The Locations of Palestine and the U.S. in the Global Map of Homelessness: Part 2.

It's now well appreciated that social determinants of health are the strongest predictors of our health and well-being. A good argument could be made that housing is at the top of the pyramid of these determinants. And, surprisingly, housing is also the social determinant that could rapidly turn on a dime-that is, with sufficient political will, creating access to housing could be radically expanded in short order. (Unfortunately, of course, it's true one can also become suddenly homeless, since few protections exist in policy or capitalist economies to prevent it). That alone sets it apart from social factors such as education and racism-conditions that take a long time to change. In contrast to long-term interventions (education) or culturally stubborn and historically rooted problems (racism), housing is rapidly malleable. In this article, we describe the social condition of homelessness in two settings, comparing and contrasting the concepts, causes, and consequences, along with how people are mobilizing to challenge the conditions that create their housing insecurity. As we review the factors that create housing conditions in each setting, we propose some universal international principles for a new approach to the human right of decent and secure housing.

The Locations of Palestine and the U.S. in the Global Map of Homelessness: Part I.

It's now well appreciated that social determinants of health are the strongest predictors of our health and well-being. A good argument could be made that housing is at the top of the pyramid of these determinants. And, surprisingly, housing is also the social determinant that could rapidly turn on a dime-that is, with sufficient political will, creating access to housing could be radically expanded in short order. (Unfortunately, of course, it's true one can also become suddenly homeless, since few protections exist in policy or capitalist economies to prevent it). That alone sets it apart from social factors such as education and racism-conditions that take a long time to change. In contrast to long-term interventions (education) or culturally stubborn and historically rooted problems (racism), housing is rapidly malleable. In this article, we describe the social condition of homelessness in two settings, comparing and contrasting the concepts, causes, and consequences, along with how people are mobilizing to challenge the conditions that create their housing insecurity. As we review the factors that create housing conditions in each setting, we propose some universal international principles for a new approach to the human right of decent and secure housing.

Because its power remains naturalized: introducing the settler colonial determinants of health.

Indigenous people suffer earlier death and more frequent and severe disease than their settler counterparts, a remarkably persistent reality over time, across settler colonized geographies, and despite their ongoing resistance to elimination. Although these health inequities are well-known, they have been impervious to comprehensive and convincing explication, let alone remediation. Settler colonial studies, a fast-growing multidisciplinary and interdisciplinary field, is a promising candidate to rectify this impasse. Settler colonialism's relationship to health inequity is at once obvious and incompletely described, a paradox arising from epistemic coloniality and perceived analytic challenges that we address here in three parts. First, in considering settler colonialism an enduring structure rather than a past event, and by wedding this fundamental insight to the ascendant structural paradigm for understanding health inequities, a picture emerges in which this system of power serves as a foundational and ongoing configuration determining social and political mechanisms that impose on human health. Second, because modern racialization has served to solidify and maintain the hierarchies of colonial relations, settler colonialism adds explanatory power to racism's health impacts and potential amelioration by historicizing this process for differentially racialized groups. Finally, advances in structural racism methodologies and the work of a few visionary scholars have already begun to elucidate the possibilities for a body of literature linking settler colonialism and health, illuminating future research opportunities and pathways toward the decolonization required for health equity.

Communal Poverty Is a Significant Risk Factor for Neonatal Seizures.

INTRODUCTION: Neonatal seizures (NS) are a severe condition with significant mortality and long-term morbidity. This study aims to identify risk factors for NS in a racially or ethnically diverse population in Israel. METHODS: This is a case-control study. The cases were all newborns born between 2001 and 2019 at Emek Medical Center in Israel and admitted with NS. Two healthy controls born in the same period were matched for each case. Demographic, maternal, and neonatal variables were abstracted from the electronic medical files. RESULTS: A total of 139 cases were matched with 278 controls. Residing in a town with lower socioeconomic status (SES), primiparity and abnormal prenatal ultrasound were significantly associated with NS. Prematurity, assisted delivery, a lower birthweight, being small for gestational age, and lower Apgar score were also associated with NS. In two different multivariable regression models, lower SES (odds ratio [OR] = 4.07) and Arab race/ethnicity (OR = 2.66) were risk factors for NS. Other significant risk factors in the multivariable regression models included an assisted mode of delivery (OR = 2.33), prematurity (OR = 2.27), and a 5-minute Apgar score below 7 (OR = 54.1). DISCUSSION: Communal poverty, as reflected by lower SES of towns of residence, was found to be a stronger risk factor than race or ethnicity, for NS. More studies should focus on social class, as a risk factor for maternal and neonatal adverse outcomes. As SES is a modifiable variable every effort should be invested in fighting communal poverty and improving the SES of impoverished towns and population.

