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Patient and therapist experiences of a self-management group programme for fatigue in primary care: a qualitative study.

Authors: Gunnink-Wennink SH, Cup EHC, Veenhuizen Y, Hoogeboom TJ, van der Wees PJ, Voet NBM, Graff M
Journal: BMC primary care
mental health psychology open access

Abstract

Pituitary neuroendocrine tumors (PitNETs), also referred to as pituitary adenomas, are the second most common type of primary intracranial tumors, accounting for approximately 15%–20% of all intracranial neoplasms []. These tumors may lead to excessive hormone secretion, resulting in corresponding endocrine syndromes. Additionally, they may cause visual field defects, neurological dysfunction, and hypopituitarism due to mass effect. Although the term PitNET has been adopted in the 5th WHO classification, the nomenclature remains controversial. Some experts have argued that the term “pituitary adenoma” should be retained because most of these tumors are biologically benign and clinically distinct from neuroendocrine tumors arising in other organs [, ]. PitNETs are believed to originate from adenohypophyseal cells and exhibit monoclonal proliferation. The 5th edition of the World Health Organization (WHO) Classification of Endocrine and Neuroendocrine Tumors (2022) recommends a more precise categorization of PitNETs based on transcription factor expression, hormone secretion profiles, and other biomarkers such as cytokeratin expression []. This heterogeneous group of tumors is thought to derive from six types of anterior pituitary cells or their progenitors and is broadly classified based on the expression of three lineage-specific transcription factors: PIT1 (pituitary-specific POU-class homeodomain transcription factor), TPIT (T-box family member TBX19), and SF1 (steroidogenic factor 1). Among these, PIT1-lineage tumors are the most heterogeneous and complex in classification. They typically secrete one or more of the following hormones: growth hormone (GH), PRL, or thyroid-stimulating hormone (TSH), potentially causing conditions such as acromegaly/gigantism, hyperprolactinemia, and central hyperthyroidism []. TPIT-lineage tumors usually secrete adrenocorticotropic hormone (ACTH), leading to Cushing’s disease. SF1-lineage tumors generally secrete luteinizing hormone (LH) and/or follicle-stimulating hormone (FSH), but most do not present with distinct clinical symptoms and are often referred to as “silent PitNETs” [, ]. Silent behavior may also be observed in other lineages. Some PitNETs express no transcription factors above and are classified as “null cell tumor,” while others co-express multiple transcription factors and secrete hormones from more than one lineage, referred to as “plurihormonal tumors” []. Acromegaly/gigantism is typically caused by GH-secreting PitNETs, which produce excessive amounts of GH. The chronic elevation of GH and its downstream effector insulin-like growth factor 1 (IGF-1) results in the characteristic clinical manifestations of acromegaly and can lead to multi-system complications affecting the respiratory, cardiovascular, musculoskeletal, and nervous systems, thereby severely impairing patients’ physical and mental health [, ]. According to the 5th edition WHO classification, GH-secreting PitNETs can be subdivided into eight pathological subtypes based on differences in cell morphology, transcription factors, co-expressed hormones, and other biomarkers such as low molecular weight cytokeratins [, ]: