Factors Effecting Mastalgia.
Eren Tunc,Aslan Adem,Ozemir Ibrahim A,Baysal Hakan,Sagiroglu Julide,Ekinci Ozgur,Alimoglu Orhan
Breast care (Basel, Switzerland)
BACKGROUND:Breast pain is one of the leading complaints that ends up with referral to breast surgery clinics. The purpose of the present study was to investigate the factors that cause mastalgia, and its relation with benign or malignant breast disease. METHODS:The study was performed in 700 patients. Data obtained from surveys, and imaging findings were prospectively recorded, and analyzed. RESULTS:The mean age was 45.20 ± 10.78 years. The mastalgia group included 500 cases; the asymptomatic group comprised 200 individuals. Stressful lifestyle, caffeine consumption, and smoking were associated with mastalgia (p < 0.05). Rates of women who had breast fed 3 times or more were higher in the mastalgia group (p < 0.05). Increased breast density, and breast imaging-reporting and data system (BI-RADS) 2 mammography findings were related with mastalgia (p < 0.05). Cysts and fibroadenomas were more common in the mastalgia group (p < 0.05). The incidence of a past history of malignant breast disease was significantly higher in the mastalgia group (p < 0.05). CONCLUSIONS:Stress, caffeine, smoking, lactation frequency, and benign disorders were factors detected to be related with mastalgia. Although a significant relation between mastalgia and malignant breast disease was detected in our study, more controlled studies are still required to investigate this issue further.
Effects of Mastalgia in Young Women on Quality of Life, Depression, and Anxiety Levels.
Kanat Burhan Hakan,Atmaca Murad,Girgin Mustafa,Ilhan Yavuz Selim,Bozdağ Ahmet,Özkan Zeynep,Yazar Fatih Mehmet,Emir Seyfi
The Indian journal of surgery
The aims of this study are to evaluate whether or not there is a relationship between mastalgia with anxiety and depression in young women with mastalgia who do not have organic breast pathology and to examine the effect of pain on the quality of life. Forty female pre-menopausal patients between the ages of 20-40 years with mastalgia and 40 totally healthy volunteers with the same characteristics were investigated with the Short Form 36 (SF-36), Hamilton Depression Scale, and the Hamilton Anxiety Rating Scale prospectively following breast examination and radiological examination. Statistical assessments were performed using the SPSS 11.5. Anxiety levels were observed to be higher in the patient group (p = 0.04). The depression level was higher in the patient group; however, this was not statistically significant (p = 0.08). The quality of life of the mastalgia group was determined to be lower than that of the control group, and the sub-parameters of physical function (p = 0.04), body pain (p = 0.02), general health (p = 0.03), and energy (p = 0.008) were found to be significantly low. There may be a relationship between mastalgia and depression in young women with mastalgia; however, a closer relationship between anxiety and mastalgia is observed. Mastalgia affects the quality of life of an individual negatively at a significant degree.
THE ROLE OF E2/P RATIO IN THE ETIOLOGY OF FIBROCYSTIC BREAST DISEASE, MASTALGIA AND MASTODYNIA.
Brkić Milena,Vujović Svetlana,Ivović Miomira,Tančić Gajić Milina,Marina Ljiljana,Franić Ivanišević Maja,Franić Damir
Acta clinica Croatica
- The aim of the study was to assess the role of the estradiol and progesterone relationship during the late luteal phase and the occurrence of fibrocystic breast disease (FBD). The concentration of estradiol/progesterone was measured in the group of women with FBD as study group (n=50) and control group of women without FBD (n=40). All women had regular ovulation cycles. Blood samples for estradiol (E2), progesterone (P) and prolactin determination were obtained in the morning at 8 am on days 21 and 24 of menstrual cycle. Significant mastalgia and mastodynia history in women with FBD was obtained with yes or no questionnaire. FBD diagnosis was confirmed with ultrasound (size and number of simple cysts). In the control group, a reduced E2/P ratio was noticed from day 21 to day 24 of the cycle (from 14.8±11.5 pg/mL to 9.1±6.1 pg/mL; p<0.05), which was not recorded in the group of women with FBD (study group). Even the slightest disturbance of the E2/P ratio may contribute to the occurrence of FBD with clinical manifestations of mastalgia and mastodynia.
