Development of breast cancer-related lymphedema: is it dependent on the patient, the tumor or the treating physicians?

Introduction

Breast cancer-related lymphedema (LE) is relatively common. The aim of this study was to identify the risk factors involved in the development of this complication.

Methodology

This was a cross-sectional study of breast cancer patients treated at our Center between 2004 and 2009. A total of 515 patients were included. Lymphedema was defined as a mid-arm or forearm circumference difference between both limbs of 2 cm or more.

Results

The incidence of LE in this population was 21.4 %. Patients with a BMI of 25 or higher had a significantly higher risk of LE (p = 0.002). The presence of lymphovascular invasion (LVI) (p = 0.05) and the number of positive lymph nodes (LN) (p = 0.001) were both associated with LE. Patients who underwent axillary dissection (AD) had a significantly higher incidence of LE than patients who had a sentinel LN biopsy (25 vs. 4.5 %). Adjuvant radiotherapy was also a significant risk factor in patients who had a mastectomy (p = 0.003).

Conclusion

There are multiple risk factors for LE. Most of those factors can be influenced by early tumor detection. Early tumors are smaller with no LVI or axillary LN metastasis. They do not usually require AD or axillary radiotherapy, which are the strongest factors associated with the development of LE.     

Inferior epigastric artery pseudoaneurysm: ultrasound diagnosis and treatment with percutaneous thrombin

A case of a pseudoaneurysm arising from the inferior epigastric artery in a patient presenting with a rectus sheath haematoma is reported. The pseudoaneurysm was successfully treated by percutaneous injection of human thrombin.     

Expression of the testis-specific gene, TSGA10, in Iranian patients with acute lymphoblastic leukemia (ALL)

Testis-specific gene antigen (TSGA10) is expressed in fetus, testis and frequently in human solid cancers and acute leukemias, making it a candidate for immunotherapy and for detection of minimal residual disease (MRD). This gene is considered as a member of cancer-testis (CT) genes. We previously demonstrated TSGA10 expression during spermatogenesis. There is also evidence for potential TSGA10 involvement in cell proliferation. TSGA10 expression has been observed in a wide spectrum of cancers but not in hematopoietic neoplasm. Here we demonstrated expression of TSGA10 by semi-quantitative RT-PCR in 44 (84.6%) out of 52 bone marrow samples and all peripheral blood samples from patients with acute lymphoblastic leukemia (ALL). Twenty-seven (52%) cases had high level of gene expression and 16 (30.7%) cases had a lower expression level of the gene in the patients bone marrow. Presence of TSGA10 expression in ALL may open a window to functional study of mitotic checkpoint proteins in leukemia. RT-PCR of TSGA10 may help in detection of residual clonal cells leading to early diagnosis and better prognostic qualification of the disease.     

Antenatal administration of Rh-immune globulin causes significant increases in the immunomodulatory cytokines transforming growth factor-beta and prostaglandin E2

BACKGROUND: Production of specific cytokines in response to administration of Rh-immune globulin (RhIG) was examined to assess the mechanism of inhibition of the anti-D production and prevention of hemolytic disease of the newborn (HDN). STUDY DESIGN AND METHODS: Plasma levels of 17 different cytokines before and 48 hours after antenatal administration of anti-D were measured in 10 women candidates for prophylaxis with RhIG. RESULTS: No striking changes were observed in levels of the cytokines interleukin (IL)-1 sRII, IL-12 p40, IL-16, or monocyte chemoattractant protein-1. Levels of IL-4, -5, -10, -13, and -17; macrophage inflammatory protein-1alpha; granulocyte-macrophage-colony-stimulating factor; tumor necrosis factor-beta; and interferon-gamma remained below detection levels both before and after testing. IL-1ra levels, however, showed a slight to moderate decrease in 7 of 10 women after RhIG administration. In contrast, levels of TGF-beta1 increased more than 1.3-fold in 7 of 10 women and more than 2-fold in 4 of 10 women; in 1 instance the increase was more than 5-fold and this woman also had a significant increase in TGF-beta2. In addition to TGF-beta, 5 of 10 women had a modest increase (>1.5-fold) in prostaglandin E2 (PGE2). Analyses of the combined results of the 10 women showed that increases in both TGF-beta1 and PGE2 after RhIG were significant. CONCLUSION: These results indicate that RhIG prophylaxis can induce higher than baseline levels of two strongly immunomodulatory cytokines, TGF-beta and PGE2. These findings represent one possible mechanism for the inhibition of the primary immune response to the D antigen in women receiving RhIG prophylaxis for prevention of HDN.     