Structural racism and the health of Palestinian citizens of Israel.

Palestinian citizens of Israel (PCI) constitute almost 20% of the Israeli population. Despite having access to one of the most efficient healthcare systems in the world, PCI have shorter life expectancy and significantly worse health outcomes compared to the Jewish Israeli population. While several studies have analysed the social and policy determinants driving these health inequities, direct discussion of structural racism as their overarching etiology has been limited. This article situates the social determinants of health of PCI and their health outcomes as stemming from settler colonialism and resultant structural racism by exploring how Palestinians came to be a racialized minority in their homeland. In utilising critical race theory and a settler colonial analysis, we provide a structural and historically responsible reading of the health of PCI and suggest that dismantling legally codified racial discrimination is the first step to achieving health equity.

Organized Violence and Organized Abandonment Beyond the Human: the Case of Brucellosis among Palestinians in Israel.

This article explores how brucellosis became a racialized disease in Israel, where almost all patients are Palestinians. Informed by legal and historical research, the article demonstrates how colonial and settler-colonial policies have targeted Palestinians and their goats and contributed to the distribution of brucellosis along ethno-national lines. Goats, once ubiquitous to the landscape, became enemies of the Israeli state and were blamed for the "destruction" of nature. Under Israeli rule, legal policies not only seized and confiscated Palestinian land but also targeted goat grazing and led to a steep reduction in the number of goats. The resulting depeasantization and concentration of Palestinians in dense poor townships shaped goat grazing as a backyard practice with lack of trust in the hostile state and its brucellosis eradication campaigns. We argue that state policies of organized violence and organized abandonment have shaped the current ecology of brucellosis as a racialized disease. IMPORTANCE The importance of this article is the novelty in combining public health, colonial studies, and legal research to understand the ecology of human brucellosis. This approach allows us to move from a "snap-shot" reading of diseases and cultural practices toward a reading of bacteria, animals, and humans within their political and historical context. The article uses a settler colonial lens to examine the racialized distribution of human brucellosis in Israel and traces colonial policies toward Palestinians and goats-both seen as unwanted intruders to the newly established Israeli nation state. We place these policies in a context of organized violence and organized abandonment, building on the work of Ruth Wilson Gilmore to read the power hierarchies of humans, animals, and diseases and how they shape practices and disease.

Resolution of iron deficiency following successful eradication of Helicobacter pylori in children.

AIM: To assess correlation between successful Helicobacter pylori (HP) eradication and resolution of iron deficiency in children, without iron supplementation. METHODS: Medical records of children diagnosed with HP infection based on endoscopy were retrospectively reviewed. Among those with non-anaemic iron deficiency (NAID) or iron deficiency anaemia (IDA), haemoglobin, ferritin and CRP levels were compared prior and 6-9 months' post-successful HP eradication. Predictors of resolution of iron deficiency following HP eradication were assessed. RESULTS: Among 60 included children (median age 14.8, IQR12.3-16 years; 62% males), 35% had IDA while the remaining 65% had NAID. Following successful HP eradication, iron normalised in 60% of patients with iron deficiency (ID), without iron supplementation. There were significant improvements in haemoglobin and ferritin concentrations following HP eradication with haemoglobin increasing from 12.3 g/dL to 13.0 g/dL and ferritin increasing from 6.3 µg/L to 15.1 µg/L (p < 0.001). In multiple logistic regression, older age was the only factor associated with resolution of anaemia following HP eradication (OR 1.65, 95% CI 1.16-2.35, p = 0.005). CONCLUSION: Successful HP eradication could be helpful in improving iron status among children with refractory NAID or IDA. Older age may predict this outcome. Screening for HP might be considered in the workup of refractory IDA or ID.

Structural Violence and its Effects on Children Living in War and Armed Conflict Zones: A Palestinian Perspective.

The recent events in Palestine-Israel once again have brought anger and frustration to people inside and outside the medical community. Especially for the pediatric community, the recent wars' toll of at least 67 children in the Gaza Strip and two children in Israel killed warrants attention. Armed conflicts have both direct effects on children's physical health and indirect harms through toxic stress and deprivation. During these troubling times, when civilians, including children, are dying and being mutilated because of conflict, it is crucial to understand the role of structural violence in perpetuating immediate violence. This article will shed light on the historical context of the recurrent wars and military aggressions in Palestine-Israel and contextualize them from a broader public health perspective.