Inflammatory biomarkers in serum in subjects with and without work related neck/shoulder complaints.
Matute Wilander Anna,Kåredal Monica,Axmon Anna,Nordander Catarina
BMC musculoskeletal disorders
BACKGROUND:Although it has recently been recognised that inflammation is important in the development of work-related musculoskeletal disorders (MSDs), the exact pathophysiological pathways are unknown. METHODS:We investigated serum concentrations of inflammatory cytokines in 35 female supermarket cashiers with repetitive work tasks and work related neck/shoulder complaints, compared with those from 25 women without MSDs (6 supermarket cashiers and 19 middle-school teachers or faculty staff). None of the subjects were pregnant or lactating, and showed no signs of rheumatoid arthritis, systemic lupus erythematosus, cancer, diabetes, coronary artery disease or inadequately controlled hypertension. Serum levels of IL-1α, IL-1β, IL-6, IL-8, IL-10, IL-12, MCP-1, MIP-1α, MIP-1β, TNF-α, GM-CSF, CTGF and CRP were analysed. RESULTS:The women with pain related to MSD had higher serum concentrations of MIP-1β (median, 25th-75th percentile: 90.0 pg/mL, 62.5-110 vs. 73.1 pg/mL, 54.6-88.3; p = 0.018), IL-12 (0.26 pg/mL, 0.26-0.26 vs. 0.26 pg/mL, 0.26-0.26; p = 0.047) and CRP (0.5 mg/L, 0.5-1.6 vs. 0.5 mg/L, 0.5-0.5; p = 0.003), than control subjects. Levels of MIP-1α, MIP-1β and CRP were correlated with the reported intensity of neck/shoulder pain (r = 0.29, p = 0.03 for MIP-1α; r = 0.29, p = 0.02 for MIP-1β and r = 0.43, p = 0.001 for CRP). No statistically significant differences in serum levels were found for the remaining cytokines. CONCLUSIONS:Otherwise healthy females with ongoing work-related neck/shoulder pain showed higher serum concentrations of MIP-1β, IL-12 and CRP than controls, and the levels of MIP-1α, MIP-1β and CRP were correlated to pain intensity. These results support previous findings that inflammatory processes play a part in work related MSDs.
Pentoxifylline Ameliorates Mechanical Hyperalgesia in a Rat Model of Chemotherapy-Induced Neuropathic Pain.
Kim Hee Kee,Hwang Seon-Hee,Lee Sing-Ong,Kim Sung Hoon,Abdi Salahadin
BACKGROUND:Chemotherapy-induced neuropathic pain is difficult to treat. Pentoxifylline inhibits the production of inflammatory cytokines including tumor necrosis factor α(TNF- α) and interleukin 1β (IL-1β). OBJECTIVE:The aims of our study were to investigate the analgesic and preventive effects of pentoxifylline on paclitaxel-induced neuropathic pain in rats and to identify its mechanisms of action. STUDY DESIGN:Controlled animal study. METHODS:Neuropathic pain was induced with intraperitoneally injected paclitaxel on 4 alternate days in male Sprague-Dawley rats. Pentoxifylline was administered systemically as a single injection and a continuous infusion before or after the injection of paclitaxel. The mechanical threshold for allodynia was measured by using von Frey filaments. Protein levels and localization of inflammatory cytokines were performed by using Western blotting and immunohistochemistry, respectively. RESULTS:After the rats developed neuropathic pain behavior, a single intraperitoneal injection and continuous infusion of pentoxifylline ameliorated paclitaxel-induced mechanical allodynia. In addition, systemic infusion of pentoxifylline in the early phase of the development of pain behavior delayed the onset of paclitaxel-induced pain behavior. Paclitaxel increased the levels of the catalytic subunit α of protein kinase A, phosphorylated nuclear factor ;κB, TNF- α, and IL-1κ in the lumbar dorsal root ganglia. Pentoxifylline decreased the paclitaxel-induced TNF- α and IL-1β levels. In addition, IL-1β was expressed in neurons and satellite cells in the lumbar dorsal root ganglia after paclitaxel. LIMITATIONS:Although this study was performed in the animal model by well-designed manner, clinical study will be needed to confirm the analgesic effect of pentoxifylline. CONCLUSION:Pentoxifylline alleviated chemotherapy-induced neuropathic pain in rats by reducing the levels of inflammatory cytokines in dorsal root ganglia and may be effective chemotherapy-induced neuropathic pain in patients.
