Blood Cell Count (blood + cell_count)

Distribution by Scientific Domains
Medical Sciences81%
Life Sciences11%
Earth and Environmental Science5%
Distribution within Medical Sciences
Dermatology14%
Hematology11%
Pharmacology & Pharmaceutical Medicine4%
Gastroenterology & Hepatology2%
28 Other Subdomains56%

Kinds of Blood Cell Count

  • complete blood cell count
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  • red blood cell count
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  • white blood cell count
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    Selected Abstracts

    White Blood Cell Count and the Occurrence of Silent Ischemia after Myocardial Infarction

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2003
    gorzata Kurpesa
    Background: Inflammation plays a role in the pathogenesis of atherosclerosis. Attempts are made to use markers of inflammation as prognostic factors in coronary artery disease and acute coronary syndromes. The correlation between inflammation and silent postinfarction ischemia is unknown. Methods: The study population consists of 104 asymptomatic patients who had uncomplicated Q-wave myocardial infarction within 6 months prior to the enrollment. After the white blood cell (WBC) count was assessed, the population was divided into two groups: group I comprising 48 patients with WBC , 7.0 × 103/,l and group II comprising 56 patients with WBC > 7.0 × 103/,l. Twenty-four-hour Holter monitoring was performed to detect the presence of silent ischemia. Results: Eighty-eight silent ischemic episodes were recorded. Ischemia on Holter monitoring was detected in 47 patients (84%) from group II and in five patients (9%) in group I (P < 0.01). We have found a significant positive correlation between WBC count and the number of ischemic episodes (r = 0.25), their maximal amplitude (r = 0.39), duration (r = 0.34), and total ischemic burden (r = 0.36). In multivariate analysis leucocytosis proved to be the only parameter independently correlated with the presence of silent ischemia. Conclusion: Postinfarction asymptomatic patients with increased WBC count are more likely to have residual ischemia. [source]

    Nitrite-Induced Methemoglobinaemia Affects Blood Ionized and Total Magnesium Level by Hydrolysis of Plasma Adenosine Triphosphate in Rat

    BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2009
    Md. Mizanur Rahman
    This study was performed on male Sprague,Dawley rats to which NaNO2 was injected (10 mg/kg i.p.) to induce methemoglobinaemia. Methemoglobin (MetHb) in blood was measured before (0 min.) and after 10, 30, 60 and 120 min. of NaNO2 injection. At respective time points, the tMg2+, blood ions and gases were measured by atomic absorption spectrometry and ion selective electrode, respectively. Haematological parameters were checked by automatic blood cell count, and blood films were observed under light microscope. Plasma ATP was measured by bioluminescence assay using a luminometer, and plasma proteins were measured by an automatic analyser. Blood cell count (RBC, WBC and platelet), haematocrit, and haemoglobin were found to be decreased with the advancement of MetHb concentration. With the gradual increase of MetHb concentration, the plasma ATP decreased and blood iMg2+ and plasma tMg2+ increased significantly as time passed by in comparison with the pre-drug values. A significant decrease of the ratio of ionized calcium to iMg2+, Na+ and increase of K+ was observed. In conclusion, NaNO2 -induced methemoglobinaemia is a cause of hydrolysis of plasma ATP which is responsible for the increase of blood iMg2+ and plasma tMg2+ in rats. [source]

    C-Kit receptor (CD117) expression on myeloblasts and white blood cell counts in acute myeloid leukemia

    CYTOMETRY, Issue 1 2004
    Jolanta Wo
    Abstract Background The c-Kit receptor is considered to play a crucial role in hematopoiesis. Induction of mobilization of hematopoietic cells in the bone marrow requires cooperative signaling through c-Kit and c-Kit ligand pathway, and these interactions are important in the retention of stem cells within the bone marrow. Therefore, we analyzed c-Kit density on the leukemic myeloblasts of patients with acute myeloid leukemia (AML) in relation to white blood cell count (WBC) in the peripheral blood. Methods Bone marrow aspirates collected from patients with AML and bone marrow aspirates and leukapheresis products after granulocyte colony-stimulating factor blood mobilization from adult volunteers were studied. To determine the level of c-Kit receptor expression, we applied quantitative (relative fluorescence intensity and antibody binding per cell) cytometric methods. Results Our data showed negative correlation between the level of c-Kit expression intensity on myeloblasts and the number of leukocytes in blood of AML patients. The c-Kit receptor density on myeloblasts in patients with low WBC was significantly stronger than that on myeloblasts in patients with high WBC. In the latter patient group, the density c-Kit receptor on myeloblasts was similar to that on CD34+ cells in mobilized peripheral blood. Conclusions The obtained data suggest an involvement of c-Kit receptor in the regulation of leukemic myeloblasts egress to the peripheral blood. © 2004 Wiley-Liss, Inc. [source]

    Association of components of the metabolic syndrome with the appearance of aggregated red blood cells in the peripheral blood.

    DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2005
    An unfavorable hemorheological finding
    Abstract Background Components of the metabolic syndrome are associated with low-grade inflammation. This can be accompanied by the synthesis of sticky proteins and erythrocyte aggregation. Methods The degree of erythrocyte aggregation was evaluated by a simple slide test and image analysis along with other markers of the acute-phase response, including the white blood cell count (WBCC), erythrocyte sedimentation rate (ESR), fibrinogen and high sensitivity C-reactive protein (hs-CRP) concentrations. Patients were categorized in four groups according to the absence or presence of 1, 2 and 3 or more components of the metabolic syndrome. Results We examined a total of 1447 individuals (576 women and 871 men) who gave their informed consent for participation. A significant cardiovascular risk factors, age and hemoglobin adjusted correlation was noted between the degree of erythrocyte aggregation and the number of components of the metabolic syndrome (r = 0.17, p < 0.0005). This correlation was better than that observed for clottable fibrinogen (r = 0.13 p < 0.0005), for ESR (r = 0.11 p < 0.0005) or WBCC (r = 0.13 p < 0.0005). A somewhat better correlation was noted for hs-CRP (r = 0.26 p < 0.0005). Conclusions The multiplicity of components of the metabolic syndrome is associated with enhanced erythrocyte aggregation, probably related to the presence of multiple adhesive macromolecules in the peripheral blood. The enhanced aggregation might contribute to capillary slow flow, tissue deoxygenation as well as vasomotor tone changes in the presence of multiple components of this syndrome. Copyright © 2004 John Wiley & Sons, Ltd. [source]

    Uterine torsion diagnosed in a mare at 515 days' gestation

    EQUINE VETERINARY EDUCATION, Issue 10 2010
    C. López
    Summary A pregnant mare with a history of prolonged gestation (,515 days) and suspected diagnosis of fetal mummification was examined. Rectal palpation revealed that the left broad ligament of the uterus was dorsal and medial to the right uterine ligament and it was not possible to observe the cervix during vaginal examination. Transabdominal ultrasound revealed fluid in the uterus, fetal membranes and the uterine walls defined and thickened. Free fluid was not seen in the peritoneal cavity. Laboratory tests (blood cell count and clinical chemistry) were normal. Based on clinical history, physical examination and ultrasound findings, a chronic uterine torsion with fetal death was diagnosed and the mare was subjected to exploratory celiotomy. The uterus was strongly adhered to the peritoneum of the ventral abdominal wall and there were multiple adhesions to the colon. Hysterotomy was performed to remove the fetus and to permit repositioning of the uterus. When the fetus was removed, a large devitalised grey tissue area of the right ventral uterine horn was observed. Multiple adhesions prevented a rescue hysterectomy and euthanasia of the patient was performed. During the necropsy, a 180° cranial cervix clockwise uterine torsion was observed. This rare case of uterine torsion appears to be the most chronic case reported in the equine literature. [source]

    Urinary L-FABP and anaemia: distinct roles of urinary markers in type 2 diabetes

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2010
    M. Von Eynatten
    Eur J Clin Invest 2010; 40 (2): 95,102 Abstract Background, Urinary liver-type fatty acid binding protein (L-FABP) and kidney injury molecule (KIM)-1, novel urinary biomarkers of renal tubulointerstitial function, have previously been associated with acute ischaemic kidney injury. We studied the clinical significance of urinary L-FABP, KIM-1 and N -acetyl-,-glucosaminidase (NAG) as potential markers of renal function and chronic ischaemic injury in patients with diabetic nephropathy. Material and methods, A total of 130 type 2 diabetes patients with early diabetic nephropathy and 40 healthy controls were studied. Urinary L-FABP, KIM-1, NAG, albumin excretion rate (AER) and creatinine clearance were obtained from 24-h urine samples, and correlated with measures of red blood cell count, renal function and metabolic control. Results, Urinary L-FABP was significantly increased in diabetes patients compared with healthy controls [8·1 (interquartile 0·6,11·6) vs. 2·4 (0·5,3·6) ,g/g creatinine, P < 0·001] and correlated with AER (r = 0·276, P = 0·002), creatinine clearance (r = ,0·189, P = 0·033) and haemoglobin levels (r = ,0·190, P = 0·030). In multivariable linear regression analysis, haemoglobin (, = ,0·247, P = 0·015) and AER (, = 0·198, P = 0·046) were significant predictors of urinary L-FABP. Prevalent anaemia was independently associated with a 6-fold risk for increased tubulointerstitial kidney damage (upper vs. lower two L-FABP tertiles: OR, 6·06; 95% CI: 1·65,22·23; P = 0·007). Urinary KIM-1 was not significantly associated with kidney function, AER, or measures of red blood cell count while urinary NAG was associated with parameters of glucose control and renal function. Conclusions, Different urinary biomarkers may reflect distinct pathophysiological mechanisms of tubulointerstitial damage in early diabetic nephropathy: Urinary L-FABP could be a novel biomarker for chronic intrarenal ischaemia. [source]

    Significance of white blood cell count and its subtypes in patients with acute coronary syndrome

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2009
    G. Huang
    Abstract Background, Inflammation plays a role in the pathogenesis of coronary atherosclerosis. Materials and methods, Six hundred twenty-three patients with acute coronary syndrome (ACS) referred for coronary angiography for the first time in our hospital were enrolled in this study. White blood cell and its subtypes were measured on admission. The study population was divided into three groups based on total white blood cell count and followed up. Clinical end points were major adverse cardiac events (MACEs), including cardiogenic death, stroke, heart failure, non-fatal myocardial infarction, rehospitalization for angina pectoris. Results, The median age was 68 years (range 31,92) and 64·2% of the patients were men. The median white blood cell count was 6·48 × 109 L,1 (range 2·34,27·10 × 109 L,1). The median follow-up duration was 21 months (range 1,116) and MACEs occurred in 167 patients. The multivariable Cox proportional hazards regression model revealed that neutrophil count [Relative risk = 1·098, 95% Confidence interval (CI): 1·010,1·193, P = 0·029) was a risk factor for MACEs. The logistic regression model revealed that lymphocyte count [Odds ratio (OR) = 1·075, 95% CI: 1·012,1·142, P = 0·018] and monocyte count (OR = 8·578, 95% CI: 2·687,27·381, P < 0·001) were predictive of stenosis , 75%; Neutrophil proportion (OR = 1·060, 95% CI: 1·007,1·115, P = 0·026), monocyte count (OR = 12·370, 95% CI: 1·298,118·761, P = 0·029) were predictive of the presence of multivessel disease. Kaplan,Meier analysis of short-term and long-term cumulative survival showed no significant statistical differences among three groups. Conclusions, Neutrophil count adds prognostic information to MACEs in ACS. Monocyte count and lymphocyte count are predictive of severity of coronary atherosclerosis. [source]

    Potential role of soluble angiopoietin-2 and Tie-2 in patients with inflammatory bowel disease

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2006
    I. E. Koutroubakis
    Abstract Background, Angiogenesis has been suggested to play an important role in inflammatory bowel disease (IBD). The aim of the study was to evaluate the serum markers of angiogenesis angiopoietin-2 (Ang-2) and soluble angiopoietin receptor Tie-2 in patients with ulcerative colitis (UC) and Crohn's disease (CD). Materials and methods, Serum Ang-2 and Tie-2 serum levels were measured in 160 IBD patients (79 UC and 81 CD) and in 80 matched healthy controls using commercially available enzyme-linked immunosorbent assays. Serum Ang-2 and Tie-2 levels were correlated with the disease activity, as well as the type, localization and treatment of the disease. Results, Median serum Ang-2 and Tie-2 levels were significantly higher in both the UC patients and the CD patients compared with the healthy controls (P < 0·05 and P < 0·001, respectively). The IBD patients with early disease (diagnosis < 2 years) had significantly higher (P = 0·04) median serum Ang-2 levels but significantly lower (P = 0·02) median serum Tie-2 levels as compared with IBD patients with late disease (diagnosis > 2 years). The CD patients with active disease had significantly higher levels of Ang-2 compared with non-active disease (P = 0·02). Serum levels of both Ang-2 and Tie-2 were not correlated with laboratory markers such as ESR, CRP, white blood cell count, platelet count and albumin. Conclusions, Serum Ang-2 and Tie-2 levels are elevated in patients with IBD. These markers may mediate angiogenesis and vascular permeability in the mucosa of patients with IBD. [source]

    Association of non-alcoholic steatohepatitis (NASH) with chronic neutrophilic leukemia

    EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 3 2004
    Chikashi Yoshida
    Abstract: A 54-yr-old female having chronic neutrophilic leukemia (CNL) associated with severe liver injury is presented. Physical examination on admission showed severe jaundice, hepatosplenomegaly, massive ascites, and pretibial edema. Complete blood count showed a hemoglobin level of 9.1 g/dL, platelet count of 25.8 × 104/,L, and white blood cell count of 36.6 × 103/,L with 89.7% neutrophils. Blood chemistry showed hyperbilirubinemia (21.9 mg/dL) with normal transaminase levels. There was no abnormality in serum cholesterol, triglyceride, or glucose levels. Neutrophil alkaline phosphatase activity was significantly elevated. Bone marrow aspiration showed myeloid hyperplasia with normal karyotype. Rearrangement of the bcr/abl was not detected by either polymerase chain reaction or fluorescence in situ hybridization. Human androgen receptor gene assay (HUMARA) of the bone marrow cells showed clonal proliferation of neutrophils. The patient was diagnosed as having CNL. To evaluate the pathogenesis of the liver injury, a needle biopsy was performed, which showed steatohepatitis with infiltration of neutrophils. As the patient had no history of alcohol abuse, a diagnosis of non-alcoholic steatohepatitis (NASH) was made. Assuming that the infiltration of abnormal neutrophils into the liver contributed to the development of NASH, she was treated with cytoreductive chemotherapy (cytosine arabinoside: 100 mg/d, 1,3 doses/wk). With decreases in white blood cell counts, serum bilirubin levels decreased gradually to 1.5 mg/mL. A postchemotherapy liver biopsy specimen showed marked improvement of the fatty degenerative change. To our knowledge, this is the first report describing the development of NASH in a myeloproliferative disorder. We believe that the infiltration of leukemic cells contributed to the development of NASH in this patient. [source]

    Endothelial Function in Patients With Migraine During the Interictal Period

    HEADACHE, Issue 1 2007
    Federico A. Silva MD
    Objectives.,The aim of this study is to evaluate endothelial function in migraineur subjects during the asymptomatic period. Background.,Migraine has been proposed as a risk factor for cerebrovascular events. The underlying mechanisms that relate these 2 pathologies are unknown. Nitric oxide (NO) has been proposed as the final causative molecule of migraine. Increased NO metabolites concentrations have been reported in migraineur subjects during acute migraine attacks, but there is no evidence indicating alterations in endothelial NO release during the symptom free period in theses subjects. Design and Methods.,Fifty migraineur subjects and 25 healthy subjects matched by gender and age were included. Every subject underwent a complete examination that included medical history, physical examination, resting electrocardiogram, forearm flow-mediated vasodilation (FMD), blood determinations of fasting nitrates and nitrites (NO2,+ NO3,), glucose, lipid profile, creatinine, C-reactive protein, and blood cell count. Results.,No differences in FMD or NO2,+ NO3, were detected among groups. The only difference between migraineurs and control subjects was a higher mean blood pressure 92.1 (8.8) mmHg versus 86.7 (8.2) mmHg P= .01. Conclusion.,The endothelial function is not altered during the interictal period in migraineur subjects. [source]

    Helicobacter pylori Infection and Gastric Autoimmune Diseases: Is There a Link?

    HELICOBACTER, Issue 6 2003
    Fabio Presotto
    ABSTRACT Background.,Helicobacter pylori is thought to be involved in atrophic body gastritis. We explored the prevalence of H. pylori infection in asymptomatic subjects with gastric parietal cell antibodies, as well as in patients with pernicious anemia, to evaluate a possible role of H. pylori gastric infection in gastric autoimmunity. Patients and Methods., We studied 79 consecutive asymptomatic subjects with parietal cell antibodies, 24 patients with pernicious anemia, and 66 parietal cell antibody-negative controls. All patients underwent gastric biopsies for histology and detection of H. pylori. Red blood cell count and volume, serum levels of gastrin, pepsinogen I, iron, folic acid, vitamin B12, and circulating antibodies to H. pylori and to intrinsic factor were also determined. Results., We found an atrophic body gastritis in 14 of the 79 asymptomatic subjects with parietal cell antibodies (18%) and in 2 of the 66 controls (3%) (p = .01). Mean levels of gastrin were increased (p < .0001), while those of pepsinogen were reduced (p < .001) compared with controls. H. pylori was identified at the gastric level and/or circulating anti- H. pylori antibodies were detected in 46 parietal cell antibody-positive subjects (58%) compared with 26 controls (39%) (p = .03). In patients with pernicious anemia we found an atrophic body gastritis in 18 of 24 cases (75%) (p < .001 vs. controls). Mean levels of gastrin were markedly increased (p < .0001) and those of pepsinogen I decreased (p < .0001) relative to controls. Only five of these patients (21%) had evidence of H. pylori infection compared with 46 of the parietal cell antibody-positive subjects (58%) (p = .003) and 26 of the controls (39%). Considering all patients with gastric autoimmunity (i.e. with parietal cell antibodies and/or with pernicious anemia), H. pylori was found in 44 of 72 of those without atrophy (61%) but in 6 of 31 with gastric body atrophy (19%) (p < .001), indicating that H. pylori infection is greatly reduced when gastric acid secretion decreases. Conclusions., The frequent detection of H. pylori infection in subjects with early gastric autoimmunity, indicated by the presence of parietal cell antibodies, suggests that H. pylori could have a crucial role in the induction and/or the maintenance of autoimmunity at the gastric level. [source]

    Determinants of C-reactive protein in chronic hemodialysis patients: Relevance of dialysis catheter utilization

    HEMODIALYSIS INTERNATIONAL, Issue 2 2008
    Adriana HUNG
    Abstract Biomarkers of inflammation, especially C-reactive protein (CRP), have been consistently shown to predict poor outcomes in chronic hemodialysis (CHD) patients. However, the determinants of CRP and the value of its monitoring in CHD patients have not been well defined. We conducted a retrospective cohort study to evaluate possible determinants of the inflammatory response in CHD patients with a focus on dialysis catheter utilization. Monthly CRP were measured in 128 prevalent CHD patients (mean age 56.6 years [range 19,90], 68% African Americans, 39% diabetics [DM]) over a mean follow-up of 12 months (range 2,26 months). There were a total of 2405 CRP measurements (median 5.7 mg/L; interquartile range [IQR] 2.4,16.6 mg/L). The presence of a dialysis catheter (p<0.002), cardiovascular disease (p=0.01), male gender (p=0.005), higher white blood cell count (p<0.0001), elevated phosphorus (p=0.03), and lower cholesterol (p=0.02) and albumin (p<0.0001) concentrations were independent predictors of elevated CRP in the multivariate analysis. Additionally, CRP levels were significantly associated with the presence of a catheter, when comparing the levels before and after catheter insertion (p=0.002) as well as before and after catheter removal (p=0.009). Our results indicate that the presence of a hemodialysis catheter is an independent determinant of an exaggerated inflammatory response in CHD patients representing a potentially modifiable risk factor. [source]

    Extranodal NK/T-cell lymphoma, nasal type, presenting after 5 years of remission

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 3 2008
    Tomonobu Ito MD
    A 76-year-old woman with multiple edematous erythemas, erosions, and ulcers on the breast and abdomen was admitted to our hospital in June 2005. She had developed granulomatous bleeding lesions in the right nostril 6 years prior to her visit to our dermatology unit. She had been observed at the otorhinolaryngology department of our hospital, and a biopsy was taken from the nasal lesion. Computerized tomography and gallium scintigraphy (67Ga single-photon emission computed tomography) did not reveal any lesions corresponding to the diagnosis of malignant lymphoma. The histologic examination of the nasal specimen rendered a diagnosis of natural killer (NK)/T-cell lymphoma, nasal. Because imaging analysis indicated a small-sized tumor without metastases, oral prednisolone at 20 mg/day was administered for 1 month. The tumor decreased in size and disappeared after 19 months of low-dose steroid therapy. ,Five years after the initial treatment, the patient developed a fever of 38 °C with infiltrated erythemas and erosions on her breast. Erysipelas was initially suspected, but the antimicrobial agent did not show any effect and the multiple infiltrated erythemas and ulcers spread throughout her chest and abdomen (Fig. 1). The lymph nodes were not palpable. The right nasal cavity showed no granulomatous lesions or other signs of abnormality. The peripheral white blood cell count (3000/µL), red blood cell count (3.54 × 106/µL), and platelet count (112 × 103/µL) were reduced. Atypical lymphocytes were not observed. The serum lactic dehydrogenase (LDH; 1770 U/L; normal, 224,454 U/L), aspartate aminotransferase (AST; 140 U/L; normal, 10,30 U/L), and alanine aminotransferase (ALT; 57 U/L; normal, 3,29 U/L) levels were elevated. The soluble interleukin-2 (IL-2) receptor level was high (25,300 U/mL; normal, 167,497 U/mL). Epstein,Barr virus (EBV) serologic examination showed the immunoglobulin G (IgG) viral capsid antigen (VCA) at 1 : 320 and the EBV nuclear antigen (EBNA) at 1 : 40. IgM VCA and EBV early antigen-diffuse restricted antibody (EA) IgA and IgG were not detectable. Histologic findings from the left chest skin showed a distribution of atypical lymphocytes from the upper dermis to the subcutaneous tissue, and many foamy cells which had phagocytosed the hemocytes (Fig. 2a,b). Immunohistochemical analysis showed that the atypical lymphocytes were sCD3,, CD4,, CD8,, CD20,, CD56+, granzyme B+, and T-cell intracellular antigen (TIA-1) positive. Furthermore, EBV-encoded small RNAs (EBER), detected by in situ hybridization, exhibited a strong signal. The nasal lesions biopsied 6 years previously showed an identical staining pattern with the skin lesions immunohistochemically. Analysis of the T-cell receptor-, (TCR-,), TCR-,, and TCR-, gene did not reveal any clonal rearrangements, but the EBV gene was detected from the skin specimens by Southern blotting. Our patient's condition was diagnosed as a case of extranodal NK/T-cell lymphoma, nasal type, but the patient had concomitantly developed hemophagocytic syndrome (HPS). She was treated with a combination of steroid pulse therapy and chemotherapy (pirarubicin hydrochloride 30 mg/m2, cyclophosphamide 500 mg/m2, vincristine 1 mg/m2, prednisolone 30 mg/m2, etoposide 80 mg/m2). After the first session of chemotherapy, the lesions on the chest and abdomen diminished, but, 2 weeks later, the skin lesions recurred, and disseminated intravascular coagulation (DIC) induced by HPS supervened. The patient died as a result of multiple organ failure induced by HPS. Figure 1. Multiple infiltrated erythemas, erosions, and ulcers on the breast and abdomen Figure 2. Histologic findings of a skin biopsy specimen from the left chest (hematoxylin and eosin staining). (a) Dense infiltration of atypical lymphocytes from the upper dermis to the subcutaneous tissue (×40). (b) Many foamy cells had phagocytosed the hemocytes (×400) [source]

    ,1-Antitrypsin deficiency presenting with panniculitis and incidental discovery of chronic obstructive pulmonary disease

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2007
    Gretchen Korver MD
    A 60-year-old man presented to the Emergency Department (ED) with large, painful, indurated plaques on the right thigh, left abdomen, left chest, and right chest, which began without any preceding trauma on the right thigh 3 weeks prior to presentation in the ED. He was initially treated with cefazolin 1 g three times daily as home infusions. When the lesions continued to progress, he was admitted to the hospital and placed on amoxicillin/clavulanate and vancomycin. He had a single episode of fever of 102°F, but his white blood cell count and differential remained normal. An initial biopsy showed a dermal inflammatory infiltrate composed primarily of neutrophils and eosinophils with rare flame figures in the dermis. There was minimal fat seen in this biopsy. A differential diagnosis of Wells or Sweet's syndrome was entertained, and he was placed on 60 mg/day prednisone with no resolution of his symptoms. The patient's past medical history included hypertension, hyperlipidemia, peripheral neuropathy, and hiatal hernia. His family history was significant for emphysema in both parents and coronary artery disease in his father. Both of his parents smoked cigarettes. His grandfather, who was a coal miner, also had emphysema. Whilst on antibiotics and prednisone, the plaques on the patient's right thigh, right abdomen, and left chest expanded and ulcerated, draining an oily liquid (Figs 1 and 2). An incisional biopsy was obtained from his thigh. Histopathology showed a septal and lobular panniculitis with fat necrosis, neutrophils, and histiocytes (Fig. 3). Special stains for organisms were negative. Tissue sent for bacterial and fungal culture had no growth. Amylase and lipase levels were normal. Rheumatoid factor, antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), cryoglobulins, and antiphospholipid antibodies were all normal. The ,1-antitrypsin level was low at 25 mg/dL (ref. 75,135). The ,1-antitrypsin phenotype was PiZZ. Figure 1. Indurated plaques on right chest and thigh and left chest Figure 2. Ulcerated plaques on left chest Figure 3. Septal and lobular panniculitis with fat necrosis. Hematoxylin and eosin ×10 The patient had a normal glucose-6-phosphate dehydrogenase level and was placed on dapsone 200 mg/day. The inflammation resolved and, over the course of several months, the involved areas healed with scarring. The patient denied any pulmonary complaints but, during his hospitalization, was found incidentally to have an oxygen saturation of 88% on room air. He was sent for evaluation by a pulmonologist, and pulmonary function tests revealed a mixed restrictive and obstructive pattern with a forced expiratory volume in 1 to forced vital capacity (FEV1/FVC) ratio of 63% of predicted. He had never smoked. He was placed on supplemental oxygen but, as his pulmonary disease has been stable, he has not been treated with intravenous antitrypsin inhibitor. [source]

    Two Japanese cases of lichen planus pigmentosus-inversus

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 7 2007
    Aki Kashima MD
    Case 1 was a 51-year-old Japanese woman. She presented with an asymptomatic brown macule located on the right axilla of 2 months' duration. The smooth macule was 2 cm in diameter with a sharp demarcation (Fig. 1A). Figure 1. Photographs of skin lesions in two patients. (A) Case 1. Well-circumscribed brown macule without an active red border in the central portion of the right axilla. (B) Case 2. Symmetric distribution of brown macules without an active red border in the popliteal fossae Case 2 was a 62-year-old Japanese man. He presented with asymptomatic, symmetric, gray,brown macules located on the groin, axillae, and popliteal region of 6 months' duration. The smooth macules were several millimeters to centimeters in diameter and sharply demarcated (Fig. 1B). Oral or nail lesions, previous inflammatory processes in affected areas, and internal malignancies were absent. A causal relationship with drugs, recent sun exposure, or trauma could not be identified. Findings for work-up, including blood cell count, fasting blood sugar levels, liver function, serum electrolyte levels, serum electrophoresis, urinalysis, antinuclear antibodies, and serological examinations for human hepatitis viruses and syphilis, were within normal limits or negative. The lesions gradually disappeared without medication within 6 months. Biopsy specimens showed a lymphocytic infiltrate with basal vacuolar changes and prominent melanin incontinence in the upper dermis (Fig. 2A). The band-like lymphocytic infiltrate was moderate in Case 1 and mild in Case 2. Immunohistochemistry showed infiltrative CD8+ T lymphocytes with keratinocytic damage, indicating cytotoxic injury of the keratinocytes (Fig. 2B). Both the epidermis and the upper dermis contained CD1a+ cells (Fig. 2C). The keratinocytes focally and weakly expressed HLA-DR (Fig. 2D). These findings were identical in samples from both patients. Figure 2. Light and immunohistochemical microphotographs. (A) Mild, band-like, lymphocytic infiltrate with basal vacuolar change and prominent melanin incontinence in the upper dermis with apoptosis or necrosis of keratinocytes. (B) Epidermal infiltrate of CD8+ T lymphocytes with keratinocytic damage. (C) CD1a+ cells in the upper dermis. (D) Keratinocytes focally and weakly express HLA-DR (original magnifications: A, ×200; B,D, ×400) [source]

    Necrotizing fasciitis: delay in diagnosis results in loss of limb

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2006
    Rajat Varma MD
    A 58-year-old man presented to the Emergency Room with a 1-day history of severe pain in the left lower extremity preceded by several days of redness and swelling. He denied any history of trauma. He also denied any systemic symptoms including fever and chills. His past medical history was significant for diabetes, hypertension, deep vein thrombosis, and Evans' syndrome, an autoimmune hemolytic anemia and thrombocytopenia, for which he was taking oral prednisone. Physical examination revealed a warm, tender, weeping, edematous, discolored left lower extremity. From the medial aspect of the ankle up to the calf, there was an indurated, dusky, violaceous plaque with focal areas of ulceration (Fig. 1). Figure 1. Grossly edematous lower extremity with well-demarcated, dusky, violaceous plaque with focal ulceration Laboratory data revealed a white blood cell count of 6.7 × 103/mm3[normal range, (4.5,10.8) × 103/mm3], hemoglobin of 11.5 g/dL (13.5,17.5 g/dL), and platelets of 119 × 103/mm3[(140,440) × 103/mm3]. Serum electrolytes were within normal limits. An ultrasound was negative for a deep vein thrombosis. After the initial evaluation, the Emergency Room physician consulted the orthopedic and dermatology services. Orthopedics did not detect compartment syndrome and did not pursue surgical intervention. Dermatology recommended a biopsy and urgent vascular surgery consultation to rule out embolic or thrombotic phenomena. Despite these recommendations, the patient was diagnosed with "cellulitis" and admitted to the medicine ward for intravenous nafcillin. Over the next 36 h, the "cellulitis" had advanced proximally to his inguinal region. His mental status also declined, and he showed signs of septic shock, including hypotension, tachycardia, and tachypnea. Vascular surgery was immediately consulted, and the patient underwent emergency surgical debridement. The diagnosis of necrotizing fasciitis was then made. Tissue pathology revealed full-thickness necrosis through the epidermis with subepidermal splitting. Dermal edema was also present with a diffuse neutrophilic infiltrate (Fig. 2). This infiltrate extended through the fat into the subcutaneous tissue and fascia. Tissue cultures sent at the time of surgery grew Escherichia coli. Initial blood cultures also came back positive for E. coli. Anaerobic cultures remained negative. Figure 2. Necrotic epidermis with subepidermal splitting. Marked dermal edema with mixed infiltrate and prominent neutrophils. Hematoxylin and eosin: original magnification, ×20 After surviving multiple additional debridements, the patient eventually required an above-the-knee amputation due to severe necrosis. [source]