Computed CD4 percentage as a low-cost method for determining pediatric antiretroviral treatment eligibility

Background  

The performance of the WHO recommendations for pediatric antiretroviral treatment (ART) in resource poor settings is insufficiently documented in routine care.     

The importance of imaging in tuberous sclerosis complex (tsc) in children: Two cases

Tuberous sclerosis complex (TSC) is an inherited, multisystemic, hamartomatous neurocutaneous disorder, with an autosomal dominant inheritance pattern. It affects multiple organs, however the most susceptible ones include the brain, skin, kidneys, lungs, the retina, and the heart. TSC is characterized by considerable clinical heterogeneity. The majority of patients present with a constellation of clinical signs and symptoms, most prominently central nervous system manifestations including epilepsy, cognitive impairment and autism spectrum disorders, cutaneous, cardiac, renal and ophthalmic manifestations. Epilepsy affects 70% – 90% of patients, representing the primary neurological feature and 1 of the foremost clinical findings of the disorder. Cardiac rhabdomyomas are the most frequent cardiac manifestations, appearing as isolated or multiple lesions.Herein, we present 2 patients diagnosed with tuberous sclerosis. A 3-month-old male patient with cardiac rhabdomyomas and hypopigmented macules and a 19-month-old male patient with partial epilepsy and mild psychomotor retardation. As brain lesions represent some of the most prevalent clinical features and early onset seizures are associated with more severe cognitive, function delay, through this article we hope to emphasize the potential role MRI can play in the diagnostic workup of TSC, to ensure a more timely diagnosis, thus modifying the natural course of the disorder and its prognosis.     

Elevated cerebrospinal fluid tumour necrosis factor is associated with acute and long‐term neurocognitive impairment in cerebral malaria

Systemic tumour necrosis factor‐α (TNF‐α) may contribute to the pathogenesis of cerebral malaria (CM) by promoting endothelial activation and parasite sequestration. However, less is known about the role of central nervous system (CNS) TNF‐α in CM. We assessed plasma (n=249) and cerebrospinal fluid (CSF) (n=167) TNF‐α levels in Ugandan children with CM, plasma TNF‐α in Ugandan community control children (n=198) and CSF TNF‐α in North American control children who had recovered from leukaemia (n=13). Plasma and CSF TNF‐α were measured by magnetic bead assay. We compared plasma and CSF TNF‐α levels in children with CM to mortality, acute and chronic neurologic deficits and long‐term neurocognitive impairment. Plasma and CSF TNF‐α levels were higher in CM than control children (P<.0001 for both). CSF TNF‐α levels were higher in children who had neurologic deficits at discharge or 6‐month follow‐up (P≤.05 for both). Elevated CSF but not plasma TNF‐α was associated with longer coma duration (Spearman's rho .18, P=.02) and deficits in overall cognition in children 5 years and older (β coefficient ?.74, 95% CI ?1.35 to ?0.13, P=.02). The study findings suggest that CNS TNF‐α may be involved in the development of acute and chronic neurologic and cognitive sequelae in children with CM.     

Association of interferon regulatory factor 5 (<Emphasis Type="Italic">IRF5</Emphasis>) gene polymorphisms with juvenile idiopathic arthritis

Interferon regulatory factor 5 (IRF5) is a member of IRF family which induce signaling pathways and are involved in modulation of cell growth, differentiation, apoptosis, and immune system activity. Juvenile idiopathic arthritis (JIA) is an auto-inflammatory syndrome where the inflammatory markers are believed to play a fundamental role in its pathogenesis. In this study, we aimed to assess the association of IRF5 gene polymorphisms with susceptibility of JIA in Iranian population. Three IRF5 single-nucleotide polymorphisms (rs10954213 A/G, rs2004640 G/T, and rs3807306 G/T) were genotyped using TaqMan assays in 55 patients with JIA and 63 matched healthy individuals. The frequency of the IRF5 rs2004640 T allele was significantly higher (69 vs 45%, P value?=?0.0013) in JIA group as compared to control. The frequency of the IRF5 rs 2004640 G allele was significantly higher in the control group in comparison to JIA group (54 vs 32%, P value?=?0.001). Allele and genotype frequencies of the rs10954213 and rs3807306 did not show any significant difference between JIA and control group. IRF5 rs 2004640 T allele can be considered as a risk factor for the development of JIA and presence of rs 2004640 G may be act as protective factor.