Dr. Shomali is a clinical assistant professor of Hematology at Stanford University School of Medicine. He is board certified in hematology & medical oncology.
Dr. Shomali specializes in the treatment of blood cancers such as myeloproliferative neoplasms and myelodysplastic syndromes. He aims to provide compassionate, personalized, and evidence-based care to each patient.
Dr. Shomali received his medical degree from the University of Jordan, followed by a postdoctoral fellowship at MD Anderson Cancer Center where he studied infections in cancer patients and the role of biomarkers in defining tumor fever. He completed his residency training in Internal Medicine at the Cleveland Clinic Foundation where he served as a Chief Medical Resident. He then joined Stanford University for his combined Hematology & Oncology fellowship training.
Dr. Shomali’s research interests include the study of novel agents in myeloproliferative neoplasms and myelodysplastic syndromes. He developed investigator-initiated clinical trials for patients with eosinophilic neoplasms and advanced myelofibrosis. In addition, he co-authored several papers and book chapters discussing the care of patients with cancer. His work has been presented in national meetings and published in peer reviewed journals including Blood, American Journal of Hematology, British Journal of Hematology, Leukemia & Lymphoma, and Cancer.
Among his honors, Dr. Shomali received the Cleveland Clinic Excellence in Teaching Award and was named to the Alpha Omega Alpha Medical Honor Society. He has received a Young Investigator Award from the Conquer Cancer Foundation, an NIH Institutional National Research Service Award, and a Stanford Cancer Institute Fellowship Award.
Dr. Shomali is a member of the American Society of Hematology and the American Society of Clinical Oncology.
Clinical Assistant Professor, Medicine - Hematology
Board Certification: American Board of Internal Medicine, Internal Medicine (2015)
Postdoctoral Fellowship, Stanford University School of Medicine, Hematology (2020)
Fellowship, Stanford University School of Medicine, Hematology & Oncology (2019)
Chief Resident, Cleveland Clinic Foundation, Ohio (2016)
Clinical Associate, Cleveland Clinic Foundation, Ohio (2016)
Residency, Cleveland Clinic, Internal Medicine (2015)
Postdoctoral Fellowship, MD Anderson Cancer Center, Infectious Diseases (2012)
Medical Degree, University of Jordan Medical School, Jordan (2009)
Refined diagnostic criteria for bone marrow mastocytosis: a proposal of the European competence network on mastocytosis.
In the current classification of the World Health Organization (WHO), bone marrow mastocytosis (BMM) is a provisional variant of indolent systemic mastocytosis (ISM) defined by bone marrow involvement and absence of skin lesions. However, no additional diagnostic criteria for BMM have been proposed. Within the registry dataset of the European Competence Network on Mastocytosis, we compared characteristics and outcomes of 390 patients with BMM and 1175 patients with typical ISM. BMM patients were significantly older, predominantly male, had lower tryptase and lower burden of neoplastic mast cells, and displayed a higher frequency of allergic reactions, mainly triggered by Hymenoptera, than patients with typical ISM. The estimated 10-year progression-free survival of BMM and typical ISM was 95.9% and 92.6%, respectively. In BMM patients defined by WHO-based criteria, the presence of one B-Finding and tryptase level ≥125ng/mL were identified as risk factors for progression in multivariate analyses. BMM patients without any of these risk factors were found to have better progression-free survival (p<0.05) and better overall survival (p<0.05) than other ISM patients. These data support the proposal to define BMM as a separate SM variant characterized by SM criteria, absence of skin lesions, absence of B-Findings, and tryptase levels <125ng/mL.
View details for DOI 10.1038/s41375-021-01406-y
View details for PubMedID 34545185
- World Health Organization-defined eosinophilic disorders: 2021 update on diagnosis, risk stratification, and management. American journal of hematology 2021
Chronic Eosinophilic Leukemia: Diagnosis and Therapy
CIG MEDIA GROUP, LP. 2021: S27-S29
View details for Web of Science ID 000691910500009
Diagnosis and Management of Neutrophilic Myeloid Neoplasms
CLINICAL ADVANCES IN HEMATOLOGY & ONCOLOGY
2021; 19 (7): 450-459
View details for Web of Science ID 000669942200006
Clinical and histopathological features of myeloid neoplasms with concurrent Janus kinase 2 (JAK2) V617F and KIT proto-oncogene, receptor tyrosine kinase (KIT) D816V mutations.
British journal of haematology
We report on 45 patients with myeloid neoplasms and concurrent Janus kinase 2 (JAK2) V617F and KIT proto-oncogene, receptor tyrosine kinase (KIT) D816V (JAK2pos . /KITpos . ) mutations, which are individually identified in >60% of patients with classical myeloproliferative neoplasms (MPN) and >90% of patients with systemic mastocytosis (SM) respectively. In SM, the concurrent presence of a clonal non-mast cell neoplasm [SM with associated haematological neoplasm (SM-AHN)] usually constitutes a distinct subtype associated with poor survival. All 45 patients presented with a heterogeneous combination of clinical/morphological features typical of the individual disorders (e.g. leuco-/erythro-/thrombocytosis and elevated lactate dehydrogenase for MPN; elevated serum tryptase and alkaline phosphatase for SM). Overlapping features identified in 70% of patients included splenomegaly, cytopenia(s), bone marrow fibrosis and additional somatic mutations. Molecular dissection revealed discordant development of variant allele frequency for both mutations and absence of concurrently positive single-cell derived colonies, indicating disease evolution in two independent clones rather than monoclonal disease in >60% of patients examined. Overall survival of JAK2pos . /KITpos . patients without additional somatic high-risk mutations [HRM, e.g. in serine and arginine-rich splicing factor 2 (SRSF2), additional sex combs like-1 (ASXL1) or Runt-related transcription factor 1 (RUNX1)] at 5years was 77%, indicating that the mutual impact of JAK2 V617F and KIT D816V on prognosis is fundamentally different from the adverse impact of additional HRM in the individual disorders.
View details for DOI 10.1111/bjh.17567
View details for PubMedID 34060083
Response Criteria in Advanced Systemic Mastocytosis: Evolution in the Era of KIT Inhibitors.
International journal of molecular sciences
2021; 22 (6)
Systemic mastocytosis (SM) is a rare clonal hematologic neoplasm, driven, in almost all cases, by the activating KIT D816V mutation that leads to the growth and accumulation of neoplastic mast cells. While patients with advanced forms of SM have a poor prognosis, the introduction of KIT inhibitors (e.g., midostaurin, and avapritinib) has changed their outlook. Because of the heterogenous nature of advanced SM (advSM), successive iterations of response criteria have tried to capture different dimensions of the disease, including measures of mast cell burden (percentage of bone marrow mast cells and serum tryptase level), and mast cell-related organ damage (referred to as C findings). Historically, response criteria have been anchored to reversion of one or more organ damage finding(s) as a minimal criterion for response. This is a central principle of the Valent criteria, Mayo criteria, and International Working Group-Myeloproliferative Neoplasms Research and Treatment and European Competence Network on Mastocytosis (IWG-MRT-ECNM) consensus criteria. Irrespective of the response criteria, an ever-present challenge is how to apply response criteria in patients with SM and an associated hematologic neoplasm, where the presence of both diseases complicates assignment of organ damage and adjudication of response. In the context of trials with the selective KIT D816V inhibitor avapritinib, pure pathologic response (PPR) criteria, which rely solely on measures of mast cell burden and exclude consideration of organ damage findings, are being explored as more robust surrogate of overall survival. In addition, the finding that avapritinib can elicit complete molecular responses of KIT D816V allele burden, establishes a new benchmark for advSM and motivates the inclusion of definitions for molecular response in future criteria. Herein, we also outline how the concept of PPR can inform a proposal for new response criteria which use a tiered evaluation of pathologic, molecular, and clinical responses.
View details for DOI 10.3390/ijms22062983
View details for PubMedID 33804174
A novel activating JAK1 mutation in chronic eosinophilic leukemia.
Hypereosinophilia (HE) has been arbitrarily defined as persistent eosinophilia >1.5 x109/L, and is broadly divided into primary (clonal or neoplastic; HEN), secondary/reactive (HER), or of undetermined significance (HEUS) when no cause is identified. The use of myeloid next generation sequencing panels has led to the detection of several mutations in patients previously diagnosed with HEUS, reassigning some patients to the category of HEN, specifically the World Health Organization category of chronic eosinophilic leukemia, not otherwise specified (CEL, NOS). Here we describe a novel somatic JAK1 pseudokinase domain mutation (R629_S632delinsSA) in a patient with HE that had been initially characterized as a variant of uncertain significance. We performed functional studies that demonstrate that this mutation results in growth factor independence of Ba/F3 cells in vitro and activation of the Janus Kinase-Signal Transducer and Activator of Transcription Proteins (JAK-STAT) pathway. These effects were abrogated by the JAK1/JAK2 inhibitor ruxolitinib. The R629_S632delinsSA is the first known somatic mutation in JAK1 linked to a clonal eosinophilic neoplasm, and highlights the importance of the JAK-STAT pathway in eosinophil survival.
View details for DOI 10.1182/bloodadvances.2021004237
View details for PubMedID 34496019
Venetoclax and hypomethylating agent therapy in high risk myelodysplastic syndromes: a retrospective evaluation of a real-world experience.
Leukemia & lymphoma
Treatment with hypomethylating agents (HMAs) azacitidine or decitabine is the current standard of care for high risk myelodysplastic syndromes (MDSs) but is associated with low rates of response. The limited number of treatment options for patients with high risk MDS highlights a need for new therapeutic options. Venetoclax is an inhibitor of the BCL-2 protein which, when combined with an HMA, has shown high response rates in unfit and previously untreated acute myeloid leukemia. We performed a retrospective study of high risk MDS patients receiving combination HMA plus venetoclax in order to determine their effectiveness in this context. We show that in our cohort, the combination results in high response rates but is associated with a high frequency of myelosuppression. These data highlight the efficacy of combination HMA plus venetoclax in high risk MDS, warranting further prospective evaluation in clinical trials.
View details for DOI 10.1080/10428194.2020.1775214
View details for PubMedID 32543932
- Late presentation of dyskeratosis congenita. British journal of haematology 2019
World Health Organization-defined eosinophilic disorders: 2019 update on diagnosis, risk stratification, and management.
American journal of hematology
The eosinophilias encompass a broad range of non-hematologic (secondary or reactive) and hematologic (primary, clonal) disorders with potential for end-organ damage.Hypereosinophilia has generally been defined as a peripheral blood eosinophil count greater than 1.5 x 109 /L and may be associated with tissue damage. After exclusion of secondary causes of eosinophilia, diagnostic evaluation of primary eosinophilias relies on a combination of morphologic review of the blood and marrow, standard cytogenetics, fluorescent in situ-hybridization, flow immunophenotyping, and T-cell clonality assessment to detect histopathologic or clonal evidence for an acute or chronic hematolymphoid neoplasm.Disease prognosis relies on identifying the subtype of eosinophilia. After evaluation of secondary causes of eosinophilia, the 2016 World Health Organization endorses a semi-molecular classification scheme of disease subtypes which includes the major category 'myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA, PDGFRB, or FGFR1 or with PCM1-JAK2', and the MPN subtype, chronic eosinophilic leukemia, not otherwise specified' (CEL, NOS). Lymphocyte-variant hypereosinophilia is an aberrant T-cell clone-driven reactive eosinophila, and idiopathic hypereosinophilic syndrome (HES) is a diagnosis of exclusion.The goal of therapy is to mitigate eosinophil-mediated organ damage. For patients with milder forms of eosinophilia (e.g. < 1.5 x 109 /L) without symptoms or signs of organ involvement, a watch and wait approach with close-follow-up may be undertaken. Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib. Corticosteroids are first-line therapy for patients with lymphocyte-variant hypereosinophilia and HES. Hydroxyurea and interferon-alfa have demonstrated efficacy as initial treatment and in steroid-refractory cases of HES. In addition to hydroxyurea, second line cytotoxic chemotherapy agents and hematopoietic stem cell transplantation have been used for aggressive forms of HES and CEL with outcomes reported for limited numbers of patients. The use of antibodies against interleukin-5 (IL-5) (mepolizumab), the IL-5 receptor (benralizumab), as well as other targets on eosinophils remains an active area of investigation. This article is protected by copyright. All rights reserved.
View details for DOI 10.1002/ajh.25617
View details for PubMedID 31423623
A Kindred with a β-Globin Base Substitution [β89(F5)Ser→Arg (AGT>AGG); HBB: c.270T>G] Resulting in Hemoglobin Vanderbilt.
High oxygen affinity hemoglobins (Hbs), characterized by a decreased ability to release oxygen to the tissues and a left-shifted oxygen dissociation curve, are a rare cause of secondary erythrocytosis. Here, we report a base substitution in the β-globin gene at codon 89 (AGT>AGG) in a kindred with familial erythrocytosis resulting in Hb Vanderbilt, a high oxygen affinity variant.
View details for DOI 10.1080/03630269.2019.1680382
View details for PubMedID 31657650
The new tool "KIT" in advanced systemic mastocytosis.
Hematology. American Society of Hematology. Education Program
2018; 2018 (1): 127–36
Mastocytosis is a rare disease characterized by KIT-driven expansion and accumulation of neoplastic mast cells in various tissues. Although mediator symptoms related to mast cell activation can impose a symptom burden in cutaneous disease and across the spectrum of systemic mastocytosis subtypes, the presence of an associated hematologic neoplasm and/or organ damage denotes advanced disease and the potential for increased morbidity and mortality. In addition to the revised 2016 World Health Organization classification of mastocytosis, a new diagnostic and treatment toolkit, tethered to enhanced molecular characterization and monitoring, is poised to transform the management of patients with advanced systemic mastocytosis (advSM). Although the efficacy of midostaurin and novel selective KIT D816V inhibitors, such as avapritinib (BLU-285), have validated KIT as a therapeutic target, the clinical and biologic heterogeneity of advSM requires that we reimagine the blueprint for tackling these diseases and use tools that move beyond KIT-centric approaches.
View details for PubMedID 30504301
Myelophthisic marrow involved by breast cancer and acute myeloid leukemia
2018; 131 (9): 1036
View details for PubMedID 29496704
- Concurrent uvulitis and epiglottitis. Cleveland Clinic journal of medicine 2016; 83 (10): 712-714
- Safe and effective use of ponatinib in a patient with chronic myeloid leukemia and acute venous thromboembolism on therapeutic anti-coagulation LEUKEMIA & LYMPHOMA 2016; 57 (1): 193-195
- Gastric Pneumatosis: An Unexpected Complication of Intractable Vomiting in Gastrointestinal Cancers JOURNAL OF PAIN AND SYMPTOM MANAGEMENT 2015; 49 (4): E3-E4
The Utility of Proadrenomedullin and Procalcitonin in Comparison to C-Reactive Protein as Predictors of Sepsis and Bloodstream Infections in Critically III Patients With Cancer
CRITICAL CARE MEDICINE
2014; 42 (12): 2500-2507
Infections in critically ill patients continue to impose diagnostic and therapeutic challenges. We seek to investigate the utility of proadrenomedullin and procalcitonin as diagnostic and prognostic biomarkers in febrile critically ill patients with cancer and compare their performance with that of C-reactive protein.Single-center prospective cohort study.Tertiary care, academic, university hospital.One hundred fourteen critically ill patients with cancer with fever.None.Blood samples were withdrawn on the day of fever onset and 4 to 7 days thereafter, and the serum proadrenomedullin, procalcitonin, and C-reactive protein levels were measured using the Kryptor technology afterward. Of the 114 adult patients, 27 had bloodstream infections, 36 had localized infections, and the remaining had no infections. The area under the receiver operating characteristic curve for bloodstream infection diagnosis was significantly greater for proadrenomedullin (0.70; 95% CI, 0.59-0.82) and procalcitonin (0.71; 95% CI, 0.60-0.83) compared with C-reactive protein (0.53; 95% CI, 0.39-0.66) (p = 0.021 and p = 0.003, respectively). Receiver operating characteristic analysis also showed that proadrenomedullin (p = 0.005) and procalcitonin (p = 0.009) each had a better performance than C-reactive protein in predicting patients' mortality within 2 months after their fever onset. Regarding patients' response to antimicrobial therapy, proadrenomedullin, procalcitonin, and C-reactive protein levels all significantly decreased from baseline to follow-up in responders (p ≤ 0.002), whereas only proadrenomedullin level significantly increased in nonresponders (p < 0.0001). In patients with documented infections, proadrenomedullin (0.81; 95% CI, 0.71-0.92) and procalcitonin (0.73; 95% CI, 0.60-0.85) each had a greater area under the curve compared with C-reactive protein (0.59; 95% CI, 0.45-0.73) as for as predicting response (p = 0.004 and p = 0.043, respectively). However, for all febrile patients, proadrenomedullin had a significantly greater area under the curve for predicting favorable response than procalcitonin (p < 0.0001).In critically ill patients with cancer, proadrenomedullin and procalcitonin both have a promising role in predicting bloodstream infections in a manner more helpful than C-reactive protein. These two biomarkers were superior to C-reactive protein in the prognostic analysis of response to antimicrobial therapy for those patients with documented infections. However, proadrenomedullin was superior to procalcitonin in predicting response in all febrile patients and was unique in showing increased levels among nonresponders.
View details for DOI 10.1097/CCM.0000000000000526
View details for Web of Science ID 000345255900005
View details for PubMedID 25083975
Granulocyte transfusions in hematologic malignancy patients with invasive pulmonary aspergillosis: outcomes and complications
ANNALS OF ONCOLOGY
2013; 24 (7): 1873-1879
Granulocyte transfusions (GTXs) have been used successfully as an adjunctive treatment option for invasive infections in some neutropenic patients with underlying hematologic malignancy (HM).We sought to determine the impact of GTX as an adjunct to antifungal therapy in 128 patients with HM and prolonged neutropenia (≥14 days) with a proven or probable invasive aspergillosis (IA) infection by retrospectively reviewing our institutional database.Fifty-three patients received GTX and 75 did not. By univariate analysis, patients with invasive pulmonary aspergillosis who received GTX were less likely to respond to antifungal therapy (P = 0.03), and more likely to die of IA (P = 0.009) when compared with the non-GTX group. Among patients who received GTX, 53% developed a pulmonary reaction. Furthermore, IA-related death was associated with the number of GTX given (P = 0.018) and the early initiation of GTX within 7 days after starting antifungal therapy (P = 0.001). By multivariate competing risk analysis, patients who received GTX were more likely to die of IA than patients who did not receive GTX (P = 0.011).Our study suggests that GTX does not improve response to antifungal therapy and is associated with worse outcomes of IA infection in HM patients, particularly those with pulmonary involvement.
View details for DOI 10.1093/annonc/mdt110
View details for Web of Science ID 000321881600024
View details for PubMedID 23519997
View details for PubMedCentralID PMC4990830
Can procalcitonin differentiate Staphylococcus aureus from coagulase-negative staphylococci in clustered gram-positive bacteremia?
DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE
2013; 76 (2): 158-161
Procalcitonin (PCT) and pro-adrenomedullin (ProADM) have been proposed as diagnostic and prognostic biomarkers of infection. Between July 2009 and January 2012, we studied the role of these biomarkers in 163 patients with clustered gram-positive and gram-negative bacteremia. PCT levels were significantly higher in patients with Staphylococcus aureus and gram-negative bacteremia than those with coagulase-negative staphylococci (CoNS) isolated from blood cultures (P = 0.29 and <0.001, respectively). ProADM levels were only significantly higher in patients with gram-negative bacteremia (median 1.46 nmol/L) than those with CoNS (median 1.01 nmol/L) (P = 0.04). Among patients with CoNS, PCT, and ProADM, levels failed to differentiate blood contamination (medians 0.24 ng/mL and 0.97 nmol/L) from true bacteremia (medians 0.26 ng/mL and 1.14 nmol/L) (P = 0.51 and 0.57, respectively). In cancer patients, PCT (and to a lesser extent, ProADM) was useful in differentiating CoNS from S. aureus and gram-negative bacteremia.
View details for DOI 10.1016/j.diagmicrobio.2013.03.004
View details for Web of Science ID 000319717500008
View details for PubMedID 23578976
Pro-adrenomedullin as a Novel Biomarker for Predicting Infections and Response to Antimicrobials in Febrile Patients With Hematologic Malignancies
CLINICAL INFECTIOUS DISEASES
2013; 56 (7): 943-950
Health professionals and researchers have become increasingly interested in biomarkers that help them in diagnosis of infections with recent growing attention to procalcitonin (PCT) and pro-adrenomedullin (proADM).This study compares proADM to PCT as diagnostic and prognostic biomarkers of infection in febrile patients with hematologic malignancies (HMs). From June 2009 to December 2010, 340 febrile HM patients were evaluated for presence of sepsis, systemic inflammatory response syndrome (SIRS), documented infections, and response to antimicrobial therapy.ProADM and PCT levels were measured at onset of fever and then on days 4-7 afterward. Of the 340 patients, 103 had definite sepsis, and 159 had SIRS. Only proADM initial levels were significantly higher in patients with localized bacterial infections than in those with no documented infection (P = .019) and in patients with definite sepsis than those with SIRS (P = .023). The initial proADM and PCT levels were significantly higher in neutropenic patients with BSIs than in those without documented infections (P = .010 and P = . 011, respectively). Follow-up, proADM, and PCT levels decreased significantly in response to antimicrobial therapy in patients with bacterial infections (BSIs or localized; P = .007 and P = .002, respectively).ProADM and PCT have promising roles in assisting clinicians in managing febrile HM patients. However, proADM appears to have the advantage of predicting localized bacterial infection and differentiating sepsis from SIRS.
View details for DOI 10.1093/cid/cis1029
View details for Web of Science ID 000316167000008
View details for PubMedID 23288950
Nephrostomy Tube Related Pyelonephritis in Patients with Cancer: Epidemiology, Infection Rate and Risk Factors
JOURNAL OF UROLOGY
2013; 189 (1): 130-135
Nephrostomy tube placement is often necessary to avert acute renal failure in patients with cancer with obstructive uropathy or in patients with ureteral leak. However, there have been limited published studies on the rate and risk of nephrostomy tube related pyelonephritis in patients with cancer. Therefore, in this study we determined rates of nephrostomy tube related pyelonephritis and predisposing risk factors in patients with cancer.We retrospectively reviewed patients who underwent nephrostomy tube placement between September 1, 2009 and September 16, 2010 at MD Anderson Cancer Center. Patients were followed for 90 days. The primary outcome assessed was the development of nephrostomy tube related pyelonephritis and the secondary outcome was the development of asymptomatic bacteriuria. We also determined risk factors associated with pyelonephritis.Of the 200 patients analyzed 38 (19%) had pyelonephritis and 15 (7.5%) had asymptomatic bacteriuria. Of the nephrostomy tube related infections 34 cases (89%) were with the primary nephrostomy tube. Subsequently 4 of the patients who underwent nephrostomy tube exchange had an episode of pyelonephritis. Pyelonephritis developed within the first month in 19 (10%) patients. Prior urinary tract infection and neutropenia were found to be significant risk factors for pyelonephritis (p = 0.047 and 0.03, respectively).The placement of nephrostomy tubes in patients with cancer is associated with a significant rate of pyelonephritis. Neutropenia and history of urinary tract infection were significant risk factors for pyelonephritis. This finding warrants further investigation into preventive strategies to reduce the infection rate.
View details for DOI 10.1016/j.juro.2012.08.094
View details for Web of Science ID 000312604800044
View details for PubMedID 23164390
Can procalcitonin distinguish infectious fever from tumor-related fever in non-neutropenic cancer patients?
2012; 118 (23): 5823-5829
Procalcitonin (PCT) has been proposed as a marker of infection and was studied in neutropenic patients. This study investigated its role in non-neutropenic febrile cancer patients (NNCPs).Between July 2009 and July 2010, a total of 248 NNCPs with fever were studied. PCT was measured in plasma within 24 hours of fever onset and 4 to 7 days thereafter, using a Kryptor system with a lower limit of quantitation of 0.075 ng/mL. Patients' clinical, microbiological, and radiological data were reviewed to make the diagnosis and were correlated with PCT levels.This study included 30 patients with bloodstream infection (BSI), 60 with localized bacterial infection, 141 with no documented infection, and 8 with tumor-related fever. Most patients (98%) were inpatients or admitted to the hospital during the study. Patients with BSI had significantly higher PCT levels than did those with documented localized infections (P = .048) and no documented infection (P = .011). PCT levels were significantly higher in septic patients than in those without sepsis (P = .012). Patients with stage IV disease or metastasis had significantly higher baseline PCT levels than did those with early stages of cancer (P < .05). PCT levels dropped significantly in patients with bacterial infections in response to antibiotics (P < .0001).Baseline PCT levels are predictive of BSI and sepsis in NNCPs. They may be predictors of metastasis and advanced cancer. Subsequent decrease in PCT levels in response to antibiotics is suggestive of bacterial infection. Larger trials are needed to confirm the results of this pilot study.
View details for DOI 10.1002/cncr.27602
View details for Web of Science ID 000311306000014
View details for PubMedID 22605389
Anomalous Inferior Vena Cava Drainage to the Left Atrium With Successful Staged Repair in a 32-Year-Old Woman With Arthritis
2010; 31 (6): 912-914
This report describes a case involving anomalous drainage of inferior vena cava (IVC) to the left atrium diagnosed when the patient was 32 years old. The tricuspid valve and the right ventricle were small. Successful surgical repair was performed, with significant improvement of the patient's clinical status. The use of exercise testing with pulse oxymetry monitoring aided in the decision of timing for closure of the iatrogenically created atrial septal defect.
View details for DOI 10.1007/s00246-010-9738-1
View details for Web of Science ID 000280405600031
View details for PubMedID 20544188