The comparison of hematological inflammatory parameters before and after surgery in women with endometriosis: retrospective cohort study

A total of 201 patients with endometriosis (48.9%) and 210 patients without endometriosis but with benign ovarian cysts (51.1%) were included, with the latter serving as the control group. The histopathological diagnoses of the control group included mature cystic teratoma in 86 patients (41%), benign cystic structure in 50 patients (23.6%), cystadenoma in 37 patients (17.6%), ovarian fibroma in 22 patients (10.5%), and paratubal cyst in 15 patients (7.1%). Demographic features, clinical characteristics and operation findings of the endometriosis and benign ovarian cysts groups were listed in Table  1 . Endometriosis and benign ovarian cyst groups were similar in terms of age ( p  = 0.1). While gravida and parity were higher in the benign ovarian cyst group, the nulliparity rate was lower in this group ( p  < 0.0001). History of pelvic surgery was lower in the endometriosis group, but history of endometriosis surgery was higher in this group ( p  = 0.004; p  = 0.001, respectively). Oral progesterone, oral contraceptive pills, gonadotropin releasing hormone agonist medical treatments were statistically higher in the endometriosis group ( p  = 0.001; p  = 0.003; p  = 0.02, respectively). While the presenting symptom of infertility was higher in the endometriosis group, the symptom of chronic pelvic pain was higher in the benign ovarian cyst group ( p  < 0.0001). Cyst diameter was found to be smaller in the endometriosis group ( p  = 0.005). On the other hand, the presence of bilateral cysts was higher in the endometriosis group ( p  < 0.0001). In the endometriosis group, the rate of cystectomy operation was higher, but the rate of oophorectomy operation was lower ( p  < 0.0001). The rate of hysterectomy + oophorectomy operation was higher in the benign ovarian cyst group ( p  = 0.01). Table 1 Demographic features, clinical characteristics and operation findings of the endometriosis and benign ovarian cysts groups Variables Endometriosis Benign ovarian cysts p value (n = 201, 48.9%) (n = 210, 51.1%) Age (years) 34 (19–51) 35 (18–52) 0.1 Gravida 0 (0–6) 1 (0–9) < 0.0001 Parity 0 (0–5) 1 (0–7) < 0.0001 Nulliparous 61.6% (124/201) 39.5% (83/210) < 0.0001 Menarche age (years) 11 (9–15) 11 (9–14) 0.9 History of pelvic surgery 23.3% (47/201) 35.8% (75/210) 0.004 History of endometriosis surgery 9.9% (20/201) 1.9% (4/210) 0.001 Medical treatment < 0.0001  None 81.5% (164/201) 97.1% (204/210) < 0.0001  Oral progesterone 9% (18/201) 1.4% (3/210) 0.001  OCP † 6.5% (13/201) 1% (2/210) 0.003  LNG IUD ‡ 0.5% (1/201) 0.5% (1/210) 0.9  GnRH agonist § 2.5% (5/201) 0% (0/210) 0.02 Symptoms < 0.0001  Infertility 20.8% (42/201) 4.8% (10/210) < 0.0001  Chronic pelvic pain 70.1% (141/201) 86.7% (182/210) < 0.0001  Abnormal uterine bleeding 9% (18/201) 8.5% (18/210) 0.8 Cyst diamater (centimeter) 5 (2–15) 5.5 (2–30) 0.005 Presence of bilateral cysts 33.3% (67/201) 12.3% (26/210) < 0.0001 Type of surgery < 0.0001  Cystectomy 83.5% (168/201) 61% (128/210) < 0.0001  Oophorectomy 7% (14/201) 21% (44/210) < 0.0001  Hysterectomy + oophorectomy 9.5% (19/201) 18% (38/210) 0.01 †OCP: Oral contraceptive pills; ‡LNG IUD: Levonorgestrel-releasing intrauterine device; §GnRH: Gonadotropin releasing hormone Demographic features, clinical characteristics and operation findings of the endometriosis and benign ovarian cysts groups †OCP: Oral contraceptive pills; ‡LNG IUD: Levonorgestrel-releasing intrauterine device; §GnRH: Gonadotropin releasing hormone Demographic features, clinical characteristics and operational findings of the subgroups were shown in Table  2 . These subgroups were categorized and compared as stage 1–2 endometriosis ( n  = 26, 6.3%), stage 3–4 endometriosis ( n  = 175, 42.6%) and benign ovarian cysts ( n  = 210, 51.1%). The gravida and parity of the benign ovarian cysts group were higher than the stage 3–4 endometriosis group ( p  < 0.0001). Nulliparity was 62.8% in the stage 3–4 endometriosis group and this rate was higher than other groups ( p  < 0.0001). The highest rate was detected in the history of endometriosis surgery stage 3–4 endometriosis group ( p  < 0.0001). Oral progesterone, oral contraceptive pills, and gonadotropin-releasing hormone agonist medical treatments were statistically higher in the stage 3–4 endometriosis group ( p  < 0.0001; p  = 0.09; p  = 0.03). Levonorgestrel-releasing intrauterine device treatment was at the highest rate in the stage 1–2 endometriosis group ( p  = 0.03). While the presenting symptom of infertility (22.9%) was highest in the stage 3–4 endometriosis group, chronic pelvic pain (86.7%) was the most common presenting symptom in the benign ovarian cyst group ( p  < 0.0001). Cyst diameter was found to be 3 cm in the stage 1–2 endometriosis group, 6 cm in the stage 3–4 endometriosis group, and 5.5 cm in the benign ovarian cysts group. The groups differed statistically from each other ( p  < 0.0001). Presence of bilateral cysts was highest in the stage 3–4 endometriosis group (37.7%; p  < 0.0001). Cystectomy operation was performed at a rate of 84.6% in the stage 3–4 endometriosis group, oophorectomy operation was performed at a rate of 21% in the benign ovarian cysts group, and hysterectomy + oophorectomy operation was performed at a rate of 19.2% in the stage 1–2 endometriosis group ( p  < 0.0001; p  < 0.0001; p  = 0.01). Table 2 Demographic features, clinical characteristics and operation findings of the subgroups Variables Stage 1–2 Endometriosis Stage 3–4 Endometriosis Benign ovarian cysts p value (n = 26, 6.3%) (n = 175, 42.6%) (n = 51.1%, 210) Age (years) 33.5 (20–51) 34 (19–49) 35 (18–52) 0.2 Gravida 1 (0–3) 0 (0–6) 1 (0–9) < 0.0001* Parity 0.5 (0–2) 0 (0–5) 1 (0–7) < 0.0001* Nulliparous 53.8% (14/26) 62.8% (110/175) 39.5% (83/210) < 0.0001 Menarche age (years) 11 (9–15) 11 (9–14) 11 (9–14) 0.9 History of pelvic surgery 26.9% (7/26) 22.8% (40/175) 35.7% (75/210) 0.02 History of endometriosis surgery 0% (0/26) 11.4% (20/175) 1.9% (4/210) < 0.0001 Medical treatment < 0.0001  None 92.4% (24/26) 80% (140/175) 97.1% (204/210) < 0.0001  Oral progesterone 0% (0/26) 10.2% (18/175) 1.4% (3/210) < 0.0001  OCP † 3.8% (1/26) 6.9% (12/175) 1% (2/210) 0.009  LNG IUD ‡ 3.8% (1/26) 0% (0/175) 0.5% (1/210) 0.03  GnRH agonist § 0% (0/26) 2.9% (5/175) 0% (0/210) 0.03 Symptoms < 0.0001  Infertility 7.7% (2/26) 22.9% (40/175) 4.8% (10/210) < 0.0001  Chronic pelvic pain 76.9% (20/26) 69.1% (121/175) 86.7% (182/210) < 0.0001  Abnormal uterine bleeding 15.4 (4/26) 8% (14/175) 8.5% (18/210) 0.4 Cyst diamater 3 (2–5) 6 (2–15) 5.5 (2–30) < 0.0001** Presence of bilateral cysts 3.8% (1/26) 37.7% (66/175) 12.3% (26/210) < 0.0001 Type of surgery < 0.0001  Cystectomy 77% (20/26) 84.6% (148/175) 61% (128/210) < 0.0001  Oophorectomy 3.8% (1/26) 7.4% (13/175) 21% (44/210) < 0.0001  Hysterectomy + oophorectomy 19.2% (5/26) 8% (14/175) 18% (38/210) 0.01 *Significance between Stage 3–4 Endometriosis group and Benign ovarian cysts group ** Significance between the each groups † OCP: Oral contraceptive pills; ‡ LNG IUD: Levonorgestrel-releasing intrauterine device; § GnRH: Gonadotropin releasing hormone Demographic features, clinical characteristics and operation findings of the subgroups *Significance between Stage 3–4 Endometriosis group and Benign ovarian cysts group ** Significance between the each groups † OCP: Oral contraceptive pills; ‡ LNG IUD: Levonorgestrel-releasing intrauterine device; § GnRH: Gonadotropin releasing hormone The comparison of laboratory findings of endometriosis and benign ovarian cysts groups were listed in Table  3 . Preoperative and postoperative values of the groups were similar in terms of leukocyte (WBC) ( p  = 0.8; p  = 0.2, respectively). Postoperative WBC values of both the endometriosis group and the benign ovarian cysts group were found to be higher compared to the preoperative period (7.8 vs. 8.4, p  < 0.0001; 7.9 vs. 9, p  < 0.0001, respectively). Red cell distribution width (RDW) was higher in the endometriosis group in the preoperative and postoperative periods (14.4 vs. 13.9, p  = 0.008; 14.3 vs. 14.1, p  = 0.03, respectively). Preoperative NLR was higher in the endometriosis group (2.3 vs. 2.1). However, this difference is not statistically significant ( p  = 0.08). The postoperative NLR values of both groups were higher compared to the preoperative period (2.3 vs. 3.5, p  < 0.0001; 2.1 vs. 3.7, p  < 0.0001, respectively). The postoperative MLR was found to be higher in the endometriosis group (0.3 vs. 0.2, p  = 0.0006). In the postoperative period, the MLR value of