Chronic Pain and Psychological Distress Among Undocumented Latinx Immigrants in the USA

BackgroundUndocumented immigration is often accompanied by multiple and complex stressors, which over time may increase the risk for chronic pain.ObjectiveThis study aimed to identify the prevalence of chronic pain and its association with psychological distress among undocumented Latinx immigrants in the USA.Design/ParticipantsWe used respondent-driven sampling to collect and analyze data from clinical interviews with 254 undocumented Latinx immigrants, enabling inference to a population of 22,000.Main MeasuresChronic pain was assessed using the World Health Organization Composite International Diagnostic Interview (CIDI) Chronic Conditions Module. For all analyses, inferential statistics accounted for design effects and sample weights to produce weighted estimates. We conducted logistic regression analyses to assess the association between chronic pain and psychological distress after controlling for age, years in the USA, and history of trauma.ResultsA total of 28% of undocumented Latinx immigrants reported having chronic pain, and 20% of those had clinically significant psychological distress. Significant differences in the prevalence of chronic pain were reported across age groups, years in the USA, and trauma history. After controlling for relevant covariates, chronic pain was significantly associated with psychological distress (OR = 1.06, 95% CI [1.02, 1.09]), age (OR = 1.05, 95% CI [1.02; 1.09]), and history of trauma (OR = 1.10 per additional traumatic event, 95% CI [1.02; 1.19]; C-statistic = 0.79).ConclusionAmong undocumented Latinx immigrants, chronic pain is significantly associated with psychological distress, older age, and trauma history. Given that undocumented immigrants have restricted access to healthcare and are at high risk for chronic pain, developing alternatives to facilitate access to chronic pain interventions and risk-reduction prevention are needed.KEY WORDS: chronic pain, distress, mental health, undocumented immigrants, Latinx

Chronic pain is a global health concern associated with detrimental pathophysiological, functional, economic, and social consequences.¹ Chronic pain is generally defined as continuous or intermittent pain or discomfort that persists for at least 3 months.² Approximately 1.5 billion people live with chronic pain worldwide, with US national estimates exceeding 100 million.³ Furthermore, in the USA, racial/ethnic disparities exist with regards to experiencing chronic pain.¹ For instance, Latinxs tend to report a lower prevalence of chronic pain and less pain interference with daily functioning when compared with non-Latinx whites, but greater pain severity.⁴ Likewise, disparities between these groups exist in accessing, seeking, and responding to treatment for pain.⁴ Nonetheless, less is known about the prevalence of pain and the pain experience among Latinxs who are hidden or hard-to-reach, such as undocumented immigrants.The undocumented immigration path is often accompanied by multiple and complex stressors, which over time may increase the risk for chronic pain. Hazardous working conditions, limited healthcare access, exploitation, and stigmatization are factors that could make undocumented immigrants vulnerable to chronic pain. For instance, undocumented immigrants are more likely than their documented counterparts to undertake physically demanding jobs in industries with high rates of injuries and exposure to hazardous conditions.^5–7 Non-job-related trauma is another cause of pain in immigrants^8,9—approximately 83% of undocumented immigrants report a lifetime history of trauma.¹⁰ Compounding these problems, limited healthcare access and lack of insurance force immigrants to pay out of pocket for healthcare; turn to unsafe or non-evidence-based healing practices (e.g., herbal remedies, hueseros, or bone/muscle therapy); or neglect healthcare altogether.¹¹ All of the aforementioned risk factors suggest that undocumented immigrants may be vulnerable population to chronic pain.Information about the prevalence of chronic pain among undocumented immigrants is needed to inform prevention, intervention, advocacy, and policy efforts. To our knowledge, no prior studies have addressed chronic pain among undocumented immigrants. Therefore, this study aimed to (1) assess the prevalence of chronic pain and associated vulnerabilities, including history of trauma, among undocumented Latinx immigrants residing near the US–Mexico border and (2) determine whether there is an association between chronic pain and psychological distress in this immigrant population.     

