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DOI: 10.1055/s-0045-1811538
Hypoprolactinemia Following Traumatic Brain Injury and Pituitary Surgery: Mechanisms, Prevalence, and Clinical Implications
- Abstract
- Introduction
- Methods
- Epidemiology and Prevalence
- Pathophysiology and Mechanisms
- Clinical Manifestations and Diagnosis
- Management and Therapeutic Approaches
- Future Research Directions
- Conclusion
- References
Abstract
Posttraumatic hypoprolactinemia is an often overlooked complication following traumatic brain injury (TBI) or pituitary surgery, characterized by abnormally low prolactin levels. Produced by the anterior pituitary gland, prolactin is essential for lactation, reproduction, and immune function. Damage to the hypothalamic-pituitary-axis can lead to hypoprolactinemia, causing symptoms such as lactation failure, reproductive dysfunction, mood disturbances, and immune impairment. The prevalence of hypoprolactinemia after TBI varies from 1 to 85%, while it is lower in postpituitary surgery. There is a lack of standardized diagnostic criteria and effective management strategies. This review covers the epidemiology, pathophysiology, clinical manifestations, and diagnostic challenges, while discussing therapeutic approaches like prolactin replacement therapy. Emphasizing the need for multidisciplinary care, the review also highlights the importance of research to establish diagnostic criteria and improve detection and treatment, as early intervention is crucial for better patient outcomes.
Keywords
hypoprolactinemia - traumatic brain injury - pituitary surgery - posttraumatic endocrine dysfunction - pituitary hormone deficiencyIntroduction
Hypoprolactinemia is a medical condition defined by unusually low levels of the hormone prolactin (PRL) in the bloodstream. Prolactin is produced by the lactotroph cells in the anterior pituitary gland and plays a crucial role in various bodily functions, particularly in lactation and reproduction. In the context of lactation, prolactin is essential for the growth and development of mammary glands. It prepares the breasts for milk production after childbirth, facilitates the synthesis of milk, and sustains milk secretion. A significant reduction in prolactin levels can result in lactation failure, which is a well-established consequence of hypoprolactinemia.[1] [2] [3]
From a reproductive perspective, prolactin is vital for regulating various functions. It supports the menstrual cycle by enhancing the luteal phase and promoting the production of progesterone. Furthermore, prolactin is instrumental in mammary gland development during pregnancy and is critical for maintaining pregnancy. A deficiency in prolactin can lead to reproductive complications, such as infertility, highlighting the hormone's essential role in the reproductive system.[4] Posttraumatic hypoprolactinemia, which can occur following a traumatic brain injury (TBI) or pituitary surgery, significantly affects both lactation and reproductive health. While hypoprolactinemia is classically described after TBI due to hypothalamic-pituitary-axis disruption, it may also occur following pituitary surgery, albeit through distinct mechanisms. Post-TBI hypoprolactinemia typically results from direct trauma to the hypothalamus/pituitary stalk or vascular damage, whereas surgical cases often reflect iatrogenic injury to lactotroph cells or transient postoperative dysfunction. This review examines both etiologies to contrast their pathophysiology, prevalence, and management, while acknowledging their clinical distinctions. This condition emerges when prolactin levels are low due to damage to the hypothalamus or pituitary gland, which are key regulators of prolactin production. Research indicates that the prevalence of hypoprolactinemia following TBI can vary widely, with studies reporting rates ranging from as low as 1% to as high as 85%.[5]
The primary aim of this review was to examine the prevalence, underlying mechanisms, and clinical implications of posttraumatic hypoprolactinemia. By synthesizing existing literature, we seek to enhance our understanding of the impact this condition has on patients and to identify potential areas for further research and improved clinical management strategies. Our analysis prioritizes human studies directly related to TBI and pituitary surgery while excluding anecdotal evidence or preclinical data lacking clinical correlations.
Methods
This review brings together insights from 33 peer-reviewed articles sourced from PubMed and other biomedical databases. We utilized keywords like hypoprolactinemia, TBI, pituitary surgery, and hypopituitarism to guide our search. Our focus was on clinical studies, meta-analyses, and systematic reviews published in respected journals such as “Reviews in Endocrine & Metabolic Disorders” and the “Journal of Neurotrauma.” In selecting studies, we concentrated on human research that presented measurable outcomes—like hormone levels and symptom profiles—while excluding animal studies and case reports with fewer than 10 participants unless they provided vital mechanistic insights, particularly regarding the neuroprotective roles of prolactin. We adhered to the PICOTS (Population, Intervention, Comparison, Outcome, Timing, and Setting) framework, focusing on patients with TBI or those who had undergone pituitary surgery, and aimed to assess key outcomes including prevalence, pathophysiology, and management strategies. This approach was designed to ensure the relevance and rigor of our findings within the field.
Epidemiology and Prevalence
Hypoprolactinemia, a condition characterized by low levels of prolactin in the blood, is observed in patients who have sustained TBI, though its prevalence can vary significantly. This variability is influenced by the specific phase of the injury as well as various associated risk factors. The prevalence rates reported in the literature stem from cohort studies and meta-analyses that adhere to specific inclusion criteria: a minimum of 50 participants, clear diagnostic criteria for hypoprolactinemia, and follow-up durations exceeding 6 months postinjury or surgery.
During the acute phase of TBI, the stress response and the severity of the injury can notably affect serum prolactin levels. Some studies indicate that abnormalities in these levels are common, with prevalence rates reported as high as 85% in the initial phase following the injury.[5] This broad range can be attributed to complex interactions involving hypothalamic and pituitary damage, as well as fluctuations in dopaminergic activity and various other mediators. As the condition evolves into the chronic phase, the prevalence of hypoprolactinemia tends to stabilize, potentially serving as an indicator of ongoing dysfunction in the pituitary gland. Long-term studies have revealed that a significant portion of TBI survivors experience hypoprolactinemia, with one meta-analysis estimating a pooled prevalence of approximately 33% of pituitary-axis dysfunction, which includes prolactin issues, in this later stage.[6]
The severity of the TBI emerges as a critical risk factor for hypoprolactinemia. Individuals who experience severe TBI are considerably more susceptible to significant hypothalamic-pituitary damage, resulting in higher rates of hypopituitarism, including hypoprolactinemia. Furthermore, the specific location of the injury plays a vital role; trauma directly affecting the hypothalamus or pituitary gland is particularly associated with disturbances in prolactin levels. Other contributing risk factors include intracranial hemorrhage, diffuse axonal injury, and basal skull fractures.[7] [8] [9] In contrast, the incidence of hypoprolactinemia following pituitary adenoma resection or other pituitary surgeries is relatively low. Research conducted by Webb et al found that new postoperative deficiencies in prolactin occurred in roughly 13% of patients, with various factors influencing these outcomes.[10]
Several elements can affect prolactin levels in the postoperative setting. For instance, the extent of tumor resection plays a vital role; complete removal of the tumor is generally associated with better normalization of hormonal levels, while the presence of residual tumor tissue following partial resection can continue to influence prolactin levels. Additionally, preexisting pituitary dysfunction is a key factor, as patients with hypopituitarism before surgery are more likely to experience persistent or exacerbated hormone deficiencies afterward. Notably, preoperative prolactin levels can also serve as predictors for postoperative outcomes, with lower levels before surgery linked to higher rates of remission.[11] [12] [13]
Tumor characteristics are also important. Larger, more invasive tumors tend to have a greater likelihood of causing persistent hypopituitarism due to extensive damage inflicted on the pituitary and hypothalamus. Surgical technique and the experience of the surgical team are other factors that play a substantial role in postoperative outcomes. Utilizing minimally invasive approaches and taking care with the handling of the pituitary gland can help mitigate the risk of postoperative hypopituitarism.[14] [15] [16]
In summary, hypoprolactinemia is a common endocrine disturbance following TBI, with a highly variable prevalence that is influenced by injury severity and phase. In contrast, it tends to be less frequent after pituitary surgery.
Pathophysiology and Mechanisms
TBI and pituitary surgery can significantly disrupt hormonal balance, particularly leading to a condition known as hypoprolactinemia. This occurs through various mechanisms, primarily involving damage to the hypothalamus or pituitary stalk, impairments in dopamine regulation, and the resultant inflammatory responses that can affect the hypothalamic-pituitary-axis. The hypothalamus plays a crucial role in producing dopamine, a neurotransmitter that inhibits prolactin secretion from the anterior pituitary. When either the hypothalamus or the pituitary stalk is injured, the regulatory pathways that maintain stable prolactin levels can become disrupted. Such injuries may reduce the inhibitory effect of dopamine on prolactin release, resulting in hormonal imbalance.[5]
Following a TBI, fluctuations in dopaminergic activity can further complicate prolactin regulation. A decrease in dopamine production or impairments in its transport along the pituitary stalk can contribute to hypoprolactinemia.[17] Additionally, TBI and pituitary surgeries can provoke vascular injuries and inflammation, which can lead to ischemia, compromising the hypothalamic-pituitary-axis and hindering the production and release of prolactin. The presence of inflammatory cytokines can exacerbate this dysfunction, adversely affecting both the hypothalamus and the pituitary gland.[18] [19]
Moreover, it is noteworthy that hypoprolactinemia might form part of a broader clinical picture known as posttraumatic hypopituitarism. TBI can induce deficiencies in several pituitary hormones, including growth hormone, adrenocorticotropic hormone, gonadotropins, and thyroid-stimulating hormone. The prevalence of hypopituitarism following a TBI varies widely, with estimates ranging from 15 to 50%. Similarly, postoperative outcomes for patients undergoing pituitary surgery can reveal new deficiencies in prolactin, affecting approximately 13% of these individuals.[20]
Understanding these conditions is essential not only for diagnosis and treatment but also for improving the quality of life for affected patients.
Clinical Manifestations and Diagnosis
The clinical presentation of hypoprolactinemia in individuals with a history of TBI or those who have undergone pituitary surgery often includes a range of symptoms that can significantly impact various aspects of health, including lactation, reproductive function, mood regulation, immune response, bone health, and metabolic processes.[2] [21] [22]
A notable challenge in accurately diagnosing hypoprolactinemia in these patients stems from the lack of standardized criteria. Symptoms associated with hypoprolactinemia often overlap with those that arise from the consequences of concussions or the recovery process following surgery, such as fatigue, cognitive impairments, and mood disturbances. This symptom overlap complicates the clinical assessment, making it difficult to ascertain whether the observed issues are specifically due to hypoprolactinemia. Additionally, the physiological stress response post-TBI or surgery can result in transient alterations in prolactin levels, further obscuring the distinction between short-lived fluctuations and chronic hypoprolactinemia.[23]
Another significant concern in this context is the lack of consensus on the optimal timing for conducting hormonal evaluations following TBI or surgery. Hormone levels can exhibit substantial variability during the acute phase, often providing a misleading representation of long-term pituitary function.[24] Furthermore, the diverse patterns of hormone deficiency among patients call for tailored testing approaches, which makes the establishment of universal diagnostic standards quite challenging.[25] Dynamic assessment methods, such as stimulation tests, are typically necessary for a precise evaluation of pituitary function. However, these tests can be resource-intensive and may not always be feasible in every clinical setting.[25]
To effectively screen at-risk populations, particularly those with TBI or individuals recovering from pituitary surgery, it is essential to conduct early and periodic assessments of prolactin levels. For TBI patients, it is advisable to screen individuals with moderate to severe injuries for hypopituitarism, including checking prolactin levels, within the first year after the injury, ideally within the initial 3 to 6 months. This timing allows for the identification of acute deficiencies, with follow-up screenings recommended at 12 months postinjury to catch any delayed onset of hypopituitarism. Further assessments may be warranted based on the symptoms presented and the outcomes of the initial screening.[26] [27]
In cases of pituitary surgery, it is crucial to conduct a thorough endocrine evaluation, including measuring prolactin levels, before the surgery to establish a baseline and to identify any existing pituitary dysfunction. Subsequent assessments of prolactin levels should follow in the first few weeks postsurgery to monitor for immediate changes. Follow-up evaluations at 3 to 6 months, and annually thereafter or more frequently if symptoms indicate pituitary dysfunction, are highly recommended.[26] [27]
Several factors also influence the screening process, particularly the severity and location of the brain injury. More severe injuries, especially those affecting the hypothalamus or the pituitary stalk, are correlated with a heightened risk of hypoprolactinemia, which may necessitate closer monitoring. Moreover, patients exhibiting signs of hypopituitarism—such as failure to lactate, reproductive issues, or mood disturbances—should be prioritized for endocrine evaluation.[26] [27]
Management and Therapeutic Approaches
Improved survival rates for individuals who have experienced TBI or have undergone pituitary surgery have led to a growing emphasis on enhancing the long-term quality of life for these survivors. Regular endocrine monitoring is essential, as these individuals frequently develop hypopituitarism, which can significantly impact their recovery and overall well-being. Consistent endocrine evaluations are crucial to address the complex needs of TBI patients and those recovering from pituitary surgery. Routine assessments combined with appropriate hormone replacement therapy can alleviate the negative consequences of hypopituitarism, ultimately leading to better patient outcomes and a higher quality of life.[28] [29] [30]
One area of emerging interest is the potential for prolactin replacement therapy for patients who have experienced TBI or pituitary surgery. Although prolactin is well known for its role in lactation and reproductive health, its possible neuroprotective effects are less understood. Unfortunately, the clinical application of prolactin replacement therapy is not yet well-established, primarily due to the absence of standardized diagnostic criteria for hypoprolactinemia. This lack of clarity complicates the identification of patients who might benefit from such an intervention.[31] [32]
Research indicates that prolactin may promote regeneration in brain injury situations by reducing inflammation and preventing cell death. These findings suggest that prolactin replacement could confer neuroprotective benefits for TBI patients. However, it is important to note that much of the supporting evidence comes from preclinical studies, underscoring the urgent need for rigorous clinical trials to confirm these advantages in human populations.[31] [32]
The clinical use of prolactin presents specific challenges, particularly its short half-life and the necessity for frequent administration. Furthermore, the potential side effects and long-term safety of prolactin replacement therapy require further investigation. Currently, most hormone replacement strategies focus on other pituitary hormones, such as growth hormone and cortisol, which have established efficacy.[31] [32]
Managing posttraumatic hypoprolactinemia effectively requires a collaborative, multidisciplinary approach that brings together the expertise of endocrinologists, neurologists, and surgeons. Each of these specialists plays a vital role in providing holistic care for patients.
Endocrinologists are key players in diagnosing and addressing hormonal deficiencies, particularly hypoprolactinemia. Their deep understanding of hormone function and replacement therapy is essential for crafting tailored treatment plans and monitoring the long-term health of the endocrine system. They work closely with patients to understand their unique challenges and help navigate the complexities of hormonal imbalances.
Neurologists contribute their insights into brain function and the implications of neurological disorders, especially in cases involving TBI or pituitary surgery. Their expertise is crucial for assessing the immediate and long-term neurological effects that can arise from these conditions, including potential cognitive, motor, and sensory challenges. This ensures that patients receive comprehensive care that addresses both their hormonal and neurological needs.
Surgeons, particularly those specializing in neurosurgery and endocrine surgery, play an essential role in executing delicate procedures such as pituitary surgery. They bring a wealth of knowledge regarding surgical implications and postoperative care to the team, highlighting the importance of a smooth recovery process and minimizing complications.
When these specialists collaborate, they can tackle the intricate challenges of posttraumatic hypoprolactinemia more effectively. This teamwork enhances patient outcomes, improves overall quality of life, and helps mitigate the risk of long-term complications. Beyond pharmacological treatments, nonpharmacological interventions can significantly aid in addressing certain aspects of hypoprolactinemia, especially for postpartum women facing lactation difficulties and individuals experiencing mood-related symptoms.
For postpartum women, accessing lactation support can be incredibly beneficial. This support may involve consultations with lactation specialists who guide effective breastfeeding techniques, helping resolve issues related to latch or milk supply. Additionally, connecting with breastfeeding support groups fosters a sense of community, offering emotional support and practical advice from fellow mothers. Tools like breast pumps or supplemental nursing systems can also help stimulate milk production, ensuring that infants receive adequate nourishment.
For those dealing with mood-related symptoms, such as anxiety or depression, psychological counseling can be an important part of their treatment journey. Cognitive-behavioral therapy is a proven approach that assists individuals in recognizing and reframing unhelpful thought patterns and behaviors. Support groups or group therapy can offer a safe space to share experiences with others facing similar challenges, thereby alleviating feelings of isolation and providing effective coping strategies. Furthermore, practices like mindfulness, yoga, and deep breathing can contribute to stress reduction and promote emotional well-being.
Incorporating these nonpharmacological interventions alongside medical treatments can enrich the management of hypoprolactinemia, ultimately enhancing the overall quality of life for individuals affected by this condition.
Future Research Directions
To effectively address the existing knowledge gaps and management challenges surrounding posttraumatic hypoprolactinemia, future research efforts should focus on several critical areas.
First, it is essential to conduct studies that delve deep into the underlying mechanisms of this condition. By investigating the molecular and cellular processes associated with posttraumatic hypoprolactinemia, we can enhance our understanding of its pathophysiology and identify potential therapeutic targets that could guide future treatments. In addition, well-structured clinical trials are crucial for assessing the safety and effectiveness of prolactin replacement therapy for individuals impacted by this condition. These trials should examine the benefits of normalizing prolactin levels, particularly regarding lactation, reproductive health, mood, and other areas potentially altered by hypoprolactinemia.
Large-scale epidemiological studies are also vital for gaining a clearer picture of the prevalence of posttraumatic hypoprolactinemia. Such research should aim to identify risk factors and evaluate the long-term health implications associated with the condition. Insights derived from these studies could inform screening protocols and enhance early detection strategies, ultimately improving patient care.
Moreover, the exploration of advancements in technology is imperative. This includes investigating potential biomarkers, employing advanced imaging methods, and utilizing artificial intelligence (AI) to analyze complex data sets. Biomarkers may assist in identifying patients at risk and predicting treatment responses, while AI can improve diagnostic accuracy. Advanced imaging techniques could provide detailed insights into the structural and functional changes within the hypothalamic-pituitary-axis.
By following these research avenues health care providers can deepen their understanding of posttraumatic hypoprolactinemia and create more effective approaches for diagnosis, prevention, and treatment, leading to improved patient outcomes. Establishing standardized diagnostic criteria for hypoprolactinemia is also vital to ensure accurate identification of affected individuals. In tandem with this, clinical trials assessing the safety and efficacy of prolactin replacement therapy must focus on its effects on lactation, reproductive function, mood, and immune health.
Additionally, exploring alternative delivery methods to enhance patient adherence to treatment is an important component of advancing therapeutic options. Developing more convenient, user-friendly approaches could significantly boost compliance and improve treatment results. Finally, gaining a deeper understanding of the broader effects of prolactin on mood and immune function may open up new therapeutic avenues. This knowledge could pave the way for targeted treatments that not only alleviate the immediate symptoms of hypoprolactinemia but also tackle its long-term impacts on mental health and immune performance.
Conclusion
In summary, posttraumatic hypoprolactinemia emerges as a notable complication arising from TBI or pituitary surgery. Its prevalence varies considerably, yet its impact on individuals can be profound. This condition typically manifests due to damage to the hypothalamic-pituitary-axis and the dopaminergic system, leading to a disrupted prolactin secretion process. From a clinical perspective, posttraumatic hypoprolactinemia can induce a range of challenges, including difficulties with lactation, reproductive issues, mood dysregulation, and potential impairment of the immune system. These serious ramifications underscore the critical need for enhanced awareness among health care professionals, particularly when managing populations that may be vulnerable to this condition.
To ensure early diagnosis and effective management, regular screening and a collaborative approach involving endocrinologists, neurologists, and surgeons are essential. Timely interventions, such as hormone replacement therapy, can significantly alleviate symptoms, enhance quality of life, and mitigate long-term health risks. Looking ahead, future research should focus on establishing standardized diagnostic criteria, thoroughly evaluating the efficacy and safety of prolactin replacement therapy, and investigating alternative treatment strategies. By addressing these gaps in knowledge, we can facilitate earlier detection, tailor treatments to individual patient needs, and ultimately improve outcomes in this often-overlooked domain of endocrinology.
Conflict of Interest
None declared.
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References
- 1 Karaca Z, Unluhizarci K, Kelestimur F. Hypoprolactinemia. Does it matter? Redefining the hypopituitarism and return from a mumpsimus : “absence of proof is not the proof of absence”. Rev Endocr Metab Disord 2024; 25 (06) 943-951
- 2 Kelestimur F, Ioachimescu AG. Hypoprolactinemia, a neglected endocrine disorder. Rev Endocr Metab Disord 2024; 25 (06) 941-942
- 3 Shimon I. Prolactin deficiency in the context of other pituitary hormone abnormalities : special issue: hypoprolactinemia: a neglected endocrine disorder. Rev Endocr Metab Disord 2024; 25 (06) 1041-1046
- 4 Goffin V, Bouchard B, Ormandy CJ. et al. Prolactin: a hormone at the crossroads of neuroimmunoendocrinology. Ann N Y Acad Sci 1998; 840: 498-509
- 5 Hacioglu A, Tanriverdi F. Traumatic brain injury and prolactin. Rev Endocr Metab Disord 2024; 25 (06) 1027-1040
- 6 Aljboor GS, Tulemat A, Al-Saedi AR, Radoi MP, Toader C, Papacocea TM. Acute and chronic hypopituitarism following traumatic brain injury: a systematic review and meta-analysis. Neurosurg Rev 2024; 47 (01) 841
- 7 Tritos NA, Yuen KC, Kelly DF. AACE Neuroendocrine and Pituitary Scientific Committee. American Association of Clinical Endocrinologists and American College of Endocrinology disease state clinical review: a neuroendocrine approach to patients with traumatic brain injury. Endocr Pract 2015; 21 (07) 823-831
- 8 Silva PP, Bhatnagar S, Herman SD. et al. Predictors of hypopituitarism in patients with traumatic brain injury. J Neurotrauma 2015; 32 (22) 1789-1795
- 9 Schneider M, Schneider HJ, Yassouridis A, Saller B, von Rosen F, Stalla GK. Predictors of anterior pituitary insufficiency after traumatic brain injury. Clin Endocrinol (Oxf) 2008; 68 (02) 206-212
- 10 Webb SM, Rigla M, Wägner A, Oliver B, Bartumeus F. Recovery of hypopituitarism after neurosurgical treatment of pituitary adenomas. J Clin Endocrinol Metab 1999; 84 (10) 3696-3700
- 11 Wang S, Li B, Ding C, Xiao D, Wei L. A novel “total pituitary hormone index” as an indicator of postoperative pituitary function in patients undergoing resection of pituitary adenomas. Oncotarget 2017; 8 (45) 79111-79125
- 12 Amar AP, Couldwell WT, Chen JC, Weiss MH. Predictive value of serum prolactin levels measured immediately after transsphenoidal surgery. J Neurosurg 2002; 97 (02) 307-314
- 13 Zhao M, Li K, Niu H, Zhao Y, Lu C. Perioperative hormone level changes and their clinical implications in patients with pituitary adenoma: a retrospective study of 428 cases at a single center. Front Endocrinol (Lausanne) 2023; 14: 1286020
- 14 Fatemi N, Dusick JR, Mattozo C. et al. Pituitary hormonal loss and recovery after transsphenoidal adenoma removal. Neurosurgery 2008; 63 (04) 709-718 , discussion 718–719
- 15 Riley G, Scheyer N, Klein M. et al. Prognostic indicators in pituitary adenoma surgery: a comprehensive analysis of surgical outcomes and complications. Front Endocrinol (Lausanne) 2024; 14: 1327404
- 16 Ottenhausen M, Conrad J, Wolters LM, Ringel F. Surgery as first-line treatment for prolactinoma? Discussion of the literature and results of a consecutive series of surgically treated patients. Neurosurg Rev 2023; 46 (01) 128
- 17 Kopczak A, Kilimann I, von Rosen F. et al. Screening for hypopituitarism in 509 patients with traumatic brain injury or subarachnoid hemorrhage. J Neurotrauma 2014; 31 (01) 99-107
- 18 Mele C, Pingue V, Caputo M. et al. Neuroinflammation and hypothalamo-pituitary dysfunction: focus of traumatic brain injury. Int J Mol Sci 2021; 22 (05) 2686
- 19 Tanriverdi F, Schneider HJ, Aimaretti G, Masel BE, Casanueva FF, Kelestimur F. Pituitary dysfunction after traumatic brain injury: a clinical and pathophysiological approach. Endocr Rev 2015; 36 (03) 305-342
- 20 Temizkan S, Kelestimur F. A clinical and pathophysiological approach to traumatic brain injury-induced pituitary dysfunction. Pituitary 2019; 22 (03) 220-228
