospholipid syndrome (APS) at the time of diagnosis. Increased fibrinogen levels were observed in 35% without relating to disease activity. The rates of C3 and C4 hypocomplementemia were 86 and 64%, respectively, and both are closely correlated with the disease activity. Moreover, C3 hypocomplementemia was more prominent in cases with renal or serosal involvement. Leukopenia and hyperfibrinogenemia were more common in patients with skin/mucosal involvements. C3 hypocomplementemia, APS and elevated IgG levels were more common in our patients with renal involvement. SLE should be kept in mind while evaluating patients with mentioned hematological findings, especially in those with accompanying organ involvements.

Impact of Helicobacter pylori on the development of vitamin B12 deficiency in the absence of gastric atrophy.

Cobalamin (vitamin B12) deficiency is associated with Helicobacter pylori infection. This study examined how serum vitamin B12 levels relate to gastric mucosa H. pylori density and histology, and to hematological findings in patients with minimal or no gastric atrophy. A second aim was to confirm that H. pylori eradication therapy increases serum B12. Biopsies of the gastric mucosa from a population of dyspeptic patients were graded for level of chronic inflammation, neutrophil activity, atrophy, and H. pylori density. A total of 145 H. pylori-infected patients with minimal or no atrophy were included in the study. Serum cobalamin level, hemoglobin level, and mean corpuscular volume were measured in the 145 patients before eradication therapy, and in 65 of the subjects after treatment. The hematologic findings before and after eradication therapy and correlations between serum vitamin B12 level and histologic parameters, hematologic findings, and patient age were statistically analyzed. There was no significant correlation between serum cobalamin level and patient age. Before treatment all the histopathological scores were inversely correlated with serum vitamin B12 level (p <.01) on univariate analysis. Only H. pylori density was significantly associated with B12 level on multivariate analysis. Serum hemoglobin and cobalamin levels were significantly increased after treatment, regardless of H. pylori eradication status (p <.001). The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with non-ulcer dyspepsia and minimal or no gastric atrophy.

Hematologic reference ranges in a population of patients with schizophrenia.

The potential hematotoxic effects of antipsychotic drugs are well known and may limit the use of some effective therapies. Although some previous studies have suggested that patients with schizophrenia may have altered "normal" values, only limited data were available. It is now believed that biological values do not usually follow a normal distribution; therefore, reference ranges are frequently used when interpreting laboratory tests in clinical practice and in research. However, it may be important to use disease-specific hematologic reference ranges when evaluating laboratory test results for patients with schizophrenia. In this study, data taken from patients with schizophrenia prior to treatment in previous phase II and phase III pharmaceutical studies were analyzed to produce reference ranges for a variety of hematologic parameters. An increased variability was shown in the reference ranges for all white blood cell indices between patients with schizophrenia and the population without schizophrenia. Certain reference values also showed heterogeneity for gender, age, and racial descent. This study suggests that abnormal hematologic findings in patients with schizophrenia should be assessed in the context of a valid reference range. This information will be of value to psychiatrists, laboratory scientists, and other physicians who encounter hematologic problems in patients with schizophrenia, as well as in the assessment of the adverse effects of new therapeutic agents.