A Survey on the association of seizure disorders with asthma and allergies in children.

Summary: Background. Little is known about the relationship between allergic diseases and seizure disorders including epilepsy. It is hypothesized that inflammation from allergic diseases may predispose children to seizures. the aim of this study is to investigate frequency of seizure disorder in children with asthma and allergy. Methods. A cross-sectional survey study of parents of 1300 children and adolescents under 20 years of age referred to the Allergy and Asthma Clinic of Imam Ali Hospital (Karaj) who were asked to complete a screening questionnaire for seizures in their children. Parents who reported any history of seizures in their children were contacted to answer a second in-depth questionnaire to determine more detail of type, triggers, and treatment of seizures. Results. A total of 705 males (62%) and 433 females (38%) participated in this study, with a mean and standard age of 6.62±4.57 years. Among them, 70.6% had asthma, 15.2% had allergic rhinitis, 5.6% had atopic dermatitis, 3.5% had urticaria, 2.7% had food allergies, 1% had drug allergies, and 1.4% had other allergic diseases. Additionally, 88 patients (7.7%) had a history of doctor-diagnosed seizures, 57 patients (5%) had febrile convulsions, and 15 patients (1.31%) had idiopathic epilepsy. There was no significant relationship found between febrile convulsions, seizures, and epilepsy with the type of allergic diseases. However, a significant association was observed between the number of comorbid allergic diseases in patients with febrile convulsions (OR=1.4, 95% CI: 1.07-1.83, P=0.013).There was also an association between the epilepsy and comorbid allergic diseases number with an odds ratio OR=1.84, 95% CI=0.28-12, however the risk of epilepsy was increased by 0.84 percent but this increase was not significant. Regarding the relation between the number of allergic diseases in parents and idiopathic epilepsy in their children, a significant association was found only for mothers (OR=1.28, 95% CI: 1.04-2.23, P=0.024), but not for fathers (P>0.05). Conclusions. Febrile convulsion is associated with the .number of comorbid allergic diseases in children and the mother's number of allergic diseases is more related to idiopathic epilepsy in children than the father's.

Non-Infectious Complications in B-Lymphopenic Common Variable Immunodeficiency.

BACKGROUND AND OBJECTIVE: Common variable immunodeficiency (CVID) is considered the most symptomatic type of inborn errors of immunity in humans. Along with infectious complications, which have numerous consequences, non-infectious complications are also a major challenge among CVID patients. METHODS: All registered CVID patients in the national database were included in this retrospective cohort study. Patients were divided into two groups based on the presence of B-cell lymphopenia. Demographic characteristics, laboratory findings, non-infectious organ involvements, autoimmunity, and lymphoproliferative diseases were evaluated. RESULTS: Among 387 enrolled patients, 66.4% were diagnosed with non-infectious complications; however, 33.6% had only infectious presentations. Enteropathy, autoimmunity, and lymphoproliferative disorders were reported in 35.1%, 24.3%, and 21.4% of patients, respectively. Some complications, including autoimmunity and hepatosplenomegaly, were reported to be significantly higher among patients with B-cell lymphopenia. Among organ involvement, dermatologic, endocrine and musculoskeletal systems were predominantly affected in CVID patients with B-cell lymphopenia. Among autoimmune manifestations, the frequency of rheumatologic, hematologic, and gastrointestinal autoimmunity was reported to be higher compared to other types of autoimmunity independent from the B cell-lymphopenia. Furthermore, hematological cancers, particularly lymphoma, were slightly introduced as the most common type of malignancy. Meanwhile, the mortality rate was 24.5%, and respiratory failure and malignancies were reported as the most common cause of death in our patients without significant differences between the two groups. CONCLUSION: Considering that some of the non-infectious complications might be associated with B-cell lymphopenia, therefore, regular patient monitoring and follow-up along with proper medications (besides immunoglobulins replacement therapy) are highly recommended to prevent further sequels and increase the patients' quality of life.

The spectrum of inborn errors of immunity: a single tertiary center retrospective study in Alborz, Iran.

Summary: Background. Inborn errors of immunity (IEIs) are a group of heterogeneous disorders with inherited faults in the immune system that increase susceptibility to infections, malignancies, lymphoproliferation, and autoimmune/autoinflammatory disorders. Methods. We retrospectively studied the demographic characteristics, clinical features, and immunological profiles of the 90 IEIs patients, who were diagnosed and classified according to the European Society for Immunodeficiencies (ESID) and International Union of Immunological Societies (IUIS) criteria from July 2010 to June 2021. The study was carried out in the Non-communicable Diseases Research Center, Imam Ali Hospital, Alborz, Iran. Results. Within a period of 11 years, 53 (58.9%) males and 37 (41.1%) females were diagnosed and followed up for 20 IEI disorders. The median (IQR) age of onset, age of clinical diagnosis and diagnostic delay was 0.7 (0.08-2.0), 3.18 (1.0-8.0) and 1.5 (0.17-5.0) years, respectively. Twelve patients (36.4%) had a positive family history of IEI, and the majority of patients (84.5%) had recurrent infections. Pneumonia (51.7%) was the most common clinical manifestation among IEI patients, followed by skin complications (46.2%). The most frequently diagnosed IEI was immunoglobulin A deficiency (IgAD) (14.4%) and severe combined immunodeficiency (SCID) (11.1%). Predominantly antibody deficiencies group (36.7%) was the most common category, followed by combined immunodeficiencies with associated or syndromic features group (27.8%). Conclusions. IEIs have different patterns within populations with high consanguinity. There is a need to search for underlying genetic and epigenetic factors in most common IEIs in Alborz.

Socioeconomic inequalities in metastasis, recurrence, stage and grade of breast cancer: a hospital-based retrospective cohort study.

INTRODUCTION: This study aims to estimate the Socio-Economic Status (SES) inequality on the metastasis, recurrence, stage and grade in Breast Cancer (BC). METHODS: This retrospective cohort study conducted on 411 BC patients in Arak, Iran. Asset-based questionnaire used to estimate the household SES. For calculate of SES inequality was used from Concentration Index (C). Moreover for investigate the association between recurrence and metastasis with other variables were used from multilevel logistic regression and analysis of variance were used to investigate the relationship between SES and other variables. The data were analyzed with Stata (v.13) software. RESULTS: Results of analysis of variance showed statistical significant relationship between SES with, insurance, surgery, grade, stage, recurrence and metastasis (p-value < 0.05). Moreover the Odds Ratio (OR) were significant of recurrence with age, academic level of education, supplementary insurance history of BC in first-degree relatives, stage and grade, also, metastasis with age of > 80 years, insurance, supplementary insurance, history of BC in first-degree relatives, chemotherapy, radiotherapy, stage and grade four. The total C index obtained 0.015 (0.002, 0.026), 0.011 (0.003, 0.031), - 0.014 (- 0.034, - 0.001) and - 0.042 (- 0.061, - 0.002) for metastasis, recurrence, stage and grade of BC respectively. CONCLUSIONS: Our results showed evidence of inequality in the metastasis, recurrence, stage and grade in BC patients.

Autoimmunity and its association with regulatory T cells and B cell subsets in patients with common variable immunodeficiency

Background: Common variable immunodeficiency (CVID) is one of the most prevalent symptomatic primary immunodeficiencies (PIDs), which manifests a wide clinical variability such as autoimmunity, as well as T cell and B cell abnormalities. Methods: A total of 72 patients with CVID were enrolled in this study. Patients were evaluated for clinical manifestations and classified according to the presence or absence of autoimmune disease. We measured regulatory T cells (Tregs) and B-cell subsets using flow cytometry, as well as specific antibody response (SAR) to pneumococcal vaccine, autoantibodies and anti-IgA in patients. Results: Twenty-nine patients (40.3%) have shown at least one autoimmune manifestation. Autoimmune cytopenias and autoimmune gastrointestinal diseases were the most common. A significant association was detected between autoimmunity and presence of hepatomegaly and splenomegaly. Among CVID patients, 38.5% and 79.3% presented a defect in Tregs and switched memory B-cells, respectively, whereas 69.0% presented CD21low B cell expansion. Among patients with a defect in Treg, switched memory and CD21low B cell, the frequency of autoimmunity was 80.0%, 52.2% and 55.0%, respectively. A negative correlation was observed between the frequency of Tregs and CD21low B cell population. 82.2% of patients had a defective SAR which was associated with the lack of autoantibodies. Conclusions: Autoimmunity may be the first clinical manifestation of CVID, thus routine screening of immunoglobulins is suggested for patients with autoimmunity. Lack of SAR in CVID is associated with the lack of specific autoantibodies in patients with autoimmunity. It is suggested that physicians use alternative diagnostic procedures (AU)

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Systematic investigation for underlying causes of recurrent infections in children: surveillance of primary immunodeficiency.