TNF-α and sTNF-RII Are Associated with Pain Following Hip Fracture Surgery in Older Adults.
Ko Fred C,Rubenstein William J,Lee Eric J,Siu Albert L,Sean Morrison R
Pain medicine (Malden, Mass.)
Objective:To explore whether plasma inflammatory mediators on postoperative day 3 (POD3) are associated with pain scores in older adults after hip fracture surgery. Design:Cross-sectional study. Setting:Mount Sinai Hospital, New York, New York. Subjects:Forty patients age 60 years or older who presented with acute hip fracture at Mount Sinai Hospital between November 2011 and April 2013. Methods:Plasma levels of six inflammatory mediators of the nuclear factor kappa B pathway were measured using blood collected on POD3. Self-reported pain scores (i.e., pain with resting, walking, and transferring) were assessed at baseline (prefracture) and on POD3. Linear regression models using log-transformed data were performed to determine associations between inflammatory mediators and postoperative pain. Results:Interleukin 18 (IL-18) was positively associated with POD3 resting pain score in the unadjusted model (β = 0.66, P = 0.03). Tumor necrosis factor α (TNF-α) and soluble TNF receptor II (sTNF-RII) were positively associated with POD3 resting pain score in the adjusted model (β = 0.99, P = 0.03, and β = 0.86, P = 0.04, respectively). Moreover, TNF-α was positively associated with POD3 walking pain score in the adjusted model (β = 1.59, P = 0.05). Pain with transferring was not associated with these inflammatory mediators. Conclusions:These findings suggest that TNF-α and its receptors may influence pain following hip fracture. Further study of the TNF-α pathway may inform future clinical applications that monitor and treat pain in the vulnerable elderly who are unable to accurately report pain.
Association of Parkinson's disease-related pain with plasma interleukin-1, interleukin-6, interleukin-10, and tumour necrosis factor-α.
Li Donghui,Song Xiangsheng,Huang Huayun,Huang Huadong,Ye Zanya
OBJECTIVE:To study the association between Parkinson's disease (PD)-related pain and plasma interleukin (IL)‑1, IL‑6, IL‑10, and tumour necrosis factor (TNF)‑α levels. METHODS:Sixty-seven participants were enrolled. Plasma inflammatory cytokine levels of IL-1, IL-6, IL-10, and TNF-α were measured with enzyme-linked immunosorbent assay. We additionally administered the third part of the Unified Parkinson's Disease Rating Scale (UPDRS III) and Hoehn and Yahr (H-Y) scale stage and recorded the course of the disease, the type and location of the pain, and the use of drugs. RESULTS:The level of IL-1 was significantly higher in the PD-with-pain than in the healthy-control group (P < 0.05). There was no significant difference among groups in the other examined cytokine levels. There was a statistically significant difference between the PD-with-pain and the PD-without-pain groups in UPDRS III and H-Y stage. Additionally, the IL-1 level was significantly higher in patients who received a levodopa dosage of >250 mg than in their counterparts who received ≤250 mg, and the IL-1 level was higher in patients with an H-Y stage of >2 and UPDRS III of >27 than in their counterparts with an H-Y stage of ≤2 and UPDRS III of ≤27. The expression of TNF-α was higher in patients aged ≥70 years than in their counterparts aged <70 years. The level of IL-10 was significantly lower in the patients with an H-Y stage of >2 than in their counterparts with an H-Y stage of ≤2. CONCLUSION:The elevated level of IL-1 and the depressed level of IL-10 in the peripheral blood of patients with PD-related pain suggests that certain inflammatory cytokines may be implicated in the occurrence and clinical symptoms of PD-related pain.
[Non-inflammatory muscle pain].