Evolution of metabolic and functional derangements of pancreatic islets in phosphate depletion.

Phosphate depletion (PD) causes a rise in basal level of cytosolic calcium ([Ca2+]i) of pancreatic islets, a decrease in their basal and stimulated ATP content, a reduction in the maximum velocity (Vmax) of Ca2+ adenosine triphosphatase (ATPase) and Na(+)-K+ ATPase, impaired glucose-induced calcium signal and decreased glucose-induced insulin secretion. The sequence of events that lead to these derangements during the evolution of PD are not defined. The present study examined this issue by measuring the metabolic and functional profile of pancreatic islets weekly during the evolution of PD over a period of 6 weeks, and whether phosphate repletion reverses these abnormalities. The results show that initial abnormalities are a rise in Vmax of Ca2+ ATPase and modest rise in basal [Ca2+]i. This was followed by a fall in basal and stimulated ATP content. With the fall in ATP content, the Vmax of Ca2+ ATPase and Na(+)-K+ ATPase decreases and the rise in [Ca2+]i becomes more pronounced. A decrease in glucose-induced insulin secretion becomes evident with the fall in ATP, the decrease in glucose-induced calcium signal, and/or delta[Ca2+]i/basal[Ca2+]i. All functional and metabolic derangements of the pancreatic islets returned to normal after phosphate repletion. Taken together, our data are consistent with the notion that PD is associated with an initial increase in calcium influx into the islets. This is followed by modest but significant rise in [Ca2+]i which, in turn, would inhibit mitochondrial oxidation and ATP generation leading to a decrease in ATP content. The latter compromises the activity of Ca2+ ATPase and Na(+)-K+ ATPase which are involved, directly or indirectly, in calcium extrusion out of the islets. The increased influx of calcium combined with decreased calcium extrusion is followed by a further rise in basal levels of [Ca2+]i. This sequence of events continues until a steady state is reached and is characterized by reduced basal and stimulated ATP content, reduced Vmax of Ca2+ ATPase and Na(+)-K+ ATPase and elevated basal level of [Ca2+]i. Phosphate repletion reverses all these abnormalities.     

Control within a virtual environment is correlated to functional outcomes when using a physical prosthesis

Background

Advances such as targeted muscle reinnervation and pattern recognition control may provide improved control of upper limb myoelectric prostheses, but evaluating user function remains challenging. Virtual environments are cost-effective and immersive tools that are increasingly used to provide practice and evaluate prosthesis control, but the relationship between virtual and physical outcomes—i.e., whether practice in a virtual environment translates to improved physical performance—is not understood.

Methods

Nine people with transhumeral amputations who previously had targeted muscle reinnervation surgery were fitted with a myoelectric prosthesis comprising a commercially available elbow, wrist, terminal device, and pattern recognition control system. Virtual and physical outcome measures were obtained before and after a 6-week home trial of the prosthesis.

Results

After the home trial, subjects showed statistically significant improvements (p <?0.05) in offline classification error, the virtual Target Achievement Control test, and the physical Southampton Hand Assessment Procedure and Box and Blocks Test. A trend toward improvement was also observed in the physical Clothespin Relocation task and Jebsen-Taylor test; however, these changes were not statistically significant. The median completion time in the virtual test correlated strongly and significantly with the Southampton Hand Assessment Procedure (p =?0.05, R =???0.86), Box and Blocks Test (p =?0.007, R =???0.82), Jebsen-Taylor Test (p =?0.003, R =?0.87), and the Assessment of Capacity for Myoelectric Control (p =?0.005,R =???0.85). The classification error performance only had a significant correlation with the Clothespin Relocation Test (p =?0.018, R =?.76).

Conclusions

In-home practice with a pattern recognition-controlled prosthesis improves functional control, as measured by both virtual and physical outcome measures. However, virtual measures need to be validated and standardized to ensure reliability in a clinical or research setting.