    Bullous variant of Sweet's syndrome

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 11 2005
    Susanne Voelter-Mahlknecht MD
    A 69-year-old woman presented to our clinic as an emergency with erythematous, well-circumscribed plaques, which were partly vesicular, on her extremities and in her armpits, and additionally hemorrhagic blisters on both her palms and her fingers (Fig. 1a), which had developed 2 days after the first appearance of the skin lesions. The rapid onset of the lesions (within a few hours) and the pain associated with them were extremely troublesome to the patient. On admission she complained of fever, tiredness and being easily fatigued. Because of a urinary tract infection 1 month prior to admission, trospiumchloride was given. On clinical examination, body temperature was found to be above 38 °C and infraclavicular lymph nodes were enlarged but not tender. Figure 1. (a) Bullae on the patient's right hand. (b) Multiple partly confluent vesicles with neutrophilic granulocytes intraepidermally and a dense interstitial perivascular infiltration of neutrophilic granulocytes and lymphomononuclear cells (H&E, ×200) Normal or negative laboratory tests included blood counts, liver and kidney parameters, electrolytes and infection screen. Laboratory examination demonstrated minor leukocytosis and absolute neutrophilia (white blood cell count 10 440 cells/µL, neutrophils 8030 cells/µL). X-ray screening, abdominal ultrasound and laboratory investigations were all normal. There was no response to antibiotics when erythromycine was given. However, there was a good response to systemic corticosteroids. The patient was treated with a low dosage of prednisolone, beginning at 50 mg/day, which was then tapered off. Skin lesions resolved within 7 days. Histology from a lesion on the patient's left forearm showed a dense interstitial inflammatory infiltration consisting predominantly of neutrophilic granulocytes from the subepidermal layer to the middle of the reticular dermis. Inflammatory cells penetrated into both blood vessels and vessel walls; vasculitis was not prominent. In the lower dermis, perivascular infiltrations of lymphomononuclear cells were found. In addition, intraepidermally multiple partly confluent vesicles, with inclusions of neutrophilic granulocytes, were found, confirming the diagnosis of this rare variant of an acute febrile neutrophilic dermatosis (Fig. 1b). [source]

    Cutaneous sarcoid-like granulomas with alveolar hemorrhage and c-ANCA PR-3

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 9 2004
    Natividade Rocha MD
    A 28-year-old woman, employed as a leather factory worker, noted asymptomatic, well-delimited plaques on both knees, 6 years ago. The plaques were violaceous with a smooth surface. One appeared over a post-traumatic scar from childhood (Fig. 1). Two years later, she began to complain of symptoms suggestive of polyarthritis, first of the small joints of the hands (proximal interphalanges) and then of the larger joints (wrists, elbows, and knees). She was diagnosed with rheumatoid arthritis and began treatment with nonsteroidal anti-inflammatory drugs for 1 month without any change. Deflazacort, 12 mg/day, and hydroxychloroquine, 400 mg/day, were administered for 3 months, with improvement of her articular complaints, but not her skin lesions. Figure 1. Well-delimited, violaceous plaques with a smooth surface on the knees, one over an old post-traumatic scar One year later, she complained of dysphonia, which remitted spontaneously after some weeks. After one additional year, she noted papules, with similar characteristics to the plaques, on the elbows, and two well-delimited orange-to-brown plaques on the forehead (Fig. 2). Figure 2. Orange,brown plaques symmetrically placed on the forehead During the fifth year of the disease, she was referred for the first time to a dermatologist, who biopsied one of the knee lesions. The histologic result was compatible with "sarcoid granuloma." At that time, she presented with skin lesions as her only complaint. Sarcoidosis was suspected based on a chest X-ray, which revealed hilar lymphadenopathy and diffuse accentuation of the interstitium. In November 2000, she suddenly developed fever (40 °C), cough with hemoptysis, dysphonia, and subcutaneous nodules on the palmar surface of the fingers of both hands that were painless, well-delimited, 5 mm in diameter, and firm (Fig. 3). She reported a weight loss of 12 kg in the previous 3 months. Pulmonary condensation was found on auscultation, and she had palpable hepatomegaly. Peripheral lymphadenopathy was not present. Figure 3. Painless, well-delimited, firm subcutaneous nodules on the palmar surface of the fingers Laboratory investigations revealed normochromic, normocytic anemia (hemoglobin, 7.7 g/dL), iron deficit, a white blood cell count of 16,000/µL with neutrophilia, an erythrocyte sedimentation rate of 130 mm/h, elevation of liver enzymes, a slight increase in angiotensin-converting enzyme (ACE) level (72 U/L), hypergammaglobulinemia (IgG, 3350 mg/dL), antinuclear antibody (ANA) of 1 : 320, and a slight increase in CD4 and decrease in CD8 lymphocytes with normal cellular morphology in blood. Renal function, urine sediment, urine and serum calcium, complement (C4), dsDNA, antimitochondrial antibody, direct and indirect Coombs test, antineutrophil cytoplasmic antibody (ANCA), tuberculin skin tests, viral markers of hepatitis B, C, and human immunodeficiency virus (HIV), electrocardiogram (ECG), ophthalmic examinations, and culture for infectious agents in blood and sputum were all normal or negative. Computed tomography (CT) scan showed an infiltrate in the upper right pulmonary lobule with a central cavity and bilateral hilar lymphadenopathy (Fig. 4). Homogeneous hepatosplenomegaly was present. The bronchoalveolar lavage (BAL) showed a slight lymphocytic increase predominantly of CD8 cells and hemosiderosis. Stains for infectious agents, including acid-fast bacillus, fungi, Mycoplasma, and Legionella, were negative. Three biopsies from the forehead, elbows, and knees showed well-formed noncaseating epithelioid cell granulomas with giant cells of the Langhans type in the dermis, suggestive of sarcoidosis (Figs 5 and 6). A fourth biopsy from a finger nodule demonstrated inflammatory infiltration of the dermis and necrosis with cellular debris. Vasculitis was not seen (Fig. 7). Figure 4. Computed tomography scan showing an infiltrate in the upper right pulmonary lobule with a central cavity Figure 5. Beneath a flattened epidermis, several sarcoid granulomas composed of epithelioid histiocytes and several multinucleated giant cells of Langhans type can be seen (hematoxylin and eosin, ×10) Figure 6. Less well-formed sarcoid granulomas in a hyperkeratotic area, surrounded by a sparse rim of lymphocytes (hematoxylin and eosin, ×20) Figure 7. Foci of necrosis and fibrinoid degeneration with some neutrophil infiltration and nuclear dusting (hematoxylin and eosin, ×40) The patient was treated with a broad-spectrum empirical antimicrobial (levofloxacin, 500 mg daily intravenously) over 12 days, with prompt improvement in her symptoms and remission of the forehead and finger lesions. Nevertheless, on the first evaluation after hospitalization, the CT scan showed persistence of the pulmonary cavity (Fig. 8). A repeat ANCA determination was positive (cytoplasmic pattern, c-ANCA) at 1 : 640 by indirect immunofluorescence (IIF). Antiproteinase-3 antibody was demonstrated at 78 by enzyme-linked immunosorbent assay (ELISA). Figure 8. Computed tomography scan showing persistence of the pulmonary cavity She underwent an open lung biopsy which revealed intra-alveolar hemorrhage and scanty noncaseating epithelioid cell granulomas of the sarcoidosis type in the peripheral blood vessels without vasculitis. A diagnosis of Wegener's granulomatosis was made and she began prednisolone (1 mg/kg/day) and oral cyclophosphamide (2 mg/kg/day). One year later, she is asymptomatic, the skin lesions have completely remitted, c-ANCA is negative, and the CT scan shows partial regression of the pulmonary cavity. [source]

    Dyskeratosis congenita with isolated neutropenia and granulocyte colony-stimulating factor treatment

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 3 2002
    Kutluhan Yilmaz
    A 3-year-old Turkish boy with a history of chronic cough, recurrent bronchopneumonia, and a borderline sweat chloride test (40 mEq/L) was referred for further evaluation to our department. He was born at term (2100 g) to a marriage with no consanguinity. His mother and father were 40 and 46 years old, respectively. Physical examination (Fig. 1) revealed hypopigmented, atrophic, and hyperkeratotic skin lesions surrounded by reticulate hyperpigmentation on the entire body, predominantly on the face, neck, arms, shoulders, and legs, which had been noticed initially at the age of 18 months. Dystrophic toenails, sparse and thin hair, and phimosis were also observed. Laboratory tests disclosed an isolated neutropenia (white blood cell count, 1800/mm3). Bone marrow (BM) aspiration showed a decreased myelopoiesis without myelodysplastic changes, but normal erythropoiesis, megakaryopoiesis, and normal stroma. Lymphocyte subgroups containing CD4, CD5, CD6, CD8, CD19, CD23, and CD25, and immunoglobulin G (IgG), IgM, IgA, and IgE, were in the normal range; hemoglobin F (HbF), 2.8%. Spontaneous and clastogen-induced chromosome breaks were not increased. A skin biopsy showed increased pigmentation at the basal layer, dyskeratotic epidermal cells, and marked IgM deposition and cytoid bodies and mild IgA and IgG deposits at the dermo-epidermal junction. Lactate response to glucose challenge, amino acid chromatography, and urine organic acid analysis were normal. Figure 1. Hypopigmented, atrophic, and hyperkeratotic skin lesions surrounded by reticulate hyperpigmentation involving predominantly the face, neck, arms, shoulders, and legs, dystrophic toenails, and sparse and thin hair A diagnosis of dyskeratosis congenita (DC) was made with typical skin lesions, dystrophic toenails, thin and sparse hair, and neutropenia with decreased myelopoiesis in BM. Treatment with granulocyte colony-stimulating factor (G-CSF) was considered for the neutropenia. As the increase in neutrophil count at a dose of 5 µg/kg was not adequate, 10 µg/kg G-CSF was tried (Fig. 2). With 10 µg/kg once to three times a week, a 1.8,4.8-fold increase in the absolute neutrophil count (ANC) was achieved with no side-effects. Treatment was more frequent during infection (days 22,28). Figure 2. Response of absolute neutrophil count (ANC) to granulocyte colony-stimulating factor (G-CSF) administration (5 µg/kg on days 1 and 3; 10 µg/kg on days 5, 10, 16, 23, 26, 28, 34, 40, 48, 54) [source]

    Lichenoid photodermatitis associated with nimesulide

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 12 2001
    Umit Tursen MD
    An 81-year-old-female patient presented with a 2 week history of erythematous to violaceous lichenoid papules and plaques exhibiting a reticulated pattern on the ,,V'' area of the chest and dorsal hands. Fine, whitish reticulated networks were present over the surface of many well developed papules. The lesions were sharply demarcated and moderately pruritic (Fig. 1). Figure 1. ,Violaceous lichenoid papules with reticular pattern located on the ,,V'' area of the chest The result of routine complete blood cell count, urinalysis, erythrocyte sedimentation rate, liver and kidney function tests were within normal limits. Antinuclear and anti-DNA antibodies were negative, and total C3 and C4 complement levels were normal. Hepatitis B surface antigen, anti-Hepatitis B surface antigen, anti-Hepatitis B core IgM antibody were negative, while anti-Hepatitis C virus antibody was positive. A skin biopsy specimen obtained from the neck of our patient revealed an interface lichenoid dermatitis accompanied by individual necrotic epidermal keratinocytes, parakeratosis and eosinophils in the infiltrate (Fig. 2). Figure 2. ,Interface lichenoid dermatitis accompanied by individual necrotic epidermal keratinocytes and parakeratosis (Hematoxylin and eosin; original magnification, × 200) Nimesulide therapy was stopped and the patient was treated with topical corticosteroids and systemic antihistamines. The eruption resolved within 5 days. The rash returned following nimesulide rechallenge. [source]

    Acute generalized exanthematous pustulosis mimicking toxic epidermal necrolysis

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 7 2001
    Arnon D. Cohen MD
    A 91-year-old patient presented with a nonfebrile, pruritic, widespread eruption that appeared 10 days after starting therapy with cefuroxime tablets, 1000 mg/day, due to stasis dermatitis with secondary infection. The patient was also treated with paracetamol tablets, 500,1000 mg/day, 10 days before the onset of the eruption. Previous diseases included congestive heart disease, hyperglycemia, and ectropion. There was no personal or family history of psoriasis. Additional medications, taken for more than 2 years at the time of the eruption, included indomethacin, captopril, hydrochlorothiazide, isosorbide-5-mononitrate tablets, and a combination drug Laxative®. Examination revealed widespread erythema involving 95% of the total body surface area, with numerous 1,2 mm nonfollicular pustules (Fig. 1). There was no predilection to the body folds. Within 24 h of hospitalization, during intravenous therapy with cefuroxime, the patient's condition worsened and bullae containing clear fluid appeared. Nikolsky's sign was positive on erythematous skin, and eventually skin detachment involved 41% of the total body surface area (Fig. 2). There were no target or target-like lesions and there was no involvement of the mucous membranes. Figure 1. Numerous, 1,2 mm, nonfollicular pustules, with confluence (viewed in the lower left part of the photograph), on erythematous skin Figure 2. Widespread skin detachment An early biopsy from a pustule revealed subcorneal and intraepidermal spongiform pustules, papillary edema, perivascular mononuclear infiltrate with a few eosinophils in the dermis, and leukocytoclastic vasculitis. A later biopsy showed similar findings with no evidence of full-thickness epidermal necrosis or necrotic keratinocytes. Direct immune fluorescence (DIF) taken from erythematous skin was negative. Laboratory studies showed the following results: sedimentation rate, 80 mm/h; white blood cell count, 26,200/mm3 with 87% polymorphonuclears and 1.8% eosinophils; hemoglobin, 13.0 g/dL; albumin, 2.8 g/dL (normal, 3.5,5.5 g/dL); other blood chemistry tests were normal. Immunologic studies for rheumatoid factor, antinuclear antibodies, antismooth muscle antibodies, antiparietal cell antibodies, antimitochondrial antibodies, C3, and C4 were normal or negative. Serology for venereal disease research laboratory (VDRL) test, Epstein,Barr virus, cytomegalovirus, hepatitis B virus, hepatitis C virus, human immunodeficiency virus, and antistreptolysin titer was negative. Chest X-ray was normal. Blood cultures were negative. Swab cultures taken from the pustules revealed Staphylococcus aureus as well as coagulase-negative Staphylococcus. All systemic drugs, including intravenous cefuroxime, were withdrawn with close monitoring for signs of heart failure or infection. Topical therapy consisted of application of wet dressings. Within 10 days, the eruption resolved with re-epithelialization of the erosions and the appearance of widespread post-pustular desquamation (Fig. 3) Figure 3. Post-pustular desquamation on the trunk [source]

    A child with spider bite and glomerulonephritis: a diagnostic challenge

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 4 2000
    Jennifer M. Lung MD
    A previously healthy 7-year-old white boy presented to St. Louis Children's Hospital with a 1-day history of headache, malaise, temperature of 38.7 °C, and a progressively erythematous, tender calf with central dusky purpura. On the morning of admission, his mother noticed a 2-mm crust on the patient's right calf with a 3-cm × 3-cm area of surrounding erythema. No history of recent trauma or bite was obtained. He had suffered two episodes of nonbloody, nonbilious emesis during the last day. In addition, over the previous 12 h, he presented brown urine without dysuria. His mother and brother had suffered from gastroenteritis over the previous week without bloody diarrhea. On initial physical examination, there was a 6-cm × 11-cm macular tender purpuric plaque with a central punctum on the right inner calf, which was warm and tender to the touch, with erythematous streaking towards the popliteal fossa ( Fig. 1). The inguinal area was also erythematous with tender lymphadenopathy and induration, but without fluctuance. Laboratory studies included an elevated white blood cell count of 20,800/,L with 6% bands, 86% segs, and 7% lymphocytes, hemoglobin of 12.5 g/dL, hematocrit of 35.1%, and platelets of 282,000/,L. The prothrombin time/activated partial tissue thromboplastin was 10.4/28.0 s (normal PT, 9.3,12.3 s; normal PTT, 21.3,33.7 s) and fibrinogen was 558 mg/dL (normal, 192,379 mg/dL). Urinalysis showed 1+ protein, 8,10 white blood cells, too numerous to count red blood cells, and no hemoglobinuria. His electrolytes, blood urea nitrogen (BUN), and creatine were normal. The urine culture was negative. Blood culture after 24 h showed one out of two bottles of coagulase negative Staphylococcus epidermidis. Figure 1. (A) 7-year-old boy with painful purpura of the calf The patient's physical examination was highly suggestive of a brown recluse spider bite with surrounding purpura. Over the next 2 days, the surrounding rim of erythema expanded. The skin within the plaque cleared and peeled at the periphery. The coagulase negative staphylococci in the blood culture were considered to be a contaminant. Cefotaxime and oxacillin were given intravenously. His leg was elevated and cooled with ice packs. The patient's fever resolved within 24 h. The lesion became less erythematous and nontender with decreased warmth and lymphadenopathy. The child was discharged on Duricef for 10 days. Because the patient experienced hematuria rather than hemoglobinuria, nephritis was suggested. In this case, poststreptococcal glomerulonephritis was the most likely cause. His anti-streptolysin-O titer was elevated at 400 U (normal, <200 U) and C3 was 21.4 mg/dL (normal, 83,177 mg/dL). His urine lightened to yellow,brown in color. His blood pressure was normal. Renal ultrasound showed severe left hydronephrosis with cortical atrophy, probably secondary to chronic/congenital ureteropelvic junction obstruction. His right kidney was normal. [source]

    Juvenile psoriatic arthritis with nail psoriasis in the absence of cutaneous lesions

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2000
    Carola Duran-McKinster MD
    A 4-year-old white boy without a significant family history had morning stiffness and painful swelling of his left knee and ankle, right elbow, and dorsolumbar region of 2 months' evolution. The following laboratory studies were within normal limits: complete blood cell count, C-reactive protein (CRP), latex, antistreptolysin, and antinuclear antibodies. Rheumatoid factor was negative and an increase in the erythrocyte sedimentation rate (ESR) was detected (56 mm/h). The pediatric department made an initial diagnosis of juvenile rheumatoid arthritis, and treatment with acetylsalicylic acid at 100 mg/kg/day and naproxen at 10 mg/kg/day was started. A thick, yellowish toenail was diagnosed as onychomycosis. No mycologic investigations were performed. Intermittent episodes of painful arthritis of different joints were present. The radiographic features of the peripheral joints included: narrow joint spaces, articular erosions, soft tissue swelling, and diffuse bony demineralization. Characteristic bilateral sacroiliitis and a swollen tendon sheath on the left ankle were detected. At 11 years of age the nail changes had extended to five other toenails and to four fingernails, were yellow,brown in color, and showed marked subungual hyperkeratosis ( Figs 1, 2). The rest of the nails showed significant nail pitting. Trials of griseofulvin alternated with itraconazole in an irregular form for five consecutive years resulted in no clinical improvement, which prompted a consultation to our dermatology department. On three different occasions, KOH nail specimens were negative for fungus, but the presence of parakeratotic cells aroused the suspicion of psoriasis. A complete physical examination was negative for psoriatic skin lesions. A nail bed biopsy specimen was characteristic of nail psoriasis ( Fig. 3). Figure 1. Thickened nails with severe subungual hyperkeratosis in five fingernails Figure 2. Secondary deformity of nail plate. No "sausage" fingers were observed Figure 3. Light microscopic appearance of a nail biopsy specimen showing parakeratotic hyperkeratosis, elongation of interpapillary processes, and Munroe abscess (arrow) (hematoxylin and eosin stain, ×40) The following human leukocyte antigens (HLAs) were positive: A9, A10, B12, B27, Cw1, Bw4, DR6, DR7, DQ1, DQ2, and DR53. A diagnosis of juvenile psoriatic arthritis associated with nail psoriasis was made. Toenail involvement became so painful that walking became very difficult. Occlusive 40% urea in vaseline applied to the affected toenails for 48 h resulted in significant improvement. Currently, the patient is 20 years old with nail involvement, but no psoriatic skin lesions have ever been observed. [source]

    ORIGINAL ARTICLE: Pro-hepcidin and iron metabolism parameters in multi-time blood donors

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 5 2010
    J. BOINSKA
    Summary A high number of blood donations may cause iron depletion. The pathophysiology behind this process may involve hepcidin, a recently discovered peptide that acts by inhibiting iron absorption and promoting iron retention in reticuloendothelial macrophages. The aim of this study was to determine serum pro-hepcidin levels and iron metabolism parameters in multi-time blood donors. The study group consisted of 132 multi-time male blood donors and 25 healthy male volunteers (nondonors). Complete blood cell count and iron status including serum iron, ferritin, soluble transferrin receptor (sTfR), total iron binding capacity (TIBC), unsaturated iron binding capacity (UIBC), erythropoietin and pro-hepcidin (ELISA) were assessed. In blood donors, ferritin level drops markedly in relation to donation frequency (P < 0.001). In contrast, TIBC and UIBC levels increase progressively corresponding to annual donation frequency. Pro-hepcidin concentration increases significantly with the number of donations per year (P = 0.0290). In blood donors having donated blood with the highest frequency per year, pro-hepcidin levels were positively correlated with haemoglobin (R = 0.31, P < 0.05) and negatively with sTfR (R = ,0.31, P < 0.05). Pro-hepcidin levels increase in relation to blood donation frequency per year. Longitudinal studies focusing on changes in serum hepcidin levels are required to address the question whether hepcidin may contribute to iron metabolism disturbances in multi-times blood donors. [source]

    EQAS for peripheral blood morphology in Spain: a 6-year experience

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 6 2008
    G. GUTIÉRREZ
    Summary The Spanish haematology external quality assessment scheme (EQAS), established in 1984, is run by the Spanish Haematology and Haemotherapy Association (AEHH) [Quality Assurance in Health Care 3 (1991) 75] and functions to evaluate the quality and reproducibility of the assessment of diagnostic samples by clinical laboratories. The Hospital Clinic of the University of Barcelona (HCB) serves as the EQAS Coordination Centre and follows the guidelines established by the International Committee for Standardization in Haematology [Annali dell'Istituto superiore di Sanità 31 (1995) 95; International Journal of Hematology 68 (1998) 45]. During the period 2001,2006, replicates of 25 different blood films were sent to 604 EQAS participants for cell morphology evaluation. Some patient details corresponding to the samples were disclosed, such us age, sex, haemoglobin value and white blood cell count. The participants were asked to select up to four significant morphology features using a coding list, provided by the Coordination Centre, which included significant morphological alterations that appear in haematopoietic cells. For each survey, individual results were assessed against the morphological reference results (MRR) established by the Cytology Group of the AEHH (,true' answers). This paper describes the organization of the 6-year-long study and the evaluation of laboratory performance for blood smear interpretation by the Spanish haematology EQAS. Different performance levels were detected relative to the laboratory category. Laboratories providing services to hospitalized patients showed higher performances compared with laboratories providing services to nonhospitalized patients. Pathological lymphoid cells were the most difficult to identify by the participants. To improve the results in EQAS peripheral blood morphology, the development of specific cytology educational trainings is discussed. [source]

    Severe antibody-mediated agranulocytosis

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 1 2008
    H. JOHNSEN
    Summary A 56-year-old female with Crohn's disease was admitted to the hospital with malaise, fever, and a low white blood cell count (0.8 × 109/l) with no granulocytes or myeloid precursor cells in the bone marrow. The leucopenia was initially thought to be the result of an infection and she was treated with antibiotics and granulocyte colony-stimulating factor (G-CSF, filgrastim). However, the bacterial cultures and viral tests were all negative. The patient's condition deteriorated and she became morbidly ill, but recovered after high dose steroid treatment. Six weeks later she relapsed whilst receiving 7.5 mg daily dose of prednisolone. She recovered quickly after being given high dose methylprednisolone in combination with filgrastim. A high maintenance dose of prednisolone was tapered over 5 months. She has not relapsed since and is currently well. Antibodies to the human neutrophil antigen (HNA)-3a were detected, but these antibodies could not easily explain her agranulocytosis as she had a HNA-3a negative phenotype. It seems plausible that her agranulocytosis was immune mediated through autoantibodies directed towards the early myeloid cells. [source]

    Venous stasis and routine hematologic testing

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 5 2006
    G. LIPPI
    Summary Prolonged venous stasis, as generated by a long tourniquet placement, produces spurious variations in several measurable analytes. To verify to what extent venous stasis influences routine hematologic testing, we assessed routine hematologic parameters, including hemoglobin, hematocrit, red blood cell count (RBC), main cell hemoglobin (MHC), main cell volume (MCV), platelet count (PLT), main platelet volume (MPV), white blood cell count (WBC) and WBC differential on the Advia 120 automated hematology analyzer in 30 healthy volunteers, either without venous stasis (no stasis) or after application of a 60 mmHg standardized external pressure by a sphygmomanometer, for 1 (1-min stasis) and 3 min (3-min stasis). Although the overall correlation between measures was globally acceptable, the mean values for paired samples were significantly different in all parameters tested, except MCV, MHC, PLT, MPV, eosinophils, basophils and large unstained cells after 1-min stasis and all parameters except MCV, MHC, MPV and basophils after 3-min venous stasis. As expected RBC, hemoglobin and hematocrit displayed a significant trend towards increase, whereas WBC and the WBC subpopulations were decreased. Difference between measurements by Bland and Altman plots exceeded the current analytical quality specifications for desirable bias for WBC, RBC, hemoglobin, hematocrit, lymphocytes and monocytes in samples collected after either 1- and 3-min stasis. These results provide clear evidence that venous stasis during venipuncture might produce spurious and clinically meaningful biases in the measurement of several hematologic parameters, prompting further considerations on the usefulness of adopting appropriate preventive measures for minimizing such influences. [source]

    Respiratory changes in human red cells

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 6 2001
    G. Aliberti
    To investigate physiological respiratory changes in human red cells, we measured automated red cell parameters in samples from the pulmonary and radial arteries of 86 patients undergoing aorto-coronary bypass and from the pulmonary artery and the aorta in 23 patients. Our results showed higher mean corpuscular volume (88.53 ± 5.06 fl vs. 88.12 ± 4.94 fl, P < 0.000001), haematocrit (0.369 ± 0.039 vs. 0.367 ± 0.038, P < 0.0005), red cell distribution width (43.38 ± 4.16 vs. 43.04 ± 4.05 fl, P < 0.000001) and a lower mean corpuscular haemoglobin concentration (338.3 ± 15.9 vs. 339.9 ± 16.8 g/l, P < 0.005) in pulmonary arterial as compared to radial arterial blood. There were no differences with respect to haemoglobin concentration, red blood cell count, or mean corpuscular haemoglobin. Similar differences were observed between pulmonary arterial and aortic blood. Our results suggest cyclic respiratory modifications of red cell parameters attributable to the CO2 Jacobs,Stewart cycle. [source]

    Automated counting of white and red blood cells in the cerebrospinal fluid

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 4 2000
    M.W. Aune
    Summary The objective of this study was to examine to what extent the automated method of the Bayer H*2 instrument could replace the visual counting of white and red blood cells in cerebrospinal fluid. The number of white blood cells as well as the percentage of mononuclear and polymorphonuclear cells were counted in the ,Baso channel' (Research screen 3) whereas the number of red cells were registered as the ,R-count' (Research screen 1). All automated cell counts were compared to visual estimates. The automated count yielded reliable results down to 5 × 106 white blood cells/l and 5 × 108 red blood cells/l. In some samples ,noise' was present in the Baso channel. A correct white blood cell count could then be obtained by counting the cells directly as dots on the screen. It was possible to differentiate between polymorphnuclear cells and mononuclear cells at all WBC concentrations. The automated counting of cerebrospinal fluid can be performed without changing thresholds or sample volumes of the instrument. Thus, in the routine practice it will be possible to alternate between automated counting of whole blood samples and cerebrospinal fluid samples. [source]

    Palpable splenomegaly in children with haemoglobin SC disease: Haematological and clinical manifestations

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 3 2000
    S.A. Zimmerman
    Summary This study aimed to investigate the prevalence of palpable splenomegaly in children with haemoglobin SC (Hb SC) disease, and to determine the haematological and clinical manifestations of splenomegaly in this patient population. We performed a retrospective chart review of 100 patients with Hb SC over 2 years of age followed by the Duke University Paediatric Sickle Cell Program with serial physical examinations and laboratory measurements. Palpable splenomegaly was present in 34% of patients and was more common in males (P = 0.029). Children with splenomegaly had a significantly lower average haemoglobin concentration (10.3 vs. 10.8 g/dl, P = 0.011) and lower platelet count (237 vs. 314 × 109/l, P < 0.001) than those without splenomegaly. Children with measurements both before and after the onset of splenomegaly had a significant decrease in the platelet count (279 vs. 216 × 109/l, P < 0.001) and white blood cell count (9.1 vs. 7.9 × 109/l, P = 0.04) after splenomegaly was identified. Clinical complications included acute splenic sequestration in 12% of children (median age 5.4 years), and hypersplenism with chronic thrombocytopenia in another 10% of patients (median age 10.6 years). Splenomegaly is a common physical finding in children with Hb SC disease and is often associated with mild cytopenias. Clinical complications of splenomegaly include acute splenic sequestration in younger patients and hypersplenism with chronic thrombocytopenia in older children. [source]