Summary: Recurrent infections seem to be a common complaint in children who are referred to general practitioners and pediatricians offices. Detection of primary immunodeficiencies (PID) etiology is very important for achieving appropriate diagnosis and treatment of these patients. The absence of appropriate treatment could lead to subsequent complications, in a hospital inpatient and/or outpatient settings. This study was performed in a group of children with recurrent infections to identify patients with underlying PID. A cross-sectional study was designed to evaluate the final clinical diagnosis obtained in 100 pediatric patients with a history of recurrent infections referred to Children s Medical Center, Tehran, Iran, during one year (2011-2012). History taking and physical examination, complementary laboratory tests including immunological investigations were done to confirm the main causes of disease according to our previously published stepwise approach to recurrent infections. Among all studied patients, 21% (11 males and 10 females) were diagnosed to have PID. Parental consanguinity (p = 0.001) and soft tissue infections (p = 0.004) were significantly higher in PID group, comparing to other causes of recurrent infections. Gender and location of infections were also linked to the type of PID including antibody deficiency, combined immunodeficiency and phagocytosis disorders. The real rate of PID as a cause of recurrent infection appears to be much higher than what is generally considered in a se-lected group of pediatric patients; so, following the suggested stepwise guideline can im-prove timely diagnosis and appropriate treatment of these patients.

Autoimmunity and its association with regulatory T cells and B cell subsets in patients with common variable immunodeficiency.

BACKGROUND: Common variable immunodeficiency (CVID) is one of the most prevalent symptomatic primary immunodeficiencies (PIDs), which manifests a wide clinical variability such as autoimmunity, as well as T cell and B cell abnormalities. METHODS: A total of 72 patients with CVID were enrolled in this study. Patients were evaluated for clinical manifestations and classified according to the presence or absence of autoimmune disease. We measured regulatory T cells (Tregs) and B-cell subsets using flow cytometry, as well as specific antibody response (SAR) to pneumococcal vaccine, autoantibodies and anti-IgA in patients. RESULTS: Twenty-nine patients (40.3%) have shown at least one autoimmune manifestation. Autoimmune cytopenias and autoimmune gastrointestinal diseases were the most common. A significant association was detected between autoimmunity and presence of hepatomegaly and splenomegaly. Among CVID patients, 38.5% and 79.3% presented a defect in Tregs and switched memory B-cells, respectively, whereas 69.0% presented CD21low B cell expansion. Among patients with a defect in Treg, switched memory and CD21low B cell, the frequency of autoimmunity was 80.0%, 52.2% and 55.0%, respectively. A negative correlation was observed between the frequency of Tregs and CD21low B cell population. 82.2% of patients had a defective SAR which was associated with the lack of autoantibodies. CONCLUSIONS: Autoimmunity may be the first clinical manifestation of CVID, thus routine screening of immunoglobulins is suggested for patients with autoimmunity. Lack of SAR in CVID is associated with the lack of specific autoantibodies in patients with autoimmunity. It is suggested that physicians use alternative diagnostic procedures.

Humoral immune consequences of Staphylococcus aureus ST239-associated bacteremia.

The humoral immune responses against 46 different staphylococcal antigens in 27 bacteremia patients infected by clonally related methicillin-resistant Staphylococcus aureus (MRSA) strains of a single sequence type (ST) 239 were investigated. A group of non-infected patients (n = 31) hospitalized for different reasons served as controls. All strains were confirmed as ST 239 by S. aureus and mecA-specific PCR, spa, and multi-locus sequence typing (MLST). In each bacteremia patient, a unique pattern of S. aureus antigen-specific immune responses after infection was observed. Antibody levels among bacteremia patients were significantly higher than controls for HlgB (P = 0.001), LukD (P = 0.009), LukF (P = 0.0001), SEA (P = 0.0001), SEB (P = 0.011), SEC (P = 0.010), SEQ (P = 0.049), IsaA (P = 0.043), IsdA (P = 0.038), IsdH (P = 0.01), SdrD (P = 0.001), SdrE (P = 0.046), EsxA (P = 0.0001), and SA0104 (P = 0.0001). On the other hand, the antibody levels were significantly higher among controls for SSL3 (P = 0.009), SSL9 (P = 0.002), and SSL10 (P = 0.007) when the IgG level on the day of infection was compared with that measured on the day of admission. Diversity was observed in the immune response against the antigens. However, a set of antigens (IsaA, IsdA, IsdH, SdrD, and HlgB) triggered a similar type of immune response in different individuals. We suggest that these antigens could be considered when developing a multi-component (passive) vaccine. SEA and/or its specific antibodies seem to play a critical role during ST239 MRSA bacteremia and SEA-targeted therapy may be a strategy to be considered.

