Tumor recurrence or residual regrowth are poor prognosis for pituitary adenoma.

A comprehensive review of the literature quantified the pituitary adenoma recurrence rates for commonly observed pituitary adenomas after transsphenoidal surgical resection with curative intent. Findings suggest that surveillance within 1 year may be of low yield. Further, clinical trials and cohort studies investigating the cost-effectiveness of surveillance schedules and their impact on the quality of life of patients under surveillance will provide further insight to optimize follow-up ¹⁾.

The old 2004 World Health Organization classification introduced atypical adenoma, which was equivocally defined as an invasion with increased mitotic activity that had a Ki67 labeling index (LI) greater than 3%, and extensive p53 immunoreactivity. However, aPAs that exhibit all of these features are rare and the predictive value for recurrent pituitary adenomas (PAs) remains uncertain.

Remission is lowest in patients with nonfunctioning adenomas, and recurrence is highest in patients with a prolactinoma. The remission rate has not improved over 3 decades of publication, but there is a modest decrease in recurrences with time. The highest incidence of tumor recurrence is between 1 and 5 years after surgery. Surgery-related hypopituitarism was highest in Cushing’s disease. The most important predictor for recurrence is the postoperative basal (non-stimulated) hormone level in functioning adenomas, while in nonfunctioning adenomas no single convincing factor could be identified ²⁾.

With a high rate of recurrence, Nonfunctioning pituitary adenomas (NFPA) should be closely followed-up over a long-term period. Improvement of surgical techniques with advanced surgical equipment and adjuvant radiosurgery would lead to reduce the recurrence rate and improve patients’ outcome ³⁾.

Postoperative residue, age, immunohistological subtypes, invasion, tumor size, hormone levels, and postoperative radiotherapy can predict the risk of recurrence in patients with PAs. Additionally, biomarkers such as Ki-67, p53, cadherin, pituitary tumor transforming gene, matrix metalloproteinase-9, epidermal growth factor receptor, fascin actin-bundling protein 1, cyclooxygenase-2, and some miRNAs and lncRNAs may be utilized as valuable tools for predicting PA recurrence. As no single marker can independently predict PA recurrence, we introduce an array of comprehensive models and grading methods, including multiple prognostic factors, to predict the prognosis of PAs, which have shown good effectiveness and would be beneficial for predicting PA recurrence ⁴⁾.

There is no validated and well-accepted prognostic classification of PAs to predict the clinical outcome and guide clinical practice. Tumor recurrence or residual regrowth identified by MRI scans and endocrine studies and associated clinical and pathological characteristics were analyzed for patients who underwent surgery in the years 2008-2016 at West China Hospital. Thereby, a new clinicopathological classification was proposed and applied.

After a median follow-up of 44.0 months, tumor recurrence and residual progression were identified in 48 (25.0%) and 29 (37.2%) cases, respectively. Proliferative potential (HR=2.188, p=0.002), invasiveness (HR=1.698, p=0.029), larger tumor size (HR=1.029, p=0.004), high-risk PA subtype (HR=2.151, p=0.004) and postoperative residual (HR=1.941, p=0.007) were risk factors for recurrence/progression in the early stage after surgery. With respect to clinicopathological classification, compared with Grade 1a tumors, Grade 1b, 2a and 2b adenomas had poorer prognoses with an increased probability of tumor recurrence/progression of 5.133-, 4.467- and 20.1-fold, respectively.

The proposed clinicopathological classification of PAs showed significant value in predicting prognosis and succeeded in identifying cases with more clinically aggressive lesions with recurrence or residual regrowth. This prognostic classification may be helpful when identifying aggressive PAs and deciding the appropriate therapeutic strategy for patients with PAs ⁵⁾.