European Journal of Cardiovascular Medicine

Pituitary adenomas (PAs) are non-metastasizing neoplasms arising from adenohypophysial cells. Although they usually occur within the sella turcica, ectopic presentations have also been reported.¹ Pituitary tumors constitute approximately 10–15% of intracranial tumors in surgical specimens and account for nearly 10–20% of all primary brain tumors. These tumors are broadly classified based on size into microadenomas (<10 mm) and macroadenomas (≥10 mm), and clinically into functioning and non-functioning pituitary adenomas (NFPAs). NFPAs do not secrete biologically active hormones and represent nearly 30% of pituitary tumors. However, advances in immunoassays, immunohistochemistry and molecular biology have shown that many clinically non-functioning tumors can synthesize glycoprotein hormones or their subunits, making NFPAs a heterogeneous group that also includes null cell adenomas and oncocytomas.²

Patients with pituitary adenomas commonly present with features of mass effect, endocrine dysfunction, or both. Endocrine abnormalities may include hypersecretion or hyposecretion of pituitary hormones. Visual disturbances such as visual field defects, impaired acuity and ocular palsies occur due to compression of the optic apparatus or cavernous sinus involvement. Destruction of normal pituitary tissue or compromised blood supply may result in partial or panhypopituitarism.³ The estimated prevalence of clinically significant pituitary adenomas ranges from 78 to 94 cases per 100,000 population. According to the WHO classification (2004), pituitary tumors are categorized as functioning—secreting ACTH, GH or prolactin—and non-functioning tumors, commonly associated with LH and FSH secretion.⁴

Pituitary apoplexy is an acute clinical syndrome characterized by sudden headache, vomiting, visual impairment and altered consciousness due to hemorrhage or infarction of the pituitary gland. It is often spontaneous, though risk factors such as hypertension, anticoagulation, surgery and radiotherapy are identified in 10–40% of cases.⁵ Apoplexy occurs more frequently in NFPAs and may be the first manifestation of pituitary disease. Due to overlapping features with conditions like meningitis and subarachnoid hemorrhage, diagnosis is challenging and requires multidisciplinary management.⁶

Aim: This study aims to evaluate the demographic characteristics, clinical presentations, and hormonal and biochemical profiles of patients diagnosed with pituitary adenoma.

This is a descriptive observational study conducted on consecutive patients diagnosed with pituitary adenoma and fulfilling the inclusion and exclusion criteria, admitted to or attending the outpatient department (OPD) of Fortis Escorts Hospital, Jaipur, from January 2021 to June 2022.

Sