Normal White Blood Cell Count Research Articles

1581 Sequential Fecal Microbiota Transplantation for Severe Acute Refractory Clostridium difficile Colitis: A Life-Saving Treatment Approach

INTRODUCTION: Fecal microbiota transplantation (FMT) is now a commonly used mode of treatment for recurrent Clostridium difficile infection (rCDI) refractory to antibiotics. We report a unique case where two sessions of sequential FMT were used to treat acute rCDI refractory to antibiotics with endoscopically documented marked improvement in disease process. CASE DESCRIPTION/METHODS: A 69 year-old female presented with 4 days of fever, large volume non-bloody diarrhea and poor appetite. She denied abdominal pain, nausea or vomiting. She reported two months before this admission, she was treated for hospital-acquired CDI, but could not recall what she was treated with. Physical examination revealed a non-tender abdomen without guarding or rigidity. Laboratory tests revealed hemoglobin 11.3 g/dL and white blood cell (WBC) count 18,700/mcL. Stool testing was positive for C. difficile toxin assay. Computed tomography of the abdomen showed diffuse pancolitis, compatible with CDI, no evidence of bowel perforation or obstruction. Despite treatment with oral vancomycin (500 mg every 6 hours), intravenous metronidazole and probiotics for 5 days, her leukocytosis increased to 32,000/mcL, hemoglobin dropped to 6 g/dL and her symptoms persisted. The decision was made to try FMT and antibiotics were stopped for 48 hours as per FMT protocol. Colonoscopy showed severe pancolitis (Figure 1) and pseudomembranes consistent with severe C. difficile colitis with distal ascending colonic mucosa concerning for ischemia. 250 mL of donor stool was delivered at the proximal transverse colon. After the first FMT, mild improvement was noted in her symptoms and leukocytosis but she persisted to have severe diarrhea. A second FMT was performed 4 days later. Repeat colonoscopy (Figure 2) showed marked improvement in the appearance of pancolonic erythema, inflammation and pseudomembranes compared to prior. 250 mL of donor stool was infused through the colonoscope into the cecum. The following day after the second FMT, the patient began having formed stool and improved leukocytosis. She was discharged from the hospital 3 days after the second FMT with normal stool consistency and normal WBC count. DISCUSSION: There have been no clear data regarding directing severe rCDI treatment with regards to the length of time in between FMTs. Clinicians should be aware that patients may need multiple FMTs to treat rCDI. A shorter duration in between FMTs may rapidly improve severe rCDI, reduce the duration of hospitalization, and improve outcomes.

Dengue rash: white islands in a sea of red

A 36-year-old Japanese woman presented to our emergency department with a 2-day history of fever, headache, eye pain, arthralgia and poor appetite after returning from Thailand. She had been sightseeing...

Risk of appendiceal cancer in patients undergoing appendectomy for appendicitis in the era of increasing nonoperative management

Management practices for acute appendicitis are changing. In cases of nonoperative treatment, the risk of missed or delayed diagnosis of malignancy should be considered. We aimed to identify predictors associated with appendiceal cancer diagnosis after appendectomy for acute appendicitis. This retrospective cohort study was performed using the National Surgical Quality Improvement Program (NSQIP) appendectomy-targeted data set from 2016 to 2017. A total of 21 069 patients with imaging-confirmed or imaging indeterminate appendicitis who underwent appendectomy were included. Logistic regression was used to identify predictors of cancer diagnosis. Increasing age had an increasing monotonic relationship with the odds of pathologic cancer diagnosis after appendectomy (age 50-59 odds ratio [OR], 2.08, 95% confidence interval [CI], 1.28-3.39, P = .003; age 60-69 OR, 2.89, 95% CI, 1.72-4.83, P < .001; age 70-79 OR, 3.85, 95% CI, 2.08-7.12, P < .001; age >80 OR, 5.32, 95% CI, 2.38-11.9, P < .001). Other significant predictors included obesity, morbid obesity, normal preoperative white blood cell count, and imaging indeterminate for appendicitis. When counseling patients regarding operative vs nonoperative treatment options for management of acute appendicitis, the rising risk of a delayed or missed cancer diagnosis with increasing age must be discussed.

An exploration of goal-setting for Cognitive Remediation Therapy in patients with bipolar disorder

Tubulo-villous adenoma is a rare benign appendiceal neoplasm often asymptomatic with the most clinical manifestation that resembles acute appendicitis. Pre-operative diagnosis is difficult by its rarity and the absence of typical symptoms. Adequate treatment is surgical resection.A 69-year-old male was admitted to the Emergency Department with a two-day history of abdominal pain associated with constipation. Abdominal examination revealed abdominal pain localized, at deep palpation, in the right iliac fossa and in hypogastrium without obvious muscle guarding or rebound tenderness. Laboratory tests showed a normal white blood cell count with 82.3% neutrophils and high C-reactive protein level. After a negative abdominal ecography, the patient was evaluated by abdominal computed tomography, which revealed acute appendicitis. The patient was submitted to surgery and open appendectomy was performed. The post-operative course was uneventful and the patient was discharged on the 5th post-operative day.Acute appendicitis may be a clinical manifestation of a benign appendiceal neoplasm. Pre-operative radiological investigations not always are useful for an early diagnosis that is mandatory because of the potential risk of malignant degeneration. Appropriate treatment of acute appendicitis is debated: some surgeons suggest operative treatment, but others advocate for non-operative management. In our case the patient was submitted to surgery avoiding the risk of diagnostic delay of neoplasm.Appendiceal tubulo-villous adenoma is a rare neoplasm difficult to diagnose and suspect because of lack of pathognomonic symptoms and specific diagnostic signs. Acute appendicitis is the most common clinical presentation. Appendectomy is the appropriate treatment.

Feeding of dried sweet orange (Citrus sinensis) peel on humoral immune response of broiler chickens

PurposeAn experiment was conducted to evaluate the effect of dried sweet orange (Citrus sinensis) peel (DCSP) on humoral immune response of broiler chickens.MethodsFour hundred 1-day-old Ross 308 broilers were distributed according to a completely randomized design into five treatments with four replicates of 20 chicks each. The following five dietary treatments were applied: control group with 0% DCSP; diet containing 1.5% DCSP from 1 to 21 days of age (starter phase) and from 1 to 42 days of age, respectively; and diet containing 3% DCSP from 1 to 21 days of age (starter phase) and from 1 to 42 days of age, respectively.ResultsThe DCSP treatments influenced positively total anti-SRBC and IgG titers on days 28 and 42, whereas no differences were found for IgM titer. The anti-NDV titers were not affected by diets; conversely, the anti-AIV titers were different among treatments. The anti-IBD titers were different on days 14 and 42 among diets, whereas anti-IBV titers were not influenced by treatments. Average white blood cell, heterophil, lymphocyte, and monocyte counts, as well as heterophil/lymphocyte (H/L) ratio, were different among treatments.ConclusionThe findings suggested that the dietary inclusion of dried Citrus sinensis promoted some effects on the immune humoral response of chickens; however, these effects were not completely effective to protect birds from the main diseases.

PB2244 CUTANEOUS HEMORRHAGE TYPES AS SUPPORTIVE FACTORS FOR PREDICTING CHRONIC IMMUNE THROMBOCYTOPENIA IN CHILDREN

Please indicate where the abstract has been published before: Journal of Pediatric Hematology OncologyBackground:Immune thrombocytopenia (ITP) of childhood is characterized by isolated thrombocytopenia (platelet count &lt;100,000/μL, with a normal white blood cell count and normal hemoglobin levels). The cause of ITP remains unknown in most cases, but it can be triggered by a viral infection or other immunologic or environmental factors.1–3 The annual incidence of ITP in children is estimated to be between 1 and 6.4 cases per 100,000 children.3–5 Affected children are young (peak age, ∼5y) and previously healthy, and they typically present with the sudden onset of petechiae or purpura a few daysorweeksafteraviralinfection.Boysandgirlsareequally affected.6 Primary ITP is categorized into 3 phases, on the basis of the time period since diagnosis:1 (1) newly diagnosedITP: ITP within 3 months of diagnosis; (2) persistent ITP: ongoing ITP between 3 and 12 months of initial diagnosis; and (3)chronicITP:ITPlasting for &gt;12 months ofdiagnosis.Immune thrombocytopenia (ITP) of childhood is characterized by isolated thrombocytopenia (platelet count &lt;100,000/μL, with a normal white blood cell count and normal hemoglobin levels). The cause of ITP remains unknown in most cases, but it can be triggered by a viral infection or other immunologic or environmental factors.Aims:Our objective was to assess risk factors for developing chronic immune thrombocytopenia (ITP) in children.Methods:All categorical variables were presented by counts and percentages and compared using the χ2 test or the Fisher exact test. Continuous variables were presented by means ± SD and compared by the Mann‐Whitney test because of the non‐normal distribution. A logistic regression model with a backward elimination method wasapplied to identifythe factors that are related to the chronic state of the disease. Significance level was defined as α = 0.05. Analyses were carried out using SPSS version 24.0.Results:Sixty‐two children were included in the study (mean age, 6.15y); 44 (71%) were found to have acute ITP, and 18 (29%) developed chronic ITP (permanent or relapsing thrombocytopenia &gt;12mo). In a univariate analysis, cutaneous hemorrhages were observed significantly more in acute patients (90.9%) than in chronic patients (61.1%). Patients who had acute ITP were more likely to present with a combination of petechiae, purpura, and/or ecchymosis (75%) than patients with chronic disease (44.4%, P = 0.010). In multivariate analysis, older age increased the risk (odds ratio = 1.1; P&lt;0.05) for chronic disease, and manifestations of combination skin hemorrhages (petechiae/ purpura/ecchymosis) reduced the risk (odds ratio = 0.167; P&lt;0.05).Summary/Conclusion:In conclusion, the most important risk factor for chronic disease is older age. Skin hemorrhage types were found to be a supportive factor for the prediction process: the combination of petechia/purpura/ecchymosis was associated with a lower risk for developing chronic disease compared with petechiae alone. Future studies should assess the prognostic value of skin hemorrhage types that are a simple way to predict the course of ITP in children

PS1436 IFN‐Α TREATMENT NORMALIZES THE PLATELET COUNTS AND REDUCES QUIESCENT STEM CELLS IN A CALR‐DEL52 TRANSGENIC MOUSE MODEL, IN VIVO

Background:Treatment options for Myeloproliferative Neoplasms (MPN) have mainly been limited to disease managing risk of thromboembolic events and long‐term transformation to acute myelogenous leukemia and myelofibrosis. To date, type I interferons (IFNs) are the only class of drugs with curative potential in MPN as they can actually reduce the allelic burden of mutant clones in patients. The mechanism of action of IFN in MPNs remains elusive. This is mainly because modelling IFN treatment in mouse models has proven to be difficult due to the short half‐life of murine non‐pegylated IFNs. This shortcoming was solved by the murine pegylated IFN‐α (murine ropeginterferon‐a, mRopeg) developed by PharmaEssentia (Taipei, Taiwan) which can be used to model IFN treatment in mouse models of MPN.Aims:Generation of a conditional transgenic mouse model for CALR‐del52 induced MPN and modelling IFN treatment in these mice using murine pegylated IFN‐α (mRopeg).Methods:The CALR‐del52 transgenic mice (with human mutant sequence) were generated on a C57BL/6 background by homologous recombination of embryonic stem cells at Ozgene (Perth, Australia). The CALR‐del52 floxed mice were bred with vavCre transgenics, thereby allowing the expression of CALR‐del52 specifically in the hematopoietic cells. MPN phenotype in the mice was characterized by peripheral blood counts and flow cytometry. IFN treated mice received mRopeg weekly (600 ng) by subcutaneous injection for 4 weeks. Control mice received the same volume of vehicle (in this case, phosphate buffered saline – PBS).Results:Heterozygous CALR‐del52fl/+;vavCre mice displayed elevated platelet counts starting from 6 weeks of age, with normal white blood cell and red blood cell counts. However, homozygous CALR‐del52fl/fl;vavCre mice developed much higher platelet counts associated with increased white blood cell and decreased red blood cell counts. Homozygous CALR‐del52 mice also developed splenomegaly starting from 6 months of age. Also at 6 months, there was significant increase in the megakaryocyte population in the bone marrow, along with significant increase in LSK cells (Lin− Sca+ kit+) and the quiescent (Fraction A) stem cell population. IFN‐α treatment of CALR‐del52 transgenic mice for 4 weeks resulted in the normalization of the platelet counts to wild type levels. Interestingly, the total stem cell population (LSK cells) in the bone marrow increased upon IFN‐α treatment. However, the percentage of quiescent stem cells (Fraction A) reduced, while the percentage of cycling stem cells (Fraction B) and multipotent stem cells (Fraction C) was increased.Summary/Conclusion:Expression of CALR‐del52 in hematopoietic cells leads to the development of MPN phenotype in mice, and the severity positively correlated with the number of mutant alleles. Heterozygous CALR‐del52 mice developed an Essential Thrombocythemia (ET) like phenotype, with high platelet counts but normal white blood and red blood cell counts. However, the homozygous CALR‐del52 mice developed signs of myelofibrosis with age, including reduced red blood cell counts and splenomegaly. IFN‐α treatment resulted in normalization of platelet numbers to wild type levels within 4 weeks of treatment. Importantly, it also resulted in significant reduction of the quiescent hematopoietic stem cells, while cycling and multipotent stem cells were increased. This suggests that IFN‐α induces proliferation of quiescent stem cells into cycling and multipotent stem cells in CALR‐del52 mutant cells.image

PS917 SAFE TARGETING OF T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA BY SUBUNIT SELECTIVE GAMMA-SECRETASE INHIBITION

Background: SPI1 fusion genes are recurrently found in Early Thymic Precursor cell Acute Lymphoblastic Leukemia (ETP-ALL) cases and represent a distinct subgroup with high frequency of RAS mutations and dismal prognosis. SPI1 (PU.1) is an important transcription factor in hematopoietic cells and its dysregulation contributes to several types of leukemia. Forced overexpression of SPI1 in T-cell progenitors is known to inhibit T-cell differentiation. Conversely, knock-out of TCF7, which is highly expressed in the earliest thymic progenitors, also leads to a T-cell differentiation block. However, the role of SPI1 fusions in driving and maintaining T-ALL remains unknown. Aims: In this study we aimed to elucidate the role of the TCF7-SPI1 fusion and its potential collaboration with RAS mutation in driving and maintaining T-ALL. Methods: We performed whole genome, transcriptome and nanopore sequencing on a patient sample with the TCF7-SPI1 fusion. Primary mouse pro-T cells were cultured on Dll4-coated plates in the presence of stem cell factor (Scf) and interleukin-7 (Il7). In vivo bone marrow transplant (BMT) assays were performed using hematopoietic stem and progenitor cells (HSPCs) isolated from CD2-Cre C57BL/6J mice and transduced with retroviral vectors for inducible expression of the TCF7-SPI1 fusion and/or NRAS (G12D) mutant within developing T-cells of recipient mice. Results: Combined short read and long read RNA-sequencing characterized the exon structure of the TCF7-SPI1 fusion transcript and confirmed the presence of a NRAS (G12D) mutation in the patient sample. Expression of TCF7-SPI1 and NRAS (G12D) transformed pro-T cells to Scf and interleukin-7 (Il7) independent growth. Using an inducible in vivo BMT model, conditional expression of TCF7-SPI1 and NRAS (G12D) within developing T-cells resulted in an aggressive immature acute T-ALL characterized by hyperleukocytosis (CD4-/CD8-, CD3+, CD117+), splenomegaly but no thymus enlargement. This was in contrast to either conditional TCF7-SPI1 alone that did not develop leukemia, or with NRAS (G12D) alone that developed a mature CD4+/CD8+ lymphoma with normal white blood cell count and no peripheral leukemic invasion of the bone marrow and spleen. Notably, a deletion construct of TCF7-SPI1, lacking the N-terminal beta-catenin binding domain of TCF7 lost its oncogenic properties. Summary/Conclusion: Here, we show that TCF7-SPI1 cooperates with NRAS (G12D) to drive an aggressive immature T-cell leukemia in vivo that is dependent on the N-terminal beta-catenin binding domain of TCF7.

PB1745 CLINICAL FEATURES AND TREATMENT OUTCOME OF ACUTE PROMYELOCYTIC LEUKEMIA IN SOUTHERN TUNISIA

Background:All‐trans retinoic acid (ATRA) is the major advance in the treatment of acute promyelocytic leukemia (APL). Its introduction in the treatment of APL has revolutionized the outcome of this disease.Aims:The current study reports the clinical features and treatment outcome of patients with acute promyelocytic leukemia (APL) treated at the hematology department of Sfax from Tunisia.Methods:Our study is retrospective; it concerned all patients with the diagnosis of APL and followed in the hematology department of Hedi Chaker Hospital Sfax, from January 2000 until December 2017. The diagnosis of APL is based on morphological, cytogenetic and molecular study. The specific treatment is similar that of the French protocol APL93 until 2013, and then similar that of Spanish protocol APL2005 since January 2014.The treatment regimen includes an induction treatment combining ATRA and chemotherapy followed by 2 consolidation courses in the APL93 protocol and 3 consolidation courses in the APL 2005 protocol followed by a 2‐year maintenance treatment with methotrexate, mercaptopurine and ATRA. We evaluate the rates of remission, death and overall survival (Kaplan‐Meier method).Results:We collected 60 patients. The sex ratio was 1.32 with a median age of 32 years (extreme: 2‐75 years). Hyperleukocytosis (GB &gt; 10000 / mm3) was noted in 20 patients (33%). The average white blood cell count was 12995 / mm3. The disseminated intravascular coagulation (DIC) was found in the majority of cases (67% of cases). The t(15,17) was found in 86.1% of cases. The PML‐RARAα transcript was positive in 100% of cases. Seven patients (11.6%) died before treatment with cerebral hemorrhage. Thirty one patients were treated by the APL 93 (group1) and twenty two patients were treated by the protocol APL2005 (group 2). Ten patients (16.7%) died early between days 2 and 5 of the induction course. Forty three patients were evaluable for induction therapy. Complete remission was obtained in thirty nine patients (91% of the evaluable patients and 70% of the treated patients) and tow patient failure (4%). No death was reported during consolidation or maintenance treatment. A late bone marrow relapse was observed in 5 patients (12%), one patient in the group 2 and four patients in the group 1. At five years of follow up, overall survival and event‐free survival are 71% and 55.9%, respectively, and relapse‐free survival is 77%.Summary/Conclusion:In our series, the DIC rates is correlated that of the literature. It would be increase the early death rate by hemorrhage syndrome. The complete remission and overall survival are improved with the APL 2005 protocol, but there remain lower than that of the literature. This is explained by a high rate of early mortality (before7 days of induction) by cerebral hemorrhage, of the higher frequency of hyper‐leukocyte forms and the delay in diagnosis and management for our patients.

IL-6, IL-8 drive LAG3/PD1 immune suppression on effector and naïve, peripheral blood CD8+ T cells in cancer patients

Abstract Cancer patients off therapy and with normal white blood cell counts are often at greater risk for infections, immune dysregulation, progressive disease or reactivation of viral infections. However, the exact mechanism of this systemic immunosuppression in cancer patients is not fully understood. We hypothesize that cancer patients may have systemic immune suppression via cytokine-driven IR expression in all CD8+ T cells subsets, including naïve cells. PBL were obtained from healthy donors and treatment-naïve NSCLC, HNSCC, and melanoma patients. IR (i.e. LAG3, PD1, CTLA4, etc) expression was assessed on CD8+ T cells, CD4+ T cells, and regulatory T cells. Plasma cytokine concentrations were compared by Luminex. Autologous micro-stimulation assays were performed on peripheral CD8+ or CD4+ T cells with antigen presenting cells plus or minus IR blockade. CD8+ T cells, including naive CD8+ T cells, from cancer patient PBL contain elevated total LAG3 expression which correlated with worse state, worse survival, and elevated expression of other IRs. Further, CD8+ T cells from these patients had decreased proliferation, which was rescued with the addition of anti-LAG3 or anti-PD1. Plasma from these patients had significantly elevated levels of cytokines that can signal via STAT3 (i.e. IL-6, IL-8), which were independently found to increase total IR expression in healthy donor, naïve CD8+ T cells. Patients with cancer have systemic elevations IL-6 and IL-8 leading to increased IR expression in naïve, peripheral CD8+ T cells making them poised for exhaustion even before TCR binding. These findings suggest that cytokine combined with IR blockade may play a role in reversing PD1 blockade resistance.

Residual cavity hydrops initially misdiagnosed as recurrent hepatic echinococcosis

A 37-year-old woman presented to our liver surgery clinic with a 12-month history of intermittent pain in the right upper quadrant of the abdomen. More than 5 years earlier, the patient had undergone routine excision of the internal capsule because of a hepatic hydatid cyst and had taken albendazole regularly after surgery (300 mg every 12 h for 6 months). A large heteroechoic hepatic mass was identified by abdominal ultrasound. Laboratory tests showed a normal white blood cell count, a normal absolute eosinophil count, and negative anti-echinococcus IgG antibody status. A CT scan showed a 5-cm low-density mass with calcification in the anterior superior segment of the right lobe of the liver, which suggested recurrence of liver hydatid cyst (figure). The patient had a laparotomy, during which the entire cyst was removed intact. The cyst wall was white and contained a small amount of bile and pigmented stones. Pathological testing showed intrahepatic cystic degeneration of liver tissue, and a large amount of bile pigment deposition inside the cyst wall. Echinococcus granulosus was not detected. At follow-up 6 months after surgery, the patient had no residual symptoms.

Higher monocyte count with normal white blood cell count is positively associated with 10-year cardiovascular disease risk determined by Framingham risk score among community-dwelling Korean individuals.

The cardiovascular disease (CVD) has been identified as a leading cause of premature mortality among middle-aged and elderly individuals globally. Inflammation plays an important role in aging and age-related diseases, such as atherosclerosis and CVD. White blood cell (WBC) count is an inexpensive, simple biomarker of systemic inflammations and includes several cell subtype counts, such as neutrophils, monocytes, lymphocytes, basophils, and eosinophils. However, which component of a WBC count has the ability to predict CVD remains controversial. The objective of this study was to assess the association between monocyte counts and 10 year-CVD risk among community-dwelling Korean individuals using the Framingham risk score (FRS). We studied a total of 627 participants aged over 30 years who underwent routine health examinations. The mean age of the study population was 48.1 ± 11.7 years, and 56.9% were male. In the multiple regression analysis, the independent contribution of monocyte count to Framingham 10-year CVD risk was 0.217 ± 0.092 (P = .018) after adjusting for confounding variables. We found that of the various WBCs, monocyte count is an independent predictor of CVD risk. Further larger-scale prospective cohort studies are warranted to determine these associations in the future.

Microbial Evidence in Congenital Pulmonary Airway Malformations of Young Asymptomatic Infants.

Introduction: Experts of pediatric endosurgery recommend early thoracoscopic resection of congenital pulmonary airway malformations (CPAM) even in asymptomatic infants due to the risk of later infections. However, neither the rate of lower airway inflammation nor the underlying microbes and their pathogenic potential have been revealed in CPAMs yet. Using latest gene-sequencing techniques, we present the first study analyzing the pulmonary microbiome in young asymptomatic infants with CPAM. Materials and Methods: Seven asymptomatic infants (age 2-3 months) underwent thoracoscopic lobectomy for CPAM. Preoperatively, blood test was taken to rule out systemic infections. Surgical specimen was screened and graded for local inflammation by hematoxylin and eosin (HE) histology. The pulmonary microbiome and mycobiome were assessed using next-generation sequencing. Results: Preoperatively, all infants had normal white blood cell counts and normal C-reactive protein (CRP) levels. Microbial evidence was found in 4/7 patients, 3 being bacteria (Pseudomonas twice, Streptococcus sp. once) and 1 fungal species (Pneumocystis jirovecii, mostly known from immunosuppressed patients, and Preussia funiculata). Histologically, both Pseudomonas and fungi were associated with low and intermediate pulmonary inflammation, whereas Streptococcus was negative for leucocyte infiltration. Conclusion: For the first time ever this study revealed genetic evidence of pathogenic microbes in 4/7 CPAMs causing lower airway inflammation in 3/7 asymptomatic young infants. Especially pseudomonas and fungi represent considerable pathogenic potential and call for a broader, age-dependent, multicenter study of CPAMs. Such data could be important for pediatric surgeons counseling parents about the necessity and timing of thoracoscopic resections.

Sympathetic Joint Effusion in an Urban Hospital.

ObjectiveSympathetic joint effusion (SJE) and sympathetic synovial effusion (SSE) are recognized as causes of noninflammatory effusion with <2000 white blood cell (WBC) WBC/mm3 in the joint and bursa, respectively. Data on normal range SJE/SSE with <200 WBC/mm3 are unknown. We aimed to investigate the incidence, disease characteristics, and associated triggers of normal range SJE/SSE and to propose diagnostic criteria.MethodsThis retrospective study included patients hospitalized at Temple University Hospital who underwent a diagnostic arthrocentesis for joint or bursal effusion of unclear etiology from 31 January 2010 to 10 December 2016. A cohort of 72 patients with normal range synovial fluid (<200 WBC/mm3) fulfilled all inclusion criteria for detailed chart review.ResultsAnnualized incidence of SJE/SSE was 1.2%. All 72 patients presented with joint pain and swelling. Twenty‐three (32%) also had warmth and 12 (17%) had erythema. Symptom onset was hours to within 6 days in 45 (63%) patients. The most commonly affected joint was the knee (61, 85%). Concurrent pathology in close anatomical proximity to SJE/SSE in the same limb was documented in 29 (40%) patients, most of which (26 of 29, 89%) were infection, deep venous thrombosis, intramuscular fluid collection, and trauma. Less common pathology included adjacent recent hip surgery, loosening of hip prosthesis, and extracorporeal membrane oxygenation catheters.Conclusion SJE/SSE is not uncommon in hospitalized patients and mimics both inflammatory and septic arthritis. It is seen with normal and noninflammatory synovial fluid. A search for a root cause in the same limb is warranted when evaluating acute or subacute painful joint effusions with normal range synovial fluid WBC count.

Substantial improvement in immune thrombocytopenic purpura associated with T-cell/histiocyte-rich B-cell lymphoma treated with chemotherapy: A case report.

Immune thrombocytopenic purpura (ITP) is characterized by antibody and immune platelet destruction, occasionally leading to life-threatening hemorrhage. ITP is a frequent complication of chronic lymphoid leukemia, but is rarely associated with diffuse large B-cell lymphoma (DLBCL). We herein describe a case of ITP associated with T-cell/histiocyte-rich B-cell lymphoma (T/HRBCL), which is a rare variant of DLBCL. A 54-year-old man presented with fever, multiple lymphadenopathies, petechial purpura and intraoral mucosal hemorrhage. Laboratory data revealed thrombocytopenia, normal white blood cell count, mild anemia, no active viral infections, and no autoimmune antibodies. Multiple lymphadenopathies were observed on computed tomography. A bone marrow biopsy revealed minor hypercellularity with increased number of megakaryocytes; however, there were no pathological cells or phagocytic cells. The patient was diagnosed with ITP; concurrently, he was also diagnosed with T/HRBCL via lymph node biopsy, and was treated accordingly with a chemotherapeutic regimen comprising rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone. Prompt reduction in the size of the superficial lymph nodes and an increase of the platelet count were observed simultaneously. To the best of our knowledge, this is the first report of T/HRBCL complicated by ITP. The findings strongly suggest a causative association between ITP and T/HRBCL.

The Case Files

Figure: Computed tomography of the abdomen and pelvis with intravenous contrast. The yellow arrows show the appendix coursing through the lower abdomen and overlying the bladder.FigureFigureThe progressive suprapubic pain was a cunning symptom. The 38-year-old man had had five days of that pain and dysuria. By the time he presented to our ED, his pain had spread to the right lower quadrant as well. He had a history of diverticulitis after a laparoscopic left hemicolectomy four years earlier. He reported no fevers, but complained of nausea and diarrhea. He was afebrile at 36.8°C with a pulse of 76 bpm. All other vital signs were normal. Physical exam was significant for suprapubic pain and right lower quadrant tenderness to palpation without rebound, guarding, or distention. His workup revealed a normal white blood cell count of 4.2, as well as a normal basic chemistry and urinalysis. A CT of the abdomen and pelvis with intravenous contrast showed a dilated appendix tip measuring 12 mm with mucosal enhancement and fat stranding. The appendix was elongated and overlying the bladder. (Photos.) Our patient was diagnosed with acute appendicitis. He was given antibiotics, intravenous fluids, kept NPO, and admitted to the surgical team. He underwent uncomplicated laparoscopic appendectomy and was discharged the next day. Suprapubic pain and right lower quadrant pain are typical chief complaints in the emergency department, but it is important to keep a broad differential diagnosis when evaluating patients. In acute appendicitis, migrating right lower quadrant pain, fever, anorexia, nausea, and vomiting are unreliable, occurring consistently in only about half of cases. (Hong Kong Med J 2000; 6[3]:254; http://bit.ly/2UiKXCh.) When considering additional diagnoses, it is important to recall anatomical structures near where the pain is reported and to be mindful of variations in appendiceal sizes and locations. The appendix in the retrocecal position can cause inflammation of the retroperitoneal organs, mimicking biliary colic or gastroenteritis. (Adv J Emerg Med 2018;2[2]:e21; http://bit.ly/2sL5uni.) A perforated appendix can cause fistula formation to the anterior abdominal wall and present as a palpable mass. (BMJ Case Rep 2016 Nov 10; http://bit.ly/2DwFa6h.) Our patient's appendix was elongated and overlying the bladder, resulting in suprapubic pain and dysuria.

Clinical Characteristics and Antibiotic Resistance of Mycoplasma Pneumoniae Pneumonia in Hospitalized Chinese Children.

To analyze the clinical characteristics and antibiotic resistance of Mycoplasma pneumoniae pneumonia (MP) in Chinese patients, providing valuable information for the management of patients with MP. A total of 120 children who were hospitalized in The First Hospital of Huzhou between January and December 2016 for respiratory tract infection due to M. pneumoniae were enrolled in this study. Infection with M. pneumoniae was confirmed by ELISA for M. pneumoniae antibody, PCR, and throat culture. Antibiotic resistance was measured from the minimum inhibitory concentrations (MICs) of antibiotics. The 23S rRNA gene of M. pneumoniae was also examined for mutations using DNA sequencing. Patients with MP were classified into antibiotic resistance (n = 98) and no resistance (n = 20) groups. For the 98 patients showing antibiotic resistance, they were further stratified into subgroups based on the antibiotics initially prescribed: azithromycin or erythromycin (n = 78) and cephalosporin or penicillin (n = 20). Clinical characteristics were compared between the patient groups. Antibiotic resistance group presented significantly longer febrile days compared to the no resistance group (P = 0.007). The number of febrile days after macrolide treatment was also longer in antibiotic resistance group than in no resistance group (P = 0.042). MP patients initially treated with azithromycin or erythromycin showed a longer average duration of respiratory symptoms (P = 0.046) and had a fever for more days after macrolide treatment (P = 0.009) compared to those received cephalosporin or penicillin. The average white blood cell count of patients treated with azithromycin or erythromycin was nearly half of those treated with cephalosporin or penicillin (P < 0.001). Nearly 90% of the resistant M. pneumoniae strains showed A to G substitution at position 2063 of the 23S rRNA gene. The clinical characteristics and antibiotic resistance of MP were analyzed in 120 Chinese patients. DNA sequencing revealed a highly prevalent A2063G mutation in the 23S rRNA gene.

Combined utility of white blood cell count and blood glucose for predicting in-hospital outcomes in acute ischemic stroke

BackgroundHigh white blood cell (WBC) count and high blood glucose level are risk factors for mortality and pneumonia after acute ischemic stroke (AIS). We investigated the combined effect of high WBC count and high blood glucose level on hospital admission and in-hospital mortality and pneumonia in acute AIS patients.MethodsA total of 3124 AIS patients enrolled from December 2013 to May 2014 across 22 hospitals in Suzhou city were included in the present study. We divided patients into four groups according to their level of WBC count and blood glucose: NWNG (normal WBC count and normal glucose), NWHG (normal WBC count and higher glucose), HWNG (higher WBC count and normal glucose), and HWHG (higher WBC count and higher glucose). Cox proportional hazard model and logistic regression model were used to estimate the combined effect of WBC count and blood glucose on all-cause in-hospital mortality and pneumonia in AIS patients.ResultsHWHG was associated with a 2.22-fold increase in the risk of in-hospital mortality in comparison to NWNG (adjusted hazard ratio [HR] 2.22; 95% confidence interval [CI], 1.21–4.07; P trend = 0.003). The risk of pneumonia was significantly higher in patients with HWHG compared to those with NWNG (adjusted odds ratio [OR] 2.61; 95% CI, 1.66–4.10; P trend < 0.001). The C-statistic for the combined WBC count and blood glucose was higher than WBC count or blood glucose alone for prediction of in-hospital mortality and pneumonia (all p < 0.01).ConclusionsHigh WBC count combined with high blood glucose level at admission was independently associated with in-hospital mortality and pneumonia in AIS patients. Moreover, the combination of WBC count and blood glucose level appeared to be a better predictor than WBC count or blood glucose alone.

Association of Severity of Posttraumatic Stress Disorder With Inflammation: Using Total White Blood Cell Count as a Marker

Background Inflammation is known to be associated with posttraumatic stress disorder. It is not known if total white blood cell count, a routinely checked inflammatory marker, is associated with posttraumatic stress disorder symptom trajectories using medical record data. Methods We used latent class growth analysis to identify three-year posttraumatic stress disorder symptom trajectories using posttraumatic stress disorder (PTSD) Checklist (PCL) scores. The outcome for each patient was maximum white blood cell count from index posttraumatic stress disorder diagnosis to last PCL. Using linear regression analysis, we then calculated and compared the average white blood cell count for each trajectory before and after controlling for age, gender, race, obesity, smoking, diabetes, hypertension, cardiovascular disease, depression, and other comorbid inflammatory conditions. Results Patients were 40.2 (SD ± 13.5) years of age, 83.7% males and 67.9% white. We identified three PCL trajectory groups based on symptom severity over time: “moderate-large decrease,” “moderate-severe-slight decrease,” and “severe-persistent.” In adjusted analyses, “severe-persistent” versus “moderate-large decrease” had significantly higher white blood cell count (B = 0.64; 95%CI = 0.18, 1.09; p = .006). Although non-significant, “moderate-severe-slight decrease” versus “moderate-large decrease” also had a higher white blood cell count (B = 0.42; 95% CI: −0.02, 0.86; p = .061). Conclusion Persistently severe posttraumatic stress disorder is associated with a higher white blood cell count than improving posttraumatic stress disorder. White blood cell appears to have utility for measuring the association between psychiatric disorders and inflammation in retrospective cohort studies involving large administrative medical record data bases.

Role of Procalcitonin as a Predictor of Clinical Outcome in Acute Diabetic Foot Infections: A Prospective Study.

Background:Prediction of outcome in diabetic foot infection (DFI) remains difficult due to lack of active signs of infection, and apparently normal white blood cell (WBC) count. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) have been studied previously in this regard and were not useful. Hence, we evaluated procalcitonin (PCT) as a prognostic marker in this study.Objectives:We aimed to study the role of PCT, CRP, and ESR levels in predicting clinical outcome of acute DFI.Materials and Methods:A total of 250 subjects (197 men, 53 women) with acute DFI were enrolled. WBC count, ESR, CRP, and PCT were done for all subjects at admission after obtaining informed consent. Subjects were managed according to hospital protocol and followed up for 1 month. Clinical outcome was assessed based on mobility and morbidity status of the subject.Results:Old age, anemia, hyponatremia, hypoalbuminemia, and elevated serum creatinine were risk factors for poor outcome. Presence of cardiac failure, diabetic retinopathy, peripheral vascular disease, previous amputations, and positive bone culture had negative influence on clinical outcome. Elevated WBC count, ESR, CRP, and serum PCT were significantly associated with bad outcome. Elevated PCT (>2 ng/ml) [odds ratio (OR) (95% confidence interval (CI)), 2.03 (1.13–5.19), P < 0.001], gangrene [OR (95% CI), 2.2 (1.02–4.73), P = 0.04], and sepsis [OR (95% CI), 10.101 (4.34–23.25), P < 0.001] were good predictors of clinical outcome in acute DFI.Conclusion:PCT proved to be a reliable marker of acute DFI and good predictor of clinical outcome than existing markers WBC count, ESR, and CRP. Hence it should be useful for clinicians while managing acute DFI.