Single nucleotide polymorphisms of IL-2, but not IL-12 and IFN-y, are associated with increased susceptibility to chronic spontaneous urticaria

Background: A clear picture of interaction of Th1/Th2 cytokines in pathogenesis of chronic spontaneous urticaria (CSU), remains elusive. Impaired IFN-γ production and decreased levels of IL-2 have been reported. The aim of this study was to evaluate the association of Th1 cytokines; IL-2, IL-12 and IFN-γ polymorphisms with CSU. Methods: 90 patients with CSU and 140 age-sex matched subjects were included in this study. DNA samples were evaluated through PCR-SSP assay in order to detect single nucleotide polymorphisms of IL-12 (A/C -1188) or (rs3212227), IFN-γ (A/T UTR5644) or (rs2069717) and IL-2 (G/T -330 and G/T +166) or (rs2069762 and rs2069763). Results: G allele at -330 at promoter region of IL-2 gene was overrepresented in CSU. Heterozygotes (GT) at this locus and heterozygotes at +166 of IL-2 gene (GT) were more prevalent in CSU group. Additionally, the haplotype GT for loci -330 and +166 of IL-2 gene was powerfully associated with CSU (OR (95%CI) = 57.29 (8.43-112.7)). Conclusions: SNP at position -330 and +166 of IL-2 gene are differently expressed in CSU. The haplotype GT of IL-2 at -330 and +166 might confer vulnerability to a number of immunological disorders in Iranian region (AU)

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Single nucleotide polymorphisms of IL-2, but not IL-12 and IFN-γ, are associated with increased susceptibility to chronic spontaneous urticaria.

BACKGROUND: A clear picture of interaction of Th1/Th2 cytokines in pathogenesis of chronic spontaneous urticaria (CSU), remains elusive. Impaired IFN-γ production and decreased levels of IL-2 have been reported. The aim of this study was to evaluate the association of Th1 cytokines; IL-2, IL-12 and IFN-γ polymorphisms with CSU. METHODS: 90 patients with CSU and 140 age-sex matched subjects were included in this study. DNA samples were evaluated through PCR-SSP assay in order to detect single nucleotide polymorphisms of IL-12 (A/C -1188) or (rs3212227), IFN-γ (A/T UTR5644) or (rs2069717) and IL-2 (G/T -330 and G/T +166) or (rs2069762 and rs2069763). RESULTS: G allele at -330 at promoter region of IL-2 gene was overrepresented in CSU. Heterozygotes (GT) at this locus and heterozygotes at +166 of IL-2 gene (GT) were more prevalent in CSU group. Additionally, the haplotype GT for loci -330 and +166 of IL-2 gene was powerfully associated with CSU (OR (95%CI)=57.29 (8.43-112.7)). CONCLUSIONS: SNP at position -330 and +166 of IL-2 gene are differently expressed in CSU. The haplotype GT of IL-2 at -330 and +166 might confer vulnerability to a number of immunological disorders in Iranian region.

Approach to the Management of Autoimmunity in Primary Immunodeficiency.

Primary immunodeficiency diseases (PIDs) consist of a genetically heterogeneous group of immune disorders that affect distinct elements of the immune system. PID patients are more prone to infections and non-infectious complications, particularly autoimmunity. The concomitance of immunodeficiency and autoimmunity appears to be paradoxical and leads to difficulty in the management of autoimmune complications in PID patients. Therefore, management of autoimmunity in patients with PID requires special considerations because dysregulations and dysfunctions of the immune system along with persistent inflammation impair the process of diagnosis and treatment.

