Paradoxical Adipose Hypertrophy (PAH) After Cryolipolysis.

BACKGROUND: Cryolipolysis is a minimally invasive technique used to decrease local adipose tissue by thermal cooling. Paradoxical adipose hypertrophy (PAH) is a rare complication of cryolipolysis with important aesthetic consequences. OBJECTIVES: The objective of this study was to describe four cases of PAH after a cryolipolysis treatment. METHODS: Between January 2014 and January 2017, all patients who had undergone a cryolipolysis treatment in a single center were reviewed. The device used was a CoolSculpting device and the same operator performed all the cryolipolysis treatments. We retrospectively included all patients who had a suspicion of PAH. RESULTS: In our study, 398 patients underwent a session of cryolipolysis. Four patients presented with a voluminous painless swelling in the treated area, between 2 and 4 months after the cryolipolysis session. One patient was treated with liposuction. Histological analysis of the adipose tissue in this patient revealed a nonspecific panniculitis. The other three patients did not receive any additional treatment, and their symptoms stabilized after several months. CONCLUSIONS: Although cryolipolysis generally yields good results, it can be complicated with PAH, which tends to occur a few months after the cryolipolysis treatment. Patients should be informed of the possibility of developing this complication and encouraged to attend regular follow up for at least 6 months, so that this condition can be readily detected. Surgical treatment should be offered if there is no spontaneous improvement of the symptoms.

A PDGFRα-Mediated Switch toward CD9high Adipocyte Progenitors Controls Obesity-Induced Adipose Tissue Fibrosis.

Obesity-induced white adipose tissue (WAT) fibrosis is believed to accelerate WAT dysfunction. However, the cellular origin of WAT fibrosis remains unclear. Here, we show that adipocyte platelet-derived growth factor receptor-α-positive (PDGFRα+) progenitors adopt a fibrogenic phenotype in obese mice prone to visceral WAT fibrosis. More specifically, a subset of PDGFRα+ cells with high CD9 expression (CD9high) originates pro-fibrotic cells whereas their CD9low counterparts, committed to adipogenesis, are almost completely lost in the fibrotic WAT. PDGFRα pathway activation promotes a phenotypic shift toward PDGFRα+CD9high fibrogenic cells, driving pathological remodeling and altering WAT function in obesity. These findings translated to human obesity as the frequency of CD9high progenitors in omental WAT (oWAT) correlates with oWAT fibrosis level, insulin-resistance severity, and type 2 diabetes. Collectively, our data demonstrate that in addition to representing a WAT adipogenic niche, different PDGFRα+ cell subsets modulate obesity-induced WAT fibrogenesis and are associated with loss of metabolic fitness.