The correlation between ABO blood types and acne vulgaris severity

Background

Acne vulgaris is a chronic inflammatory disease with multifactorial etiology. Studies on the pathogenesis of acne are still important. Recently, various studies have been conducted on the significance of genetics in the pathogenesis of acne. Blood group is transferred genetically and could affect the development, progress, and severity of certain diseases.

Aim

In the current study, the correlation between the severity of acne vulgaris and ABO blood groups was investigated.

Materials and Methods

A total of 380 patients (263 mild and 117 severe acne vulgaris patients) and 1000 healthy individuals were included in the study. Severity of acne vulgaris patients and healthy controls was determined based on the blood group and Rh factor data obtained retrospectively from the patient files in the hospital automation system.

Results

In the study, the rate of females was significantly higher in the acne vulgaris group (X²:154.908; p:0.000). The mean age of the patient was significantly lower when compared to the controls (t:37.127; p:0.0001). The mean age of the patients with severe acne was significantly lower when compared to those with mild acne. When compared to the control group, the incidence of severe acne was higher in those A blood type when compared to the patients with mild acne, while the incidence of mild acne was higher in other blood groups when compared to the control (X²:17.756; p:0.007). No significant difference was determined between the Rh blood groups of the patients with mild, severe acne and the control group (X²:0.812; p:0.666).

Conclusion

The results revealed a significant correlation between acne severity and ABO blood groups. Future studies that would be conducted with larger samples in different centers could confirm the current study findings.     

ER stress and inflammation crosstalk in obesity

The endoplasmic reticulum (ER) governs the proper folding of polypeptides and proteins through various chaperones and enzymes residing within the ER organelle. Perturbation in the ER folding process ensues when overwhelmed protein folding exceeds the ER handling capacity, leading to the accumulation of misfolded/unfolded proteins in the ER lumen—a state being referred to as ER stress. In turn, ER stress induces a gamut of signaling cascades, termed as the “unfolded protein response” (UPR) that reinstates the ER homeostasis through a panel of gene expression modulation. This type of UPR is usually deemed “adaptive UPR.” However, persistent or unresolved ER stress hyperactivates UPR response, which ultimately, triggers cell death and inflammatory pathways, termed as “maladaptive/terminal UPR.” A plethora of evidence indicates that crosstalks between ER stress (maladaptive UPR) and inflammation precipitate obesity pathogenesis. In this regard, the acquisition of the mechanisms linking ER stress to inflammation in obesity might unveil potential remedies to tackle this pathological condition. Herein, we aim to elucidate key mechanisms of ER stress-induced inflammation in the context of obesity and summarize potential therapeutic strategies in the management of obesity through maneuvering ER stress and ER stress-associated inflammation.