both groups was higher than the preoperative period ( p  < 0.0001; p  = 0.007, respectively). Preoperative PLR was higher in the endometriosis group (153 vs. 135.8, p  = 0.002). Postoperative PLR of both groups were higher than preoperative PLR (153 vs. 160, p  = 0.003; 135.8 vs. 150.1, p  < 0.0001; respectively). Preoperative and postoperative CA-125 were higher in the endometriosis group (43.3 vs. 15, p  < 0.0001; 21.5 vs. 14.5, p  < 0.0001; respectively). Postoperative values were lower in both the endometriosis and benign ovarian cysts groups (43.3 vs. 21.5, p  < 0.0001; 15 vs. 14.5, p  < 0.0001; respectively). Table 3 Comparison of laboratory findings of endometriosis and benign ovarian cysts groups Variables Endometriosis Benign ovarian cysts p value** (n = 201, 48.9%) (n = 210, 51.1%) Hemoglobin (g/dL) Preoperative 12.2 (11.1–13.1; 2) [7.6–15.1] 12.6 (11.6–13.3; 1.7) [7.2–15.1] 0.01 Postoperative 11.7 (10-3-12.8; 2.45) [7.1–15] 12 (10.8–12.9;2.1) [7.1–14.8] 0.08 p value* < 0.0001 < 0.0001 Platelet (10 3 / µl) Preoperative 291 (248-337.5; 89.5) [114–509] 285.5 (235–328; 93) [105–569] 0.1 Postoperative 259 (219.5–307; 87.5) [122–706] 253 (204.2-311.2; 107) [101–500] 0.6 p value* < 0.0001 < 0.0001 Leukocyte (WBC) (10 3 / µl) Preoperative 7.8 (6.6–9.1; 2.5) [3.9–14.6] 7.9 (6.4–9.4; 3) [4.2–14.7] 0.8 Postoperative 8.4 (7-11.4; 4.4) [3.4–16.4] 9 (7.2–12; 4.8) [4-16.4] 0.2 p value* < 0.0001 < 0.0001 Neutrophil (10 3 / µl) Preoperative 4.8 (3.8–6.2; 2.4) [1.7–10.9] 4.8 (3.7–6.2; 2.5) [1.8–10.9] 0.7 Postoperative 6 (4.4–9.3; 4.9) [1.9–18.7] 6.4 (4.4–9.9; 5.5) [1.3–18.5] 0.4 p value* < 0.0001 < 0.0001 Monocyte (10 3 / µl) Preoperative 0.5 (0.4–0.6; 0.2) [0.1-1] 0.5 (0.4–0.7; 0.3) [0.1–1.3] 0.4 Postoperative 0.5 (0.4–0.7; 0.3) [0.1–1.7] 0.5 (0.4–0.7; 0.3) [0.1–1.6] 0.2 p value* 0.2 0.1 Lymphocyte (10 3 / µl) Preoperative 2 (1.6–2.5; 0.9) [0.3–3.9] 2.1 (1.7–2.5; 0.8) [0.6–5.4] 0.05 Postoperative 1.6 (1.1–2.2; 1.1) [0.3-4] 1.8 (1.1–2.3; 1.2) [0.4–5.6] 0.1 p value* < 0.0001 < 0.0001 Mean platelet volume (MPV) (fL) Preoperative 8.7 (8.1–9.3; 1.2) [6.7–12.6] 8.6 (8.1–9.3; 1.2) [6.2–13] 0.4 Postoperative 8.8 (8.2–9.5; 1.3) [7-12.6] 8.7 (8.1–9.3; 1.2) [6.7–11.8] 0.2 p value* 0.1 0.2 Red cell distribution width (RDW) (%) Preoperative 14.4 (13.6–16; 2.4) [12-20.5] 13.9 (13.2–15.4; 2.2) [12-20.8] 0.008 Postoperative 14.3 (13.6–15.9; 2.3) [12.3–20.9] 14.1 (13.3–15.3; 2) [12-20.5] 0.03 p value* 0.1 0.6 Neutrophil to Lymphocyte Ratio (NLR) Preoperative 2.3 (1.7–3.4; 1.7) [0.5–24.3] 2.1 (1.6-3; 1.4) [0.7–15] 0.08 Postoperative 3.5 (2.2–8.2; 6) [0.6–25.8] 3.7 (1.9-8; 6.1) [0.4–36.2] 0.8 p value* < 0.0001 < 0.0001 Monocyte to Lymphocyte Ratio (MLR) Preoperative 0.2 (0.2–0.3; 0.1) [0.03–2.6] 0.2 (0.2–0.3; 0.1) [0.09–1.3] 0.4 Postoperative 0.3 (0.2–0.4; 0.2) [0.08–1.3] 0.2 (0.2–0.4; 0.2) [0.07–1.45] 0.006 p value* < 0.0001 0.007 Platelet to Lymphocyte Ratio (PLR) Preoperative 153 (115.1-190.8; 75.7) [60–750] 135.8 (105.2-166.2; 61) [46-423.7] 0.002 Postoperative 160 (115.5- 236.6; 121.1) [64.7–692] 150.1 (110.9–202; 91.1) [47.8–665] 0.1 p value* 0.003 < 0.0001 CA-125 (u/ml) Preoperative 43.3 (22.2–67; 44.8) [2.8–540] 15 (9.3–28.5; 19.2) [2.3–383] < 0.0001 Postoperative 21.5 (15.6–34.4; 18.8) [2.2-120.6] 14.5 (9.8–20.5; 10.7) [4.4–105] < 0.0001 p value* < 0.0001 < 0.0001 p * value: Wilcoxon signed-rank test (Values are presented as medain (Q1-Q3; interquartile range (IQR)), and [minimum-maximum]); p ** value: Mann whitney u test Comparison of laboratory findings of endometriosis and benign ovarian cysts groups p * value: Wilcoxon signed-rank test (Values are presented as medain (Q1-Q3; interquartile range (IQR)), and [minimum-maximum]); p ** value: Mann whitney u test Table  4 shows comparison of laboratory findings of the subgroups. Postoperative WBC values of each group were higher compared to the preoperative period ( p  = 0.08; p  < 0.0001; p  < 0.0001, respectively). Postoperative NLR values increased in all three groups compared to the preoperative period (2.2 vs. 4.4, p  = 0.001; 2.4 vs. 3.4, p  < 0.0001; 2.1 vs. 3.7, p  < 0.0001, respectively). In stage 3–4 endometriosis and benign ovarian cyst groups, the MLR values in the postoperative period were statistically higher than the preoperative period ( p  < 0.0001; p  = 0.007). PLR values increased in all three groups in the postoperative period (152.9 vs. 172.9, p  = 0.007; 153 vs. 160, p  = 0.02; 135.8 vs. 150.1, p  < 0.0001, respectively). Preoperative and postoperative CA-125 were statistically different between the stage 3–4 Endometriosis group and the benign ovarian cysts group (46.4 vs. 15, p  < 0.0001; 24.4 vs. 14.5, p  < 0.0001, respectively). Compared to the preoperative period, the CA-125 value of the stage 3–4 endometriosis group was statistically significantly lower in the postoperative period. When the postoperative period was compared with the preoperative period, CA-125 values of stage 3–4 endometriosis and benign ovarian cyst groups showed a statistically significant decrease (46.4 vs. 24.4, p  < 0.0001; 15 vs. 14.5, p  < 0.0001, respectively). Table 4 Comparison of laboratory findings of the subgroups Variables Stage 1–2 Endometriosis Stage 3–4 Endometriosis Benign ovarian cysts p value** (n = 26, 6.3%) (n = 175, 42.6%) (n = 51.1%, 210) Hemoglobin (g/dL) Preoperative 12.3 (11.1–13.2; 2.2) [9.2–14.3] 12.2 (11.2–13.2; 2) [7.6–15.1] 12.6 (11.6–13.3; 1.7) [7.2–15.1] 0.04** Postoperative 12.4 (10-12.8; 2.8) [7.9–13.9] 11.6 (10.3–12.7; 2.4) [7.1–15] 12 (10.8–12.9;2.1) [7.1–14.8] 0.2 p value* 0.01 < 0.0001 < 0.0001 Platelet Preoperative 295 (213.5–355; 141.5) [144–388] 291 (249–337; 88) [114–509] 285.5 (235–328; 93) [105–569] 0.1 (10 3 / µl) Postoperative 258.5 (201.2-311.7; 110.5) [122–363] 259 (221–307; 86) [142–706] 253 (204.2-311.2; 107) [101–500] 0.6 p value* < 0.0001 < 0.0001 < 0.0001 Leukocyte (WBC) Preoperative 7.3 (5.8–9.1; 3.3) [4.4–13.4] 7.9 (6.6–9.2; 2.6) [3.9–14.6] 7.9 (6.4–9.4; 3) [4.2–14.7] 0.8 (10 3 / µl) Postoperative 8.6 (6.8–11; 4.2) [4.3–16.9] 8.4 (7-11.4; 4.4) [3.4–16.8] 9 (7.2–12; 4.8) [4-16.4] 0.2 p value* 0.08 < 0.0001 < 0.0001 Neutrophil (10 3 / µl) Preoperative 4.7 (3.3–5.3; 2) [2.5–10.6] 4.8 (4-6.3; 2.3) [1.7–10.9] 4.8 (3.7–6.2; 2.5) [1.8–10.9] 0.7 Postoperative 6.5 (4.7–9.8; 5.1) [2.1–18.7] 5.9 (4.3–9.2; 4.9) [1.9–16.7] 6.4 (4.4–9.9; 5.5) [1.3–18.5] 0.4 p value* 0.02 < 0.0001 < 0.0001 Monocyte (10 3 / µl) Preoperative 0.5 (0.4–0.7; 0.3) [0.3-1] 0.5 (0.4–0.6; 0.2) [0.1-1] 0.5 (0.4–0.7; 0.3) [0.1–1.3] 0.4 Postoperative 0.5 (0.3–0.6; 0.3) [0.1–1.1] 0.5 (0.4–0.7; 0.3) [0.1–1.7] 0.5 (0.4–0.7; 0.3) [0.1–1.6] 0.2 p value* 0.08 0.09 0.1 Lymphocyte (10 3 / µl) Preoperative 2.1 (1.6–2.3; 0.7) [0.3–3.3] 2 (1.6–2.5; 0.9) [0.5–3.9] 2.1 (1.7–2.5; 0.8) [0.6–5.4] 0.05 Postoperative 1.4 (1-1.8; 0.8) [0.3–2.9] 1.7 (1.2–2.3; 1.1) [0.4-4] 1.8 (1.1–2.3; 1.2) [0.4–5.6] 0.1 p value* < 0.0001 < 0.0001 < 0.0001 Mean platelet volume Preoperative 8.7 (8–9; 1) [7.4–11.5] 8.7 (8.1–9.4; 1.3) [6.7–12.6] 8.6 (8.1–9.3; 1.2) [6.2–13] 0.4 (MPV) (fL) Postoperative 8.9 (8-9.6; 1.6) [7.3–11.4] 8.8 (8.2–9.4; 1.2) [7-12.6] 8.7 (8.1–9.3; 1.2) [6.7–11.8] 0.2 p value* 0.3 0.2 0.2 Red cell distribution width Preoperative 14.4 (13.5–15.9; 2.4) [12.2–19.5] 14.5 (13.7–16.2; 2.5) [12-20.5] 13.9 (13.2–15.4; 2.2) [12-20.8] 0.09** (RDW) (%) Postoperative 14.6 (13.8–15.9; 2.1) [12.5–17.1] 14.2 (13.6–15.9; 2.3) [12.3–20.9] 14.1 (13.3–15.3; 2) [12-20.5] 0.03* p value* 0.1 0.3 0.6 Neutrophil to Lymphocyte Preoperative 2.2 (1.6–2.6; 1) [1.2–24.3] 2.4 (1.8–3.5; 1.7) [0.5–22] 2.1 (1.6-3; 1.4) [0.7–15] 0.08 Ratio (NLR) Postoperative 4.4 (2.8–9.6; 6.8) [1.5–21.6] 3.4 (2.2-8; 5.8) [0.6–25.8] 3.7 (1.9-8; 6.1) [0.4–36.2] 0.8 p value* 0.001 < 0.0001 < 0.0001 Monocyte to Lymphocyte Preoperative 0.2 (0.2–0.3; 0.1) [0.1–2.6] 0.2 (0.2–0.3; 0.1) [0.03–1.2] 0.2 (0.2–0.3; 0.1) [0.09–1.3] 0.4 Ratio (MLR) Postoperative 0.3 (0.2–0.4; 0.2) [0.09–1.3] 0.3 (0.2–0.4; 0.2) [0.08–1.3] 0.2 (0.2–0.4; 0.2) [0.07–1.45] 0.02** p value* 0.1 < 0.0001 0.007 Platelet to Lymphocyte Preoperative 152.9 (109.5-172.6; 63.1) [60–750] 153 (116.3-195.8; 79.5) [60.6–584] 135.8 (105.2-166.2; 61) [46-423.7] < 0.008* Ratio (PLR) Postoperative 172.9 (122.6-257.3; 134.7) [87.1-633.3] 160 (113.8-234.6; 120.8) [64.7–692] 150.1 (110.9–202; 91.1) [47.8–665] 0.1 p value* 0.007 0.02 < 0.0001 CA-125 (u/ml) Preoperative 15.1 (8.2–28.8; 20.6) [3.5–285] 46.4 (27-69.7; 42.7) [2.8–540] 15 (9.3–28.5; 19.2) [2.3–383] < 0.0001* Postoperative 15.8 (8.7–20.6; 11.9) [6.4-120.6] 24.4 (16.4–35.4; 19) [2.2–110] 14.5 (9.8–20.5; 10.7) [4.4–105] < 0.0001* p value* 0.2 < 0.0001 < 0.0001 p * value: Wilcoxon signed-rank test p * value: Wilcoxon signed-rank test (Values are presented as medain (Q1-Q3; interquartile range (IQR)), and [minimum-maximum]); p ** value: Kruskal wallis test; *Significance between Stage 3–4 Endometriosis group and Benign ovarian cysts group.; ** Significance between the each groups Comparison of laboratory findings of the subgroups p * value: Wilcoxon signed-rank test p * value: Wilcoxon signed-rank test (Values are presented as medain (Q1-Q3; interquartile range (IQR)), and [minimum-maximum]); p ** value: Kruskal wallis test; *Significance between Stage 3–4 Endometriosis group and Benign ovarian cysts group.; ** Significance between the each groups The clinical diagnostic sensitivity and specificity predicting endometriosis for each of the preoperative variable measurements were shown in Table  5 ; Figs.  1 and 2 . RDW > 13.5 was determined as the cut-off value to predict endometriosis (sensitivity 77.1%; specificity 36.5%, p  = 0.008). PLR > 123.4 was determined as the cut-off value to predict endometriosis (sensitivity 71.6%; specificity 40%, p  = 0.002). CA-125 > 35 was determined as the cut-off value to predict endometriosis (sensitivity 62.2%; specificity 84.8%, p  < 0.0001). Table 5 Clinical diagnostic sensitivity and specificity predicting endometriosis for each of the preoperative variable measurements Variables AUC (95% CI) Sensitivity (%) Specificity (%) Cut off value p value Mean platelet volume 0.523 (0.467–0.579) 54.70% 53.80% 8.65 0.4 (MPV) (fL) Red cell distribution width 0.576 (0.521–0.631) 77.10% 36.70% 13.5 0.008 (RDW) (%) Neutrophil to Lymphocyte 0.550 (0.494–0.605) 71.60% 41.40% 1.89 0.08 Ratio (NLR) Monocyte to Lymphocyte 0.524 (0.468–0.580) 71.60% 35.70% 0.2 0.4 Ratio (MLR) Platelet to Lymphocyte 0.586 (0.531–0.641) 71.60% 40% 123.4 0.002 Ratio (PLR) Ca-125 (u/ml) 0.774 (0.728–0.820) 62.20% 84.80% 35 < 0.0001 Clinical diagnostic sensitivity and specificity predicting endometriosis for each of the preoperative variable measurements Fig. 1 Receiver operating characteristic curves of preoperative variables in diagnosing endometriosis Receiver operating characteristic curves of preoperative variables in diagnosing endometriosis Fig. 2 STARD diagram to report participants’ flow by preoperative variables throughout the study STARD diagram to report participants’ flow by preoperative variables throughout the study

This was a retrospective cohort study conducted at a tertiary center. Informed consent was obtained from all individual participants included in this study. The study was performed in line with principles of Declaration of Helsinki. Institutional ethics committee approval was provided (File number:8659-GOA, Registration number: 2024/04–16). Data were collected from 411 patients who underwent laparoscopic surgery between January 2018 and December 2023. Postoperatively, the pathology reports indicated ovarian endometrioma in 201 patients (48.9%) and other benign ovarian cysts in 210 patients (51.1%). Patients with histopathologically confirmed ovarian endometrioma comprised the endometriosis group, while the control group consisted of patients who underwent laparoscopic surgery during the same period for benign ovarian cysts other than endometrioma, such as serous, mucinous, or dermoid cysts. In cases of ovarian endometrioma accompanied by superficial or deep endometriosis, appropriate surgical procedures were performed concominantly. Endometriosis was staged according to the revised American Society for Reproductive Medicine (ASRM) Stages I-IV [ 8 ]. Inclusion criteria were: patients aged 18 to 55 years; presence of a sonographically identified adnexal mass and histopathological confirmation of ovarian endometrioma or benign ovarian cyst. Exclusion criteria were: postmenopausal women; presence of pelvic inflammatory disease; uterine fibroids or adenomyosis; malignancy; endometrial polyps or hyperplasia; systemic inflammatory or autoimmune disease; active infection; recurrence of endometrioma by postoperative week 6, and current smoking. Endometrioma and benign ovarian cysts diameters were measured by taking the mean of the largest horizontal and vertical components. The endometrioma and benign ovarian cysts size was recorded in centimeters. Demographic characteristics, clinical features, laboratory findings and operation findings of the endometriosis and benign ovarian cyst groups were obtained from the hospital data recording system. Laboratory findings were evaluated in our clinic one week before the operation and six weeks after the operation. The six-week postoperative timepoint was selected because it corresponds to the routine clinical follow-up period after gynecologic surgery and is considered sufficient for the resolution of acute inflammatory responses. The hematologic inflammatory markers evaluated in this study included the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-lymphocyte ratio (MLR), which were calculated from the complete blood count data. Hematological inflammatory markers for endometriosis were examined, considering the variations of these biomarkers throughout the menstrual cycle The medical treatment conditions of the patients one year before the operation were evaluated. Preoperative ultrasound findings were evaluated within one week before surgery. The mentioned preoperative evaluation and postoperative follow-up process was carried out routinely in our clinic. Statistical analysis was performed by SPSS version 26.0 (IBM Inc., Chicago, IL, USA). The normality of the distribution was evaluated with Kolmogorov-Smirnov test. Not normally distributed parameters were analyzed with the Kruskal Wallis, post hoc and Mann-Whitney U tests. Wilcoxon signed-rank test was used to determine changes before and after treatment. Chi-square test and Fisher precision test were used in the analysis of categorical data. Quantitative data were presented as median (minimum-maximum), and qualitative data were presented as numbers and percentages (%). Receiver operating characteristic (ROC) analysis was performed to calculate the area under the curve (AUC), which indicates the average sensitivity of variables and its 95% confidence interval (CIs) are reported for each assessed parameter. The appropriate cut-off value indicating the sum of the highest sensitivity and specificity was calculated for the most predictive variable. The p value considered statistically significant was < 0.05.

Endometriosis is a prevalent condition affecting 5–10% of women of reproductive age. It manifests with a wide spectrum of symptoms, from infertility to pelvic pain [ 1 , 2 ]. The precise pathophysiology of endometriosis remains unclear; nevertheless, it is widely accepted that endometriosis is a multifactorial disorder, with chronic inflammation being fundamental to its pathogenesis [ 3 , 4 ]. Inflammatory mediators, particularly cytokines such as TNF-α, are important factors in the onset of endometriosis [ 5 , 6 ]. Inflammatory factors are thought to be implicated in the pathogenesis of endometriosis. Although a systematic review and meta-analysis reported no relationship between hematological inflammatory parameters and the stage of endometriosis, it was emphasized that these results should be interpreted with caution due to the limited number of included studies [ 7 ]. Additionally, there are no studies in the literature comparing hematological inflammatory parameters before and after endometriosis treatment [ 7 ]. In this study, we hypothesized that hematologic inflammatory markers would decrease in the postoperative period following surgical excision of endometriotic lesions. This expectation was based on the assumption that surgical removal of ectopic endometrial tissue would reduce the chronic inflammatory stimulus associated with endometriosis. Since elevated levels of these ratios are thought to reflect ongoing systemic inflammation and immune activation, we anticipated that eliminating the underlying pathology would result in a measurable decline in inflammatory indices. However, given the potential for a transient postoperative inflammatory response related to surgical healing, we also acknowledged the possibility of temporary increases in some parameters during early follow-up. Therefore, our aim was to compare preoperative and postoperative hematological inflammatory parameters in women with endometriosis.

In conclusion, during the follow-ups, we revealed that CA-125 still maintains its effectiveness. There is a lack of existing literature that directly compares hematological inflammatory parameters before and after treatment for endometriosis. We anticipate that our investigation will fill this gap by assessing the short-term outcomes of patients under our follow-up.