Trial registration

This is a registered clinical trial: NCT03097978.

     

The role of ADAMTS‐13 in the coagulopathy of sepsis

Summary

The interaction between platelets and the vessel wall is mediated by various receptors and adhesive proteins, of which von Willebrand factor (VWF) is the most prominent. The multimeric size of VWF is an important determinant of a more intense platelet–vessel wall interaction, and is regulated by the VWF‐cleaving protease ADAMTS‐13. A deficiency in ADAMTS‐13 leads to higher concentrations of ultralarge VWF multimers and pathological platelet–vessel wall interactions, in its most typical and extreme form leading to thrombocytopenic thrombotic purpura, a thrombotic microangiopathy characterized by thrombocytopenia, non‐immune hemolysis, and organ dysfunction. Thrombotic microangiopathy associated with low levels of ADAMTS‐13 may be a component of the coagulopathy observed in patients with sepsis. Here, we review the potential role of ADAMTS‐13 deficiency and ultralarge VWF multimers in sepsis, and their relationship with sepsis severity and prognosis. In addition, we discuss the possible benefit of restoring ADAMTS‐13 levels or reducing the effect of ultralarge VWF as an adjunctive treatment in patients with sepsis.

     

The mechanism of the obstruction in calcific aortic stenosis with bicuspid valve: a reason for failure of balloon aortic valvuloplasty in the elderly

Percutaneous aortic balloon valvuloplasty failed to relieve the obstruction in 2 elderly patients with calcific aortic stenosis. Intraoperative and pathologic examination showed bicuspid aortic valve with symmetric cusps, straight and fibrotic cusp edges and fractured calcific nodules of the aortic valve. Failure of balloon valvuloplasty in these patients, in spite of successful fractures of calcific nodules, was due to inability to influence the spring-like action of the thickened edges of the valve which represents a specific additional cause of obstruction in calcific bicuspid aortic valve of the elderly.     

Selective release of glutamate from cerebellar granule cells differentiating in culture

The aim of the present study was to assess whether endogenous and newly synthesized glutamate can be released from differentiating cultured cerebellar granule cells in a way compatible with a neurotransmitter role. Granule cells from 8-day-old rat cerebella were grown in basal Eagle's medium with 10% fetal calf serum for 2-12 days in vitro (DIV), then washed with Krebs-Ringer medium, and labeled for 45 min with tracer amounts of radioactive glutamine. Subsequently, the release of endogenous glutamate and of newly formed radioactive glutamate was measured in basal conditions and upon depolarization with elevated K⁺ concentration or veratridine. At 2 DIV, the release of endogenous and newly synthesized glutamate evoked by high K⁺ concentration was small and Ca²⁺ independent, but it progressively and steadily increased (up to 8- to 10-fold) and became Ca²⁺ dependent (up to 80-85%) at later stages (4, 8, and 12 DIV). Veratridine was almost ineffective with cells at 2 DIV but greatly increased glutamate release (endogenous and neosynthesized) at 8 DIV, and its action was totally antagonized by tetrodotoxin. The level and synthesis of glutamate remained fairly constant in cells from 2 to 12 DIV. γ-Aminobutyric acid synthesis from radioactive glutamine was about 3% of that of glutamate, and γ-aminobutyric acid release (endogenous and neosynthesized) was not measurable. Aspartate synthesis was about 10% of that of glutamate, and the high K⁺ concentration-evoked release of this amino acid was modest and scarcely affected by Ca²⁺. Neither high K⁺ concentration nor veratridine was able to induce glutamate release from confluent cerebellar astrocyte cultures at 14 DIV, although the level and synthesis of the amino acid were comparable to those in granule cells. In conclusion, the data show that a stimulus-coupled release of endogenous and neosynthesized glutamate is progressively expressed by cerebellar granule cells differentiating in culture, and this strongly supports the concept that glutamate is the neurotransmitter of these cells.