Renal function in ß-thalassemia major patients treated with two different iron-chelation regimes.

BACKGROUND: Renal injury in transfusion dependent ß thalassemia patients (TDT) has been attributed to iron overload, chronic anemia and iron-chelation therapy (ICT) toxicity. We studied renal function in TDT patients treated with two different ICT regimes. PATIENTS AND METHODS: We studied 36 TDT patients: 26 received deferasirox (DFX) and 10 were treated with deferoxamine (DFO) +/- deferiprone (DFP). RESULTS: Increased uNAG was found in 30% of the DFX group vs. 10% of the DFO+/-DFP group, the mean uNAG level in the DFX group was significantly higher than in the DFO+/-DFP group, (P < 0.05). A moderate negative correlation was found between uNAG levels and mean serum ferritin for the prior 10 years (P = 0.03), more pronounced for the DFO+/-DFP group. Twenty nine patients had had their renal function evaluated 10 years earlier; eGFR significantly declined in patients switched to DFX (P = 0.0093) but not in patients who continued DFO+/-DFP. CONCLUSIONS: A high prevalence of renal tubular damage was observed in our TDT patients, particularly those treated with DFX; uNAG was negatively associated with mean 10-year serum ferritin, suggesting ICT's involvement in tubular injury. A significant decline in eGFR compared to a decade earlier was observed only in patients currently treated with DFX. Strict follow-up of renal function in TDT patients is warranted.

Risk Factors for Mortality among Newborns with Neonatal Seizures.

OBJECTIVE: The aim of the study is to examine the incidence and risk factors for death among neonates who developed neonatal seizures (NS) in an ethnically distinctive community with high consanguinity rate in Israel. METHODS: Retrospective study was conducted at a single institution on data between January 2001 and January 2016. All neonates diagnosed with NS developed up to age 28 days were included. Mortality was defined as death within the first year of life. RESULTS: Of all 69,460 neonates born during the study period, 118 (1.7 per 1,000 live births) developed NS; 35 (29.7%) died within the first year while 83 (70.3%) survived. The leading causes of death were developmental brain malformation (31.4%), genetic/metabolic (20%), hypoxic ischemic encephalopathy (20%), intracranial hemorrhage (11.4%) and infections (11.4%). Any consanguinity between the parents was found in 18 and 14.6% among the survivors and deceased groups, respectively (p = 0.24). Developmental brain malformations that lead to death were present in 3.6 and 31.4% in the survivors and deceased groups, respectively (p = 0.001; relative risk 8.70; 95% confidence interval 2.58-29.27). Stepwise backward logistic regression analysis revealed that developmental brain malformations (p < 0.0001), use of more than one antiepileptic medication (p = 0.006), and multiorgan failure (p = 0.004) were significant risk factors that predicted death. CONCLUSION: The results of the current study show that developmental brain malformations that cause NS were the leading risk factor for death.

Immune Thrombocytopenia Secondary to Hodgkin's Lymphoma in Children

BACKGROUND: Immune thrombocytopenia (ITP) is an autoimmune disorder of variable origin that results in bleeding and decreased platelet count. Autoimmune abnormalities have been described in patients with malignancies including non-Hodgkin's lymphoma but are rarely described in patients with Hodgkin's lymphoma. OBJECTIVES: To describe an unusual presentation of Hodgkin's lymphoma in an unusual age and alarm pediatricians of the challenging diagnosis. METHODS: We present two cases that highlight an unusual clinical presentation of childhood Hodgkin's lymphoma occurring at an atypical age. RESULTS: Over a 4-year period, two children aged 5 and 6 years were admitted for suspected ITP, both had cervical lymphadenopathy. Bone marrow examination showed no evidence of tumor or fibrosis. Biopsy of the lymph node was possible only after administration of intravenous immunoglobulins and normalization of the platelet count. Platelet counts increased after initiation of chemotherapy. CONCLUSIONS: The identification of the clinical presentation of ITP as a possible presentation of Hodgkin's lymphoma is important to facilitate timely diagnosis and management.

Elevated anti-tissue transglutaminase antibodies in children newly diagnosed with type 1 diabetes do not always indicate coeliac disease.

AIM: Elevated levels of anti-tissue transglutaminase (anti-tTG) antibody may spontaneously normalise in children with newly diagnosed type 1 diabetes, even if they eat gluten. The prevalence of this phenomenon and predictors of a subsequent coeliac disease (CD) diagnosis were determined. METHODS: The medical records of children diagnosed with type 1 diabetes at Ha'Emek Medical Centre, Israel, from 2007 to 2015, were retrospectively reviewed for elevated anti-tTG antibody levels. Demographic, clinical, laboratory and histological findings were compared between CD patients and those with transient coeliac serology. RESULTS: Of 425 patients with new onset type 1 diabetes, 34 (8%) had elevated anti-tTG antibodies: CD was diagnosed in 14, anti-tTG normalisation occurred in 13 and duodenal biopsies did not suggest CD in seven without anti-tTG antibody normalisation. Protective factors for a subsequent CD diagnosis were older age (p = 0.009) and mildly elevated anti-tTG antibody levels at the time of the type 1 diabetes diagnosis (p = 0.007), and decreased anti-tTG levels within six months of diagnosis (p = 0.03). CONCLUSION: Serological follow-up of a diet containing gluten is recommended for children who have newly diagnosed type 1 diabetes and slightly elevated anti-tTG antibodies with no symptoms that suggest CD.

Diagnosis of familial Mediterranean fever following the initial presentation of monoarthritis.

AIMS: To determine if familial Mediterranean fever (FMF) genetic testing should be advised in children with initial presentation of monoarthritis and to identify clinical parameters associated with FMF-induced arthritis that warrant genetic investigation. METHODS: A prospective study of 71 otherwise healthy children admitted to our pediatric department between 2010-2013 with a first episode of idiopathic monoarthritis. Demographic, clinical and laboratory data were documented and genetic assay of the five common mutations in our population of the MEFV gene that cause FMF syndrome were analyzed in the entire study population. Statistical analysis compared two groups according to FMF status (FMF arthritis and idiopathic arthritis). RESULTS: Among the cohort seven (10%) children harbored two pathogenic mutations in the MEFV gene, thus confirming diagnosis of FMF. This FMF-induced arthritis group had a statistically significant female predominance compared with the idiopathic arthritis group (six [86%] vs. 19 [30%], respectively) (P = 0.006, odds ration [OR] = 14.2). In addition, associated abdominal pain during the attack (two [28%] vs. two [3%], respectively) (P = 0.04, OR = 12.4) and a family history of FMF (two [29%] vs. five [8%], respectively) (P = 0.1, OR 4.7,) were more common in the FMF-induced arthritis group. CONCLUSIONS: In Mediterranean populations where FMF is relatively common we recommend for every child with a first episode of arthritis, without an identifying cause to strongly consider MEFV genetic testing of the common mutations in the relevant population.

Evaluating platelet function disorders in children with bleeding tendency - A single center study.

Platelet function disorders (PFDs) are a common cause of mild bleeding tendency. However, they cannot be recognized by standard screening studies. The gold standard test for PFD is platelet aggregation, performed by light transmission aggregometry (LTA). A newer and less validated method is the closure time (CT), performed by the platelet function Analyzer 100 (PFA-100). Data regarding the validity of these tests in children are limited. The aim of this study was to evaluate the usefulness of LTA and PFA-100 for the diagnosis of pediatric patients with bleeding tendency. This retrospective study included patients one month-18 year old that had LTA tests performed at the coagulation laboratory of Rabin Medical Center between the years 2006-2015. Bleeding severity was assessed using a pediatric bleeding score. Patients were excluded from analysis if they had thrombocytopenia, thrombocytosis or coagulation factors deficiencies. One hundred and thirty-seven (137) patients were included in the analysis. The median age was 7.5 years (range one month-18 years). Most patients (93%) had a bleeding score of 2 or more. Abnormal LTA was found in 40% and prolonged CT in 23% of the patients. Abnormal LTA was significantly more common in patients with a bleeding score of 2 or more compared to patients with a lower bleeding scores (P = 0.04). No significant correlation was found between the bleeding severity and the number of agonists which induced abnormal responses (p = 0.52) or the CT (p = 0.35). Furthermore, no correlation was found between abnormal LTA and prolonged CT. To conclude, we were able to diagnose 40% of children who presented with bleeding tendency with platelet aggregation defects by LTA. Abnormal LTA was significantly more prevalent in patients with a bleeding score of 2 and above. In contrast, CT was not found to be sensitive as a screening tool for PFD. Therefore, our data extend the validity of the use of LTA for the evaluation of pediatric patients with bleeding tendency.