FLG single nucleotide polymorphisms in chronic idiopathic urticaria

BACKGROUND: Filaggrin (FLG), which is formed from profilaggrin protein during epidermal terminal differentiation, is a prerequisite to squame biogenesis and thus for perfect formation of the skin barrier. Yet, the relationship between genetic polymorphisms of FLG and chronic idiopathic urticaria (CIU) has not been investigated. METHODS: The study population consisted of 93 CIU patients and 93 healthy control subjects without a history of allergic, autoimmune or any other systemic disease. Five single nucleotide polymorphisms (SNPs) of FLG were investigated: rs2485518, rs3126065, rs2786680, rs3814300, and rs3814299. RESULTS: For all the investigated polymorphisms, 100% of both CIU patients and control subjects exhibited one given allele and consequently one given genotype as following: A/A genotype for two SNPs, rs3126065 and rs2786680, C/C genotype for two SNPs, rs2485518 and rs3814300, and G/G genotype for one SNP rs3814299 of FLG, and hence no association was found between either allele frequencies or genotype distributions of FLG SNPs and CIU in an Iranian population. CONCLUSIONS: The present study examined the possible relationship between SNPs of FLG and CIU for the first time, and demonstrated that none of five investigated SNPs (rs2485518, rs3126065, rs2786680, rs3814300, and rs3814299) are correlated with CIU in an Iranian population. Further investigations are required to address whether ethnicity/race impacts on relationship between SNPs of FLG and CIU

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FLG single nucleotide polymorphisms in chronic idiopathic urticaria.

BACKGROUND: Filaggrin (FLG), which is formed from profilaggrin protein during epidermal terminal differentiation, is a prerequisite to squame biogenesis and thus for perfect formation of the skin barrier. Yet, the relationship between genetic polymorphisms of FLG and chronic idiopathic urticaria (CIU) has not been investigated. METHODS: The study population consisted of 93 CIU patients and 93 healthy control subjects without a history of allergic, autoimmune or any other systemic disease. Five single nucleotide polymorphisms (SNPs) of FLG were investigated: rs2485518, rs3126065, rs2786680, rs3814300, and rs3814299. RESULTS: For all the investigated polymorphisms, 100% of both CIU patients and control subjects exhibited one given allele and consequently one given genotype as following: A/A genotype for two SNPs, rs3126065 and rs2786680, C/C genotype for two SNPs, rs2485518 and rs3814300, and G/G genotype for one SNP rs3814299 of FLG, and hence no association was found between either allele frequencies or genotype distributions of FLG SNPs and CIU in an Iranian population. CONCLUSIONS: The present study examined the possible relationship between SNPs of FLG and CIU for the first time, and demonstrated that none of five investigated SNPs (rs2485518, rs3126065, rs2786680, rs3814300, and rs3814299) are correlated with CIU in an Iranian population. Further investigations are required to address whether ethnicity/race impacts on relationship between SNPs of FLG and CIU.

A Comparative Analysis of the Safety, Efficacy, and Cost of Islet Versus Pancreas Transplantation in Nonuremic Patients With Type 1 Diabetes.

Few current studies compare the outcomes of islet transplantation alone (ITA) and pancreas transplantation alone (PTA) for type 1 diabetes (T1D). We examined these two beta cell replacement therapies in nonuremic patients with T1D with respect to safety, graft function and cost. Sequential patients received PTA (n = 15) or ITA (n = 10) at our institution. Assessments of graft function included duration of insulin independence; glycemic control, as measured by hemoglobin A1c; and elimination of severe hypoglycemia. Cost analysis included all normalized costs associated with transplantation and inpatient management. ITA patients received one (n = 6) or two (n = 4) islet transplants. Mean duration of insulin independence in this group was 35 mo; 90% were independent at 1 year, and 70% were independent at 3 years. Mean duration of insulin independence in PTA was 55 mo; 93% were insulin independent at 1 year, and 64% were independent at 3 years. Glycemic control was comparable in all patients with functioning grafts, as were overall costs ($138 872 for ITA, $134 748 for PTA). We conclude that with advances in islet isolation and posttransplant management, ITA can produce outcomes similar to PTA and represents a clinically viable option to achieve long-term insulin independence in selected patients with T1D.

Effect of Immigration Status on Outcomes in Pediatric Kidney Transplant Recipients.

