High cost of illness in fibromyalgia patients in Iran, irrespective of disease severity: A prospective cost study.

AIMS: This study aimed to estimate the economic burden of fibromyalgia (FM) in 6 months, using a cost-diary, and to evaluate its relationship with the disease severity. METHODS: This is a prospective cost-of-illness study on 62 participants with an FM diagnosis within a 6 month period. Patients completed the questionnaires, including FIQR (Revised Fibromyalgia Impact Questionnaire) and SF-12 (12-item short-form survey). The cost-diary method was used to track the cost of the disease. The participants received six cost-diary booklets during the study period to report their FM-related costs, hours, and days of productivity loss. The final costs are reported in US dollars. RESULTS: Most of the participants were women (90.3%) with a mean (±SD) age of 40.80 (±5.50) years and a mean (±SD) FIQR score of 54.38 (±14.13). Moreover, 45.2% of patients fulfilled all six booklets, whereas 24.2% returned only one booklet. The participants showed a mean (±SD) direct healthcare, non-healthcare, and indirect cost of $ 2817.08 (±$ 1860.04), $ 1497.98(±$ 1358.21), and $ 1449.05(±$ 3637.41) per patient for 6 months, respectively. CONCLUSION: Fibromyalgia is associated with high health-related and non-health-related costs in our country, irrespective of its severity. This study warrants urgent consideration in managing the disease burden on both patients and society.

Pro-tumorigenic functions of macrophages at the primary, invasive and metastatic tumor site.

The tumor microenvironment (TME) not only facilitates cancer progression from the early formation to distant metastasis, but also it differs itself from time to time alongside the tumor evolution. Tumor-associated macrophages (TAMs), whether as pre-existing tissue-resident macrophages or recruited monocytes, are an inseparable part of this microenvironment. As their parents are broadly classified into a dichotomic, simplistic M1 and M2 subtypes, TAMs also exert paradoxical and diverse phenotypes as they are settled in different regions of TME and receive different microenvironmental signals. Briefly, M1 macrophages induce an inflammatory precancerous niche and flame the early oncogenic mutations, whereas their M2 counterparts are reprogrammed to release various growth factors and providing an immunosuppressive state in TME as long as abetting hypoxic cancer cells to set up a new vasculature. Further, they mediate stromal micro-invasion and co-migrate with invasive cancer cells to invade the vascular wall and neural sheath, while another subtype of TAMs prepares suitable niches much earlier than metastatic cells arrive at the target tissues. Accordingly, at the neoplastic transformation, during the benign-to-malignant transition and through the metastatic cascade, macrophages are involved in shaping the primary, micro-invasive and pre-metastatic TMEs. Whether their behavioral plasticity is derived from distinct genotypes or is fueled by microenvironmental cues, it could define these cells as remarkably interesting therapeutic targets.