Roicke Hannes,Köhler Wolfgang,Baum Petra,Baerwald Christoph,Krasselt Marco
Deutsche medizinische Wochenschrift (1946)
Muscle pain as a common symptom in daily practice frequently occurs as a non-specific accompanying symptom in multiple internal and neurological diseases. Primarily inflammatory or autoimmune muscular diseases are causing muscle pain. However, a number of non-inflammatory causes of pain can also be considered for differential diagnosis. These are presented in this article. In principle, a distinction must be made between focal and diffuse muscle pain. As an invasive diagnostic procedure, a muscle biopsy should only be performed as the last step in the diagnostic alogorithm. If diffuse muscle pain is only associated with slight muscle weakness or is completely absent, there is usually a primary rheumatic cause. Statins (HMG-CoA reductase inhibitors) can lead to rhabdomyolysis, muscle fiber atrophy and muscle necrosis by damaging the muscle fiber membrane. Myotonias are autosomal dominant or autosomal recessive inherited disorders of muscle function. The genetic defect leads to pronounced muscle stiffness. The cause of metabolic myopathies can be disorders of the carbohydrate, fat or purine metabolism. Fibromyalgia syndrome (FMS) is a non-inflammatory disease and, according to the current knowledge, recognized as the result of an exposure to physical, biological and psychosocial factors (biopsychological disease model). To help diagnosing FMS, pain regions and core symptoms (fatigue, sleep disturbances) can be detected using questionnaires (Widespread Pain Index [WPI] and Symptom Severity Scale [SSS]).
Differential expression of systemic inflammatory mediators in amputees with chronic residual limb pain.
Chamessian Alexander,Van de Ven Thomas,Buchheit Thomas,Hsia Hung-Lun,McDuffie Mary,Gamazon Eric R,Walsh Colin,Bruehl Stephen,Buckenmaier Chester 'Trip',Shaw Andrew
Chronic postsurgical pain impacts most amputees, with more than half experiencing neuralgic residual limb pain. The transition from normal acute postamputation pain to chronic residual limb pain likely involves both peripheral and central inflammatory mechanisms. As part of the Veterans Integrated Pain Evaluation Research study, we investigated links between systemic inflammatory mediator levels and chronic residual limb pain. Subjects included 36 recent active duty military traumatic amputees with chronic residual limb pain and 40 without clinically significant pain. Blood samples were obtained and plasma concentrations of an array of inflammatory mediators were analyzed. Residual limb pain intensity and pain catastrophizing were assessed to examine associations with inflammatory mediators. Pro-inflammatory mediators including tumor necrosis factor (TNF)-α, TNF-β, interleukin (IL)-8, ICAM-1, Tie2, CRP, and SAA were elevated in patients with chronic residual limb pain. Across all patients, residual limb pain intensity was associated positively with levels of several proinflammatory mediators (IL-8, TNF-α, IL-12, TNF-β, PIGF, Tie2, SAA, and ICAM-1), and inversely with concentrations of the anti-inflammatory mediator IL-13, as well as IL-2 and Eotaxin-3. Pain catastrophizing correlated positively with IL-8, IL-12, TNF-β, PIGF, and ICAM-1, and inversely with IL-13. Significant associations between catastrophizing and residual limb pain intensity were partially mediated by TNF-α, TNF- β, SAA, and ICAM-1 levels. Results suggest that chronic postamputation residual limb pain is associated with excessive inflammatory response to injury or to inadequate resolution of the postinjury inflammatory state. Impact of pain catastrophizing on residual limb pain may be because of part to common underlying inflammatory mechanisms.
Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain.
Barkai Omer,Puig Stephanie,Lev Shaya,Title Ben,Katz Ben,Eli-Berchoer Luba,Gutstein Howard B,Binshtok Alexander M
Endogenous inflammatory mediators contribute to the pathogenesis of pain by acting on nociceptors, specialized sensory neurons that detect noxious stimuli. Here, we describe a new factor mediating inflammatory pain. We show that platelet-derived growth factor (PDGF)-BB applied in vitro causes repetitive firing of dissociated nociceptor-like rat dorsal root ganglion neurons and decreased their threshold for action potential generation. Injection of PDGF-BB into the paw produced nocifensive behavior in rats and led to thermal and mechanical pain hypersensitivity. We further detailed the biophysical mechanisms of these PDGF-BB effects and show that PDGF receptor-induced inhibition of nociceptive M-current underlies PDGF-BB-mediated nociceptive hyperexcitability. Moreover, in vivo sequestration of PDGF or inhibition of the PDGF receptor attenuates acute formalin-induced inflammatory pain. Our discovery of a new pain-facilitating proinflammatory mediator, which by inhibiting M-current activates nociceptive neurons and thus contributes to inflammatory pain, improves our understanding of inflammatory pain pathophysiology and may have important clinical implications for pain treatment.
Vitamin D Levels, Vitamin D Receptor Polymorphisms, and Inflammatory Cytokines in Aromatase Inhibitor-Induced Arthralgias: An Analysis of CCTG MA.27.
Niravath Polly,Chen Bingshu,Chapman Judy-Anne W,Agarwal Sandeep K,Welschhans Robert L,Bongartz Tim,Kalari Krishna R,Shepherd Lois E,Bartlett John,Pritchard Kathleen,Gelmon Karen,Hilsenbeck Susan G,Rimawi Mothaffar F,Osborne C Kent,Goss Paul E,Ingle James N
Clinical breast cancer
BACKGROUND:Approximately half of women taking aromatase inhibitor (AI) therapy develop AI-induced arthralgia (AIA), and many might discontinue AI therapy because of the pain. Using plasma samples from the MA.27 study, we assessed several factors potentially associated with AIA. PATIENTS AND METHODS:MA.27 is a phase III adjuvant trial comparing 2 AIs, exemestane versus anastrozole. Within an 893-participant nested case-control AIA genome-wide association study, we nested a 72 AIA case-144 control assessment of vitamin D plasma concentrations, corrected for seasonal and geographic variation. We also examined 9 baseline inflammatory cytokines: interleukin (IL)-1β, IL-6, tumor necrosis factor-α, interferon (IFN)γ, IL-10, IL-12p70, IL-17, IL-23, and chemokine ligand (CCL)-20. Finally, we analyzed the multivariate effects of baseline factors: vitamin D level, previously identified musculoskeletal single nucleotide polymorphisms, age, body mass index, and vitamin D receptor (VDR) Fok-I variant genotype on AIA development. RESULTS:Changes in vitamin D from baseline to 6 months were not significantly different between cases and controls. Elevated inflammatory cytokine levels were not associated with development of AIA. The multivariate model included no clinical factors associated with AIA. However, women with the VDR Fok-I variant genotype were more likely to have a lower IL-1β level (P = .0091) and less likely to develop AIA after 6 months of AI compared with those with the wild type VDR (P < .0001). CONCLUSION:In this nested case-control correlative study, vitamin D levels were not significantly associated with development of AIA; however, patients with the Fok-I VDR variant genotype were more likely to have a significant reduction in IL-1β level, and less likely to develop AIA.
Effects of Parecoxib on Pain Threshold and Inflammatory Factors IL-1β, IL-6 and TNF-𝜶 in Spinal Cord of Rats with Bone Cancer Pain.
Chen Jun,Cong Xiufeng,Zhan Xiuzhu,Zhou Zheng,Zheng Wei
Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
OBJECTIVE:To investigate the effects of parecoxib on pain threshold and inflammatory factors interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in spinal cord of rats with bone cancer pain. STUDY DESIGN:An experimental study. PLACE AND DURATION OF STUDY:Department of Oncology, Shengjing Hospital of China Medical University, China, from March 2017 to May 2018. METHODOLOGY:Twenty-four healthy female Sprague-Dawley rats were selected and the bone cancer pain model was inoculated with W256 breast cancer cell into the bone marrow. Rats with bone cancer pain were randomly divided into the model group and the parecoxib group on the 7th day postoperation, with 12 rats in each group. Another 12 rats were taken as the control group. Rats in the parecoxib group were given intraperitoneal injection of parecoxib (8 mg/kg) for 10 consecutive days since the 15th day after operation. Mechanical pain threshold, thermal pain threshold, and the levels of inflammatory factors IL-1β, IL-6 and TNF-α in spinal cord of rats in each group were compared. RESULTS:On the 14th postoperative day, mechanical pain threshold and thermal pain threshold of rats in the model group and the parecoxib group were significantly decreased compared with those in the control group (p<0.001). After 5 and 10 days of administration, mechanical and thermal pain threshold of rats in the parecoxib group were significantly higher than those in the model group and the control group (p<0.001). After 10 days of administration, levels of IL-1β, IL-6 and TNF-α in spinal cord of the model group were higher than those of the control group (p<0.001); and levels of IL-1β, IL-6 and TNF-α in spinal cord of the parecoxib group were significantly lower than those in the model group and the control group (p<0.001). CONCLUSION:Parecoxib can alleviate hyperalgesia in rats with bone cancer pain, increase pain threshold and inhibit the up-regulation of inflammatory factors in the spinal cord. Parecoxib may achieve analgesic effects by down-regulating the expression of IL-1β, IL-6 and TNF-α in the spinal cord.
Yoga reduces inflammatory signaling in fatigued breast cancer survivors: a randomized controlled trial.
Bower Julienne E,Greendale Gail,Crosswell Alexandra D,Garet Deborah,Sternlieb Beth,Ganz Patricia A,Irwin Michael R,Olmstead Richard,Arevalo Jesusa,Cole Steve W
BACKGROUND:Yoga is a popular mind-body therapy that has demonstrated beneficial effects on psychological, behavioral, and functional outcomes. However, few studies have investigated effects on inflammatory processes. This study tested the hypothesis that an Iyengar yoga intervention specifically designed for fatigued breast cancer survivors would lead to decreases in inflammation-related gene expression and circulating markers of proinflammatory cytokine activity. METHODS:Breast cancer survivors with persistent cancer-related fatigue were randomized to a 12-week Iyengar yoga intervention (n=16) or a 12-week health education control condition (n=15). Blood samples were collected at baseline, post-intervention, and at a 3-month follow-up for genome-wide transcriptional profiling and bioinformatic analyses. Plasma inflammatory markers and salivary cortisol were also assessed. RESULTS:In promoter-based bioinformatics analyses, the yoga group showed reduced activity of the pro-inflammatory transcription factor nuclear factor kappa B (NF-κB), increased activity of the anti-inflammatory glucocorticoid receptor, and reduced activity of cAMP response element-binding protein (CREB) family transcription factors relative to controls (all ps<.05). There was also a significant intervention effect on the soluble tumor necrosis factor receptor type II (sTNF-RII), a marker of TNF activity; plasma levels of sTNF-RII remained stable in the yoga group, whereas levels of this marker increased in the health education group (p=.028). A similar, non-significant trend was observed for the interleukin 1 receptor antagonist (p=.16). No significant changes in C reactive protein (CRP), interleukin 6 (IL-6), or diurnal cortisol measures were observed. CONCLUSIONS:A 12-week restorative Iyengar yoga intervention reduced inflammation-related gene expression in breast cancer survivors with persistent fatigue. These findings suggest that a targeted yoga program may have beneficial effects on inflammatory activity in this patient population, with potential relevance for behavioral and physical health.
The effects of exercise on mastalgia.
Genç Aysun,Çelebi Mehmet Mesut,Çelik Süleyman Utku,Atman Ebru Düşünceli,Kocaay Akın Fırat,Zergeroğlu Ali Murat,Elhan Atilla Halil,Genç Volkan
The Physician and sportsmedicine
OBJECTIVE:Mastalgia is often ignored by physicians although it is the most common breast-related complaint among women. The effectiveness of exercise therapy for mastalgia is unclear. The aim of this study is to investigate the effects of exercise on mastalgia. METHODS:A randomized controlled trial was conducted with twenty women with complaints of mastalgia fulfilling the inclusion and exclusion criteria. Patients were randomly assigned to the control group and to the exercise group. Sports brassiere, refraining from caffeine- and methylxanthine-containing foods, and simple analgesics were recommended for two groups. In the exercise group, an exercise program was conducted three times a week for 6 weeks. Participants in both groups were evaluated for breast pain and using the Short-Form Health Survey (SF-36) questionnaire before and six weeks after study. Serum cytokine levels were also collected and analyzed. RESULTS:No significant differences were detected with respect to age, body mass index, menopausal status, psychiatric condition, and existence of unexplained pain syndromes between the groups. Total breast pain scores were similar in both groups. The sensory component of breast pain questionnaire and visual analogue scale values significantly improved via exercise in only exercise group (p = 0.012 and p = 0.016). There was no significant difference between groups in serum levels of cytokines. SF-36 subscale scores for general health and social functioning significantly improved in the control group and scores for role physical, bodily pain, and social functioning improved in exercise group. CONCLUSIONS:Based on our preliminary findings, exercise treatment is beneficial for patients with mastalgia and it can be suggested by clinicians.