Kidney transplantation is the optimal treatment for children with end-stage renal disease. For children with undocumented immigration status, access to kidney transplantation is limited, and data on transplant outcomes in this population are scarce. The goal of the present retrospective single-center study was to compare outcomes after kidney transplantation in undocumented children with those of US citizen children. Undocumented residency status was identified in 48 (17%) of 289 children who received a kidney transplant between 1998 and 2010. In undocumented recipients, graft survival at 1 and 5 years posttransplantation was similar, and mean estimated glomerular filtration rate at 1 year was higher than that in recipients who were citizens. The risk of allograft failure was lower in undocumented recipients relative to that in citizens at 5 years posttransplantation, after adjustment for patient age, donor age, donor type, and HLA mismatch (p < 0.04). In contrast, nearly one in five undocumented recipients who reached 21 years of age lost their graft, primarily because they were unable to pay for immunosuppressive medications once their state-funded insurance had ended. These findings support the ongoing need for immigration policies for the undocumented that facilitate access to work-permits and employment-related insurance for this disadvantaged group.

Interleukin-6 and tumor necrosis factor-alpha gene polymorphisms in chronic idiopathic urticaria

BACKGROUND: This study was performed to evaluate association of gene polymorphisms among proinflammatory cytokines and susceptibility to chronic idiopathic urticaria (CIU). METHODS: Ninety patients with prolonged urticaria more than 6 weeks were included as case group. Single nucleotide polymorphisms (SNPs) of IL-6 (G/C −174, G/A nt565) and TNF-α (G/A −308, G/A −238) were evaluated, using polymerase chain reaction (PCR); and the results were compared to the control group. RESULTS: Gallele was significantly higher in the patients at locus of −238 of promoter of TNF-α gene (p < 0.001). Frequency of following genotypes were significantly lower in patients with CIU, compared to controls: AG at −308 and GA at −238 of TNF-α gene (p < 0.05 and p < 0.001, respectively), CG at −174 and GG at +565 of IL-6 gene (p < 0.05). Additionally, following genotypes were more common among patients with CIU: GG at −308 and −238 of TNF-α gene (p < 0.05 and p < 0.001, respectively), GG at −174 and GA at +565 of IL-6 gene (p < 0.05). CONCLUSIONS: Pro-inflammatory cytokine gene polymorphisms can affect susceptibility to CIU. TNF-α promoter polymorphisms as well as IL-6 gene polymorphisms are associated with CIU

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Interleukin-6 and tumor necrosis factor-alpha gene polymorphisms in chronic idiopathic urticaria.

BACKGROUND: This study was performed to evaluate association of gene polymorphisms among proinflammatory cytokines and susceptibility to chronic idiopathic urticaria (CIU). METHODS: Ninety patients with prolonged urticaria more than 6 weeks were included as case group. Single nucleotide polymorphisms (SNPs) of IL-6 (G/C -174, G/A nt565) and TNF-α (G/A -308, G/A -238) were evaluated, using polymerase chain reaction (PCR); and the results were compared to the control group. RESULTS: G allele was significantly higher in the patients at locus of -238 of promoter of TNF-α gene (p<0.001). Frequency of following genotypes were significantly lower in patients with CIU, compared to controls: AG at -308 and GA at -238 of TNF-α gene (p<0.05 and p<0.001, respectively), CG at -174 and GG at +565 of IL-6 gene (p<0.05). Additionally, following genotypes were more common among patients with CIU: GG at -308 and -238 of TNF-α gene (p<0.05 and p<0.001, respectively), GG at -174 and GA at +565 of IL-6 gene (p<0.05). CONCLUSIONS: Pro-inflammatory cytokine gene polymorphisms can affect susceptibility to CIU. TNF-α promoter polymorphisms as well as IL-6 gene polymorphisms are associated with CIU.

Reducing infection transmission in solid organ transplantation through donor nucleic acid testing: a cost-effectiveness analysis.

For solid organ transplant (SOT) donors, nucleic acid-amplification testing (NAT) may reduce human immunodeficiency virus (HIV) and hepatitis C virus (HCV) transmission over antibody (Ab) testing given its shorter detection window period. We compared SOT donor NAT + Ab versus Ab alone using decision models to estimate incremental cost-effectiveness ratios (ICERs; cost per quality-adjusted life year [QALY] gained) from the societal perspective across a range of HIV/HCV prevalence values and NAT costs. The cost per QALY gained was calculated for two scenarios: (1) favorable: low cost ($150/donor)/high prevalence (HIV: 1.5%; HCV: 18.2%) and (2) unfavorable: high cost ($500/donor)/low prevalence (HIV: 0.1%; HCV: 1.5%). In the favorable scenario, adding NAT screening cost $161 013 per QALY gained for HIV was less costly) for HCV, and cost $86 653 per QALY gained for HIV/HCV combined. For the unfavorable scenario, the costs were $15 568 484, $221 006 and $10 077 599 per QALY gained, respectively. Universal HCV NAT + Ab for donors appears cost-effective to reduce infection transmission from SOT donors, while HIV NAT + Ab is not, except where HIV NAT is ≤$150/donor and prevalence is ≥1.5%. Our analyses provide important data to facilitate the decision to implement HIV and HCV NAT for deceased SOT donors and shape national policy regarding how to reduce infection transmission in SOT.

Laparoscopic sleeve gastrectomy is safe and efficacious for pretransplant candidates.

BACKGROUND: Morbid obesity is a relative contraindication for organ transplant because it is associated with higher postoperative morbidity and mortality. The safety and efficacy of laparoscopic sleeve gastrectomy (LSG) as a weight loss method for patients awaiting transplant has not been examined. METHODS: A retrospective review was performed on morbidly obese patients awaiting liver or kidney transplant who underwent LSG from 2006 to 2012. Data included patient demographic characteristics, operative details, 30-day complications, percentage of excess weight loss, postoperative laboratory data, and status of transplant candidacy. RESULTS: Twenty-six pretransplant patients underwent LSG. The mean age was 57 years, and 17 (65%) were women. Six patients had end-stage renal disease, and 20 patients had end-stage liver disease. The preoperative mean body mass index was 48.3 kg/m(2) (range 38-60.4 kg/m(2)). There were no deaths, and there were 6 postoperative complications: 2 superficial wound infections, 1 staple line leak, 1 postoperative bleed requiring blood transfusion, 1 transient encephalopathy, and 1 temporary renal insufficiency. The mean percentage of excess weight loss at 1, 3, and 12 months was 17% (n = 24/26), 26% (n = 23/26), and 50% (n = 18/20), respectively. All patients met our institution's body mass index cutoffs for transplantation by 12 months after the procedure. One patient's renal function stabilized, and he was taken off the transplant list. Eight patients eventually underwent solid organ transplant. Six received liver transplants, 1 patient received a combined liver and kidney transplant, and 1 received a kidney transplant. The mean time between LSG and transplant was 16.6 months. CONCLUSIONS: This is the largest case series involving LSG in patients awaiting solid organ transplantation. LSG is well tolerated, is technically feasible, and improves candidacy for transplantation.

Safety and feasibility of sleeve gastrectomy in morbidly obese patients following liver transplantation.

BACKGROUND: Obesity, steroid-induced diabetes, hypercholesterolemia, and steatohepatitis can occur after liver transplantation and may respond to bariatric surgery. The safety and feasibility of bariatric surgery after liver transplantation is unknown. METHODS: Nine morbidly obese patients with prior liver transplants underwent sleeve gastrectomy in a pilot program. Sleeve gastrectomy was chosen over gastric banding to avoid foreign body implantation, and over gastric bypass to maintain endoscopic access to the biliary system and reduce surgical complexity. We reviewed patient demographics, operative details, 30-day complications, weight loss, postoperative hepatic and renal functions, and resolution of comorbidities. RESULTS: Sleeve gastrectomy was performed laparoscopically in eight patients and as an open procedure in one patient. The mean operative time was 165 min and mean postoperative length of stay was 5 days. Follow-up ranged from 3 to 36 months. In the first 30 days, there were three complications in three patients: mesh dehiscence after a synchronous incisional hernia repair, bile leak from the liver surface requiring laparoscopic drainage, and postoperative dysphagia that required reoperation. Calcineurin inhibitor levels and hepatic and renal functions remained stable. There were no episodes of graft rejection. At 3 months liver function tests remained stable. Excess weight loss averaged 55.5% at 6 months. CONCLUSION: Sleeve gastrectomy is technically feasible after liver transplantation and resulted in weight loss without adversely affecting graft function and immunosuppression. Early complications may be more frequent as a result of adhesions of the left upper quadrant. Late complications were rare.