Endometriosis is linked to heightened inflammatory activity and a higher prevalence of autoimmune inflammatory diseases, asthma, and allergies [ 9 ]. Research has demonstrated that the peritoneal microenvironment in women with endometriosis is characterized by elevated levels of inflammatory cytokines, chemokines, and prostaglandins, which may significantly contribute to the development of the disease [ 10 ]. Our study differs from previous research by longitudinally evaluating hematological inflammatory markers both before and after surgical treatment for endometriosis. While numerous studies have assessed NLR, PLR, and other markers cross-sectionally, our cohort provides the first direct comparison of pre- and postoperative values within the same patients. This design allows a unique insight into the short-term inflammatory dynamics following surgical intervention and highlights potential limitations of single time-point biomarker assessments in endometriosis. Studies have indicated that the levels of certain WBC subtypes vary in the endometrial tissue, peripheral blood, and peritoneal fluid of women with endometriosis. In these patients, an elevated WBC, especially macrophages, is linked to subclinical peritoneal inflammation [ 11 , 12 ]. Tokmak et al. and Moini et al. have observed alterations in WBC counts among endometriosis patients, specifically an increase in neutrophils and a decrease in lymphocytes, which confirmed the presence of a chronic inflammatory state [ 13 , 14 ]. Conversely, another study reported no significant differences in lymphocyte and neutrophil counts or the NLR between endometriosis patients, women with ovarian cysts, and healthy controls [ 15 ]. In a recently meta-analysis, it was reported that patients with endometriosis exhibited higher levels of NLR compared to individuals with other benign tumors [ 7 ]. Additionally, NLR level of patients with stage 3 and 4 endometriosis was not different from that of patients with stage 1 and 2 endometriosis [ 7 ]. In our study, no differences in preoperative WBC were observed when comparing endometriosis patients to those with benign ovarian cysts, nor within our subgroup analysis. The NLR in the Stage 3–4 endometriosis group was observed to be higher compared to the other groups; however, this difference was consistent across all groups. Although the endometriosis group exhibited a higher NLR value than the benign ovarian cyst group, this distinction did not reach statistical significance. The cut-off values of NLR determined to predict endometriosis vary in terms of sensitivity and specificity in the literature [ 14 , 16 , 17 ]. In our study, the cut-off value of NLR was found to be 1.89, with a sensitivity of 71.6% and a specificity of 41.4%. Other markers indicative of systemic chronic inflammation include the MLR and the PLR [ 18 , 19 ]. Various studies have evaluated the predictive power of these markers, but they have produced conflicting results [ 14 , 15 , 17 ]. In our study, MLR did not differ between groups in either the main group comparison or the subgroup comparison. PLR was higher in the endometriosis group compared with the benign ovarian cyst group. In subgroup analysis, it was highest in the stage 3–4 endometriosis group. In our study, the cut-off value of MLR was found to be 0.2, with a sensitivity of 71.6% and a specificity of 35.7%. Moreover, the cut-off value of PLR was found to be statistically significant at 123.4, with a sensitivity of 71.6% and a specificity of 40%. Recently, Mean platelet volume (MPV) has been increasingly utilized as a marker of chronic inflammation [ 20 ]. RDW, also assessed in blood counts, indicates the variability in red blood cell size and has traditionally been used for the differential diagnosis of anemia [ 21 ]. However, RDW has more recently been identified as a marker related to inflammation and has been proposed to play a role in predicting mortality in diseases associated with inflammation [ 21 ]. In Moini et al.‘s study, the MPV value was found to be statistically higher in the endometriosis group. The cut-off value of MPV predicting endometriosis was 9.2, with a sensitivity of 71% and a specificity of 60%. In another study, MPV and RDW values did not show any significant difference in the endometriosis group. In our main group and subgroup comparisons, the groups were similar in terms of MPV. Additionally, the cut-off value of MPV in predicting endometriosis was 8.65, with a sensitivity of 54.7% and a specificity of 53.8%. When the main groups were compared, the median RDW of endometriosis group showed a statistically significant difference from the benign cyst group. Furthermore, upon examination of the subgroups, it was observed that the stage 3–4 endometriosis group exhibited a statistically significant difference in RDW compared to the benign cyst group. The cut-off value of RDW in predicting endometriosis was 13.5, with a sensitivity of 77.1% and a specificity of 36.7%. In line with our findings, recent research by Guney et al. demonstrated that serum levels of neutrophil gelatinase-associated lipocalin (NGAL), an acute-phase protein associated with inflammation and tissue remodeling, were significantly elevated in patients with ovarian endometrioma compared to those with other benign ovarian cysts [ 22 ]. Their study also confirmed increased NGAL expression in endometrioma tissue samples through immunohistochemical analysis, supporting the role of NGAL in the inflammatory microenvironment of endometriosis. These results reinforce the growing body of evidence that systemic and local inflammatory markers — including NGAL, CA-125, NLR, and PLR — may be integrated to improve the noninvasive diagnosis of endometriosis. Further large-scale, prospective studies are warranted to evaluate the diagnostic value of NGAL alongside established hematologic indices and to determine its potential utility in clinical practice. Supporting this, Kaya et al. investigated the predictive role of serum caspase-3 levels and found that they were significantly higher in patients with advanced-stage endometriosis [ 23 ]. In their study, caspase-3 showed high diagnostic performance (AUC: 0.93, sensitivity: 90%, specificity: 87%) for distinguishing stage 3–4 from stage 1–2 disease. These findings suggest that apoptosis-related biomarkers, such as caspase-3, may complement hematological inflammatory indices in predicting disease severity and may help refine noninvasive stratification of patients with suspected endometriosis. The association between endometriosis and high serum CA-125 levels was discovered a long time ago [ 24 ]. Studies have shown that serum CA-125 increases, especially in patients with advanced endometriosis [ 25 , 26 ]. A recent meta-analysis indicated that CA-125 is effective as a rule-in test when a blood level of ≥ 30 u/ml is used as the cutoff value [ 27 ]. However, a CA-125 level < 30 u/ml, which resulted in 49% of women with endometriosis testing negative, could not exclude the presence of endometriosis [ 27 ]. Recent findings by Oliveira et al. corroborated the diagnostic significance of CA-125, reinforcing evidence from earlier research [ 28 ]. In our study, the CA-125 values were found to be statistically higher in the endometriosis group during the primary group comparison, and specifically in cases of advanced endometriosis during the subgroup analysis. The statistically significant cut-off value predicting endometriosis was 35 u/ml with 62.2% sensitivity and 84.8% specificity. However, it is important to note that elevated CA-125 levels are not specific to endometriosis. CA-125 may also increase in various benign and malignant conditions, including pelvic inflammatory disease, uterine fibroids, adenomyosis, liver cirrhosis, menstruation, and even pregnancy. One notable example is the study by Kaya et al., which reported markedly elevated CA-125 and CA 19 − 9 levels in a patient with a transverse vaginal septum — a benign congenital anomaly [ 29 ]. These findings underscore the necessity of interpreting CA-125 levels in the appropriate clinical context and ideally in combination with other clinical, radiological, or serological findings. When comparing the postoperative laboratory values of both the endometriosis group and the benign ovarian cyst group with their respective preoperative values, a statistically significant increase was observed in the NLR, MLR, and PLR values during the postoperative period. On the other hand, postoperative CA-125 values showed a significant decrease. In the subgroup analysis, postoperative MLR, NLR and PLR values, except for the MLR value of stages 1–2, were increasing statistically. CA-125 value of stages 1–2 in the postoperative period was similar to the preoperative period. However, CA-125 values of stage 3–4 and benign ovarian cyst groups showed a statistically significant decrease. Especially the decreases in CA-125 values were in line with the literature. However, the observed increase in other inflammatory markers was unexpected. We hypothesize that there were two reasons for this observation. Firstly, it was possible that the healing/inflammatory process persists during the sixth postoperative week, and a regression in these markers may occur during a longer follow-up period. Secondly, a comprehensive theory explaining the origin of endometriosis has remained elusive, with multiple theories emerging to explain the diverse observations regarding its pathogenesis. These theories generally fall into two categories: those suggesting that implants originate from uterine endometrium and those proposing origins from tissues outside the uterus. These theories incorporate inciting factors and genetic susceptibilities, the roles of which are being progressively elucidated, although not yet sufficiently established to confirm causality and subsequent development of endometriosis. For instance, reports linking endocrine-disrupting chemicals with endometriosis suggest their involvement, alongside endogenous/exogenous estrogens, as potential factors in the pathogenesis of endometriosis. The developmental timing of action of such agents, as well as their influence on other systems predisposing to endometriosis (endocrine, immune, stem/progenitor cells, epigenetic modifications), must be considered in the context of genetic background and stimulus-driven reprogramming of the female reproductive tract. Although the observed changes in NLR, PLR, and MLR were statistically significant in the postoperative period, their clinical significance warrants careful interpretation. There is currently no universally accepted threshold that defines a clinically meaningful change in these hematologic indices in the context of endometriosis. In our study, while the median increase in NLR and PLR was modest, the trend was consistent across all subgroups, suggesting a systemic inflammatory response potentially related to postoperative healing. However, these fluctuations did not correspond with clinical deterioration or postoperative complications. Therefore, the clinical utility of such short-term changes should be evaluated in longitudinal studies with longer follow-up and correlation to symptom resolution or recurrence risk. We acknowledge this as a limitation and propose that future prospective research should establish clinically meaningful cut-off points and minimal clinically important differences for these parameters. Notably, WBC, lymphocyte, and platelet counts did not show significant variation between the preoperative and postoperative periods. This observation implies that the changes in NLR, PLR, and MLR may be due to alterations in the proportions of leukocyte subtypes rather than total cell count elevation. This supports the hypothesis that the postoperative inflammatory response may be subtle and localized, rather than systemic. We believe these findings highlight the importance of interpreting hematologic ratios in the context of stable absolute cell counts. Our decision to evaluate hematologic inflammatory parameters before and after surgery was based on the growing interest in systemic markers of inflammation in endometriosis. These indices are easily obtainable from routine complete blood count tests and may serve as adjunctive markers to monitor treatment response. In clinical practice, they could offer a low-cost and accessible tool to estimate the inflammatory burden before surgery and track its reduction postoperatively. Although not yet standard, these markers may support clinical follow-up, particularly in settings with limited access to imaging or CA-125 testing. The strengths of our study include its large cohort size, comprehensive main and subgroup analyses, and the diverse cosmopolitan population served by our tertiary care hospital. However, weaknesses of our study include its retrospective design and the discontinuation of patient follow-up after the sixth postoperative week. Endometriosis staging was performed using the rASRM classification. Although the inflammatory markers were not stratified by stage in our analysis, the inclusion of patients across all stages reflects real-world clinical diversity and may contribute to the observed variability. This aspect is acknowledged as a potential limitation and an opportunity for future studies. Furthermore, although potential confounding variables such as age, gravidity, parity, and medical treatment were recorded and compared between the groups, BMI data were not consistently available in the retrospective records and therefore could not be analyzed. This limitation will be addressed in future prospective studies through multivariate adjustments. In addition, although some patients may have received hormonal treatment (e.g., oral contraceptives, progestins, or GnRH analogs), data on the timing, duration, and type of such therapy were not systematically collected. This limitation prevents us from assessing the potential impact of hormonal therapy on hematologic inflammatory parameters. Given that hormonal agents may modulate systemic inflammatory responses, this represents a relevant source of variability. Future studies should evaluate and control for hormonal therapy exposure in a standardized manner.

Below is the link to the electronic supplementary material. Supplementary Material 1 Supplementary Material 1