Table 2.

Studies on inflammation and HPA axis dysregulation in BPD.

Authors	Study Design	States	Sample Characteristics	Outcomes
Spitzer et al. [11]	cross-sectional study	Germany	12 PTSD patients (8 BPD–PTSD patients); 38 with no PTSD (27 BPD patients)	In BPD, when trauma is present (BPD–PTSD), dysfunction of the hypothalamic–pituitary–adrenal axis may contribute to low-grade inflammation, as indicated by elevated CRP levels.
Aleknaviciute et al. [46]	case–control study	Netherlands	26 BPD patients; 20 CPD patients; 35 healthy controls (female)	BPD patients showed distinct physiological patterns, as follows: lower baseline cortisol, blunted stress responses in cortisol and HR, but higher SCL, indicating autonomic imbalance. These attenuated responses were linked to HPA axis hyporeactivity, potentially due to early-life trauma.
Boström et al. [47]	RCT	Sweden	97 BPD females with prior history of two or more potentially lethal suicide attempts vs. 32 controls (18–50 yo)	Women with BPD and a recent history of suicide attempts exhibit EAA compared to healthy controls.
Wang et al. [14]	correlational study	China	60 BD–BPD patients (18–45 yo)	Elevated serum levels of Hcy and hs-CRP may regulate inflammatory responses, exacerbating cognitive impairment in patients with BD and BPD.

BPD: borderline personality disorder; CPD: cluster c personality disorders; HPA: hypothalamic–pituitary–adrenal axis; PTSD: post-traumatic stress disorder; HR: heart rate; Hcy: homocysteine; BD: bipolar disorder; hs-CRP: C-reactive protein; EAA: epigenetic age acceleration; SCL: skin conductance levels.