- 21 Munro V, Wilkinson M, Imran SA. Neuropsychological complications of hypoprolactinemia. Rev Endocr Metab Disord 2024; 25 (06) 1121-1126
- 22 Caputo M, Mele C, Prodam F, Marzullo P, Aimaretti G. Clinical picture and the treatment of TBI-induced hypopituitarism. Pituitary 2019; 22 (03) 261-269
- 23 Glynn N, Agha A. The frequency and the diagnosis of pituitary dysfunction after traumatic brain injury. Pituitary 2019; 22 (03) 249-260
- 24 Quinn M, Agha A. Post-traumatic hypopituitarism-who should be screened, when, and how?. Front Endocrinol (Lausanne) 2018; 9: 8
- 25 Karamouzis I, Pagano L, Prodam F. et al. Clinical and diagnostic approach to patients with hypopituitarism due to traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and ischemic stroke (IS). Endocrine 2016; 52 (03) 441-450
- 26 Glynn N, Agha A. Which patient requires neuroendocrine assessment following traumatic brain injury, when and how?. Clin Endocrinol (Oxf) 2013; 78 (01) 17-20
- 27 Tan CL, Hutchinson PJ. A neurosurgical approach to traumatic brain injury and post-traumatic hypopituitarism. Pituitary 2019; 22 (03) 332-337
- 28 Garrahy A, Sherlock M, Thompson CJ. Management of endocrine disease: neuroendocrine surveillance and management of neurosurgical patients. Eur J Endocrinol 2017; 176 (05) R217-R233
- 29 Dassa Y, Crosnier H, Chevignard M. et al. Pituitary deficiency and precocious puberty after childhood severe traumatic brain injury: a long-term follow-up prospective study. Eur J Endocrinol 2019; 180 (05) 281-290
- 30 Reifschneider K, Auble BA, Rose SR. Update of endocrine dysfunction following pediatric traumatic brain injury. J Clin Med 2015; 4 (08) 1536-1560
- 31 Yousefvand S, Hadjzadeh MA, Vafaee F, Dolatshad H. The protective effects of prolactin on brain injury. Life Sci 2020; 263: 118547
- 32 Baxter D, Sharp DJ, Feeney C. et al. Pituitary dysfunction after blast traumatic brain injury: the UK BIOSAP study. Ann Neurol 2013; 74 (04) 527-536
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Publication History
Article published online:
22 August 2025
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References
- 1 Karaca Z, Unluhizarci K, Kelestimur F. Hypoprolactinemia. Does it matter? Redefining the hypopituitarism and return from a mumpsimus : “absence of proof is not the proof of absence”. Rev Endocr Metab Disord 2024; 25 (06) 943-951
- 2 Kelestimur F, Ioachimescu AG. Hypoprolactinemia, a neglected endocrine disorder. Rev Endocr Metab Disord 2024; 25 (06) 941-942
- 3 Shimon I. Prolactin deficiency in the context of other pituitary hormone abnormalities : special issue: hypoprolactinemia: a neglected endocrine disorder. Rev Endocr Metab Disord 2024; 25 (06) 1041-1046
- 4 Goffin V, Bouchard B, Ormandy CJ. et al. Prolactin: a hormone at the crossroads of neuroimmunoendocrinology. Ann N Y Acad Sci 1998; 840: 498-509
- 5 Hacioglu A, Tanriverdi F. Traumatic brain injury and prolactin. Rev Endocr Metab Disord 2024; 25 (06) 1027-1040
- 6 Aljboor GS, Tulemat A, Al-Saedi AR, Radoi MP, Toader C, Papacocea TM. Acute and chronic hypopituitarism following traumatic brain injury: a systematic review and meta-analysis. Neurosurg Rev 2024; 47 (01) 841
- 7 Tritos NA, Yuen KC, Kelly DF. AACE Neuroendocrine and Pituitary Scientific Committee. American Association of Clinical Endocrinologists and American College of Endocrinology disease state clinical review: a neuroendocrine approach to patients with traumatic brain injury. Endocr Pract 2015; 21 (07) 823-831
- 8 Silva PP, Bhatnagar S, Herman SD. et al. Predictors of hypopituitarism in patients with traumatic brain injury. J Neurotrauma 2015; 32 (22) 1789-1795
- 9 Schneider M, Schneider HJ, Yassouridis A, Saller B, von Rosen F, Stalla GK. Predictors of anterior pituitary insufficiency after traumatic brain injury. Clin Endocrinol (Oxf) 2008; 68 (02) 206-212
- 10 Webb SM, Rigla M, Wägner A, Oliver B, Bartumeus F. Recovery of hypopituitarism after neurosurgical treatment of pituitary adenomas. J Clin Endocrinol Metab 1999; 84 (10) 3696-3700
- 11 Wang S, Li B, Ding C, Xiao D, Wei L. A novel “total pituitary hormone index” as an indicator of postoperative pituitary function in patients undergoing resection of pituitary adenomas. Oncotarget 2017; 8 (45) 79111-79125
- 12 Amar AP, Couldwell WT, Chen JC, Weiss MH. Predictive value of serum prolactin levels measured immediately after transsphenoidal surgery. J Neurosurg 2002; 97 (02) 307-314
- 13 Zhao M, Li K, Niu H, Zhao Y, Lu C. Perioperative hormone level changes and their clinical implications in patients with pituitary adenoma: a retrospective study of 428 cases at a single center. Front Endocrinol (Lausanne) 2023; 14: 1286020
- 14 Fatemi N, Dusick JR, Mattozo C. et al. Pituitary hormonal loss and recovery after transsphenoidal adenoma removal. Neurosurgery 2008; 63 (04) 709-718 , discussion 718–719
- 15 Riley G, Scheyer N, Klein M. et al. Prognostic indicators in pituitary adenoma surgery: a comprehensive analysis of surgical outcomes and complications. Front Endocrinol (Lausanne) 2024; 14: 1327404
- 16 Ottenhausen M, Conrad J, Wolters LM, Ringel F. Surgery as first-line treatment for prolactinoma? Discussion of the literature and results of a consecutive series of surgically treated patients. Neurosurg Rev 2023; 46 (01) 128
- 17 Kopczak A, Kilimann I, von Rosen F. et al. Screening for hypopituitarism in 509 patients with traumatic brain injury or subarachnoid hemorrhage. J Neurotrauma 2014; 31 (01) 99-107
- 18 Mele C, Pingue V, Caputo M. et al. Neuroinflammation and hypothalamo-pituitary dysfunction: focus of traumatic brain injury. Int J Mol Sci 2021; 22 (05) 2686
- 19 Tanriverdi F, Schneider HJ, Aimaretti G, Masel BE, Casanueva FF, Kelestimur F. Pituitary dysfunction after traumatic brain injury: a clinical and pathophysiological approach. Endocr Rev 2015; 36 (03) 305-342
- 20 Temizkan S, Kelestimur F. A clinical and pathophysiological approach to traumatic brain injury-induced pituitary dysfunction. Pituitary 2019; 22 (03) 220-228
- 21 Munro V, Wilkinson M, Imran SA. Neuropsychological complications of hypoprolactinemia. Rev Endocr Metab Disord 2024; 25 (06) 1121-1126
- 22 Caputo M, Mele C, Prodam F, Marzullo P, Aimaretti G. Clinical picture and the treatment of TBI-induced hypopituitarism. Pituitary 2019; 22 (03) 261-269
- 23 Glynn N, Agha A. The frequency and the diagnosis of pituitary dysfunction after traumatic brain injury. Pituitary 2019; 22 (03) 249-260
- 24 Quinn M, Agha A. Post-traumatic hypopituitarism-who should be screened, when, and how?. Front Endocrinol (Lausanne) 2018; 9: 8
- 25 Karamouzis I, Pagano L, Prodam F. et al. Clinical and diagnostic approach to patients with hypopituitarism due to traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and ischemic stroke (IS). Endocrine 2016; 52 (03) 441-450
- 26 Glynn N, Agha A. Which patient requires neuroendocrine assessment following traumatic brain injury, when and how?. Clin Endocrinol (Oxf) 2013; 78 (01) 17-20
- 27 Tan CL, Hutchinson PJ. A neurosurgical approach to traumatic brain injury and post-traumatic hypopituitarism. Pituitary 2019; 22 (03) 332-337
- 28 Garrahy A, Sherlock M, Thompson CJ. Management of endocrine disease: neuroendocrine surveillance and management of neurosurgical patients. Eur J Endocrinol 2017; 176 (05) R217-R233
- 29 Dassa Y, Crosnier H, Chevignard M. et al. Pituitary deficiency and precocious puberty after childhood severe traumatic brain injury: a long-term follow-up prospective study. Eur J Endocrinol 2019; 180 (05) 281-290
- 30 Reifschneider K, Auble BA, Rose SR. Update of endocrine dysfunction following pediatric traumatic brain injury. J Clin Med 2015; 4 (08) 1536-1560
- 31 Yousefvand S, Hadjzadeh MA, Vafaee F, Dolatshad H. The protective effects of prolactin on brain injury. Life Sci 2020; 263: 118547
- 32 Baxter D, Sharp DJ, Feeney C. et al. Pituitary dysfunction after blast traumatic brain injury: the UK BIOSAP study. Ann Neurol 2013; 74 (04) 527-536