Raising Physician Awareness to Reduce Childhood Lead Exposure: The Massachusetts Community Lead Progress Report

Massachusetts has been at the forefront of childhood lead poisoning prevention, enacting one of the nation\u27s first Lead Laws in the 1970\u27s. The Massachusetts Lead Law is stringent, requiring universal screening of children for lead poisoning multiple times before age three, and the removal or covering of lead paint hazards in all homes built before 1978 where a child under age six lives. Owing to such a robust law, Massachusetts screening rates are high and the prevalence and incidence of lead poisoning has been steadily decreasing since 2000. Despite these successes, there is wide variation in screening and prevalence rates at the community level, with some communities showing a need for a more targeted approach. Additionally, scientific evidence increasingly suggests that even low levels of lead exposure cause severe and irreversible health effects, underlining the fact that lead remains a significant health risk for children in Massachusetts. To address these concerns, Massachusetts DPH has developed a direct mailing tool for physician outreach providing community-specific indicators of childhood lead screening and exposure and highlighting areas of needed improvement in screening, follow-up, and prevention. The Childhood Lead Poisoning Community Progress Report focuses on awareness of the CDC reference level of 5 µg/dL and the dangers of low-level lead exposure, educating medical providers on their role in preventing lead exposure by screening all children, following proper testing practices, and educating parents on available resources. Qualitative and quantitative approaches will be used to measure the impact of the Community Progress Report over time

Turning psychology into policy: a case of square pegs and round holes?

This paper problematizes the ways in which the policy process is conceived in published psychological research. It argues that these conceptions of the policy process fail to ade- quately reflect the real-world dynamism and complexity of the processes and practices of social policy-making and implementation. In this context, psychological evidence needs to be seen as one type of evidence (amongst many others). In turn this requires researchers to take account of broader political processes that favour certain types of knowledge and disparage others. Rather than be regarded as objective and scientific, policy in this characterisation is regarded as a motivated form of politics. This multi-layered, multi-level hybrid structure is not immediately amenable to the well-intentioned interventions of psychologists. While the tendency of many psychologists is to overestimate the impact that we can have upon policy formation and implementation, there are examples where psychological theory and research has fed directly into UK policy developments in recent years. This paper draws on the recent Improving Access to Psychological Therapies (IAPT) initiative and the work of personality researcher Adam Perkins on the UK’s social security system to ask whether psychology has a sufficiently elaborated sense of its own evidence base to legitimately seek to influence key national areas of public policy. The article cautions against dramatic changes to policy pre- dicated upon any one reading of the variegated and, at times, contradictory psychological evidence base. It concludes that, in order to meaningfully contribute to the policy develop- ment process in a way which increases equality and social justice, psychologists need to be more strategic in thinking about how their research is likely to be represented and mis- represented in any particular context. Finally some possible directions for psychologists to take for a more meaningful relationship with policy are suggested

Zollinger-Ellison syndrome associated with neurofibromatosis type 1: a case report

BACKGROUND: Neurofibromatosis type 1 is an autosomal dominant neurocutaneous disorder with characteristic features of skin and central nervous system involvement. Gastrointestinal involvement is rare, but the risk of malignancy development is considerable. Zollinger-Ellison syndrome is caused by gastrin-secreting tumors called gastrinomas. Correct diagnosis is often difficult, and curative treatment can only be achieved surgically. CASE PRESENTATION: A 41-year-old female affected by neurofibromatosis type 1 presented with a history of recurrent epigastric soreness, diarrhea, and relapsing chronic duodenal ulcer. Her serum fasting gastrin level was over 1000 pg/mL. An abdominal CT scan revealed a 3 × 2-cm, well-enhanced mass adjacent to the duodenal loop. She was not associated with multiple endocrine neoplasia type 1. Operative resection was performed and gastrinoma was diagnosed by immunohistochemical staining. The serum gastrin level decreased to 99.1 pg/mL after surgery, and symptoms and endoscopic findings completely resolved without recurrences. CONCLUSION: Gastrinoma is difficult to detect even in the general population, and hence symptoms such as recurrent idiopathic peptic ulcer and diarrhea in neurofibromatosis type 1 patients should be accounted for as possibly contributing to Zollinger-Ellison syndrome

Possible Primary Lymph Node Gastrinoma: Occurrence, Natural History, and Predictive Factors: A Prospective Study

OBJECTIVE: To analyze the results of a prospective study of 176 patients with Zollinger-Ellison syndrome (ZES) (138 sporadic, 38 MEN1) undergoing 207 operations over a 17-year period. SUMMARY BACKGROUND DATA: The existence of lymph node (LN) primary gastrinoma causing ZES is controversial. METHODS: Three groups of patients were compared: LN only resected, cured, and no relapse (likely LN primary); same criteria but relapse (unlikely LN primary); and duodenal primary and LN metastases (Duo-LN). RESULTS: Forty-five (26%) had only LN(s) as the initial tumor found. Twenty-six of the 45 (58%) fit the definition of a likely LN primary because they were apparently cured postresection. At 10.4 ± 1.2 years, 69% of the 26 patients with likely LN primary tumors have remained cured and have LN primaries. In the 8 of 26 with recurrent ZES, it occurred at 5 ± 1 years, and 3 had duodenal gastrinoma that had been missed. Ten percent (13/138) of all patients with sporadic ZES and 0% (0/38) with ZES and MEN1 remained cured with only a LN tumor removed. In patients with sporadic gastrinomas no clinical, laboratory, or radiographic localization feature differed among patients with likely LN primary (n = 16) and those with unlikely LN primary (n = 6) or those with Duo-LN (n = 37). In the likely LN primary group, the largest LN was 2.2 ± 0.2 cm, the number of LNs removed was 1.3 ± 0.1 (25% ≥1 LN), and 78% were in the gastrinoma triangle, which also did not differ from the other 2 groups. Disease-free survival was similar in the likely LN primary group, patients with Duo-LN, and those with pancreatic primaries. CONCLUSIONS: These results support the conclusion that primary LN gastrinomas occur and are not rare (approximately 10% of sporadic cases). These results suggest that a proportion (25%) of these tumors are either multiple or malignant. Because no clinical, laboratory, or tumoral characteristic distinguishes patients with LN primary tumors, all patients with ZES undergoing surgery should have an extensive exploration to exclude duodenal or pancreatic tumors and routine removal of lymph nodes in the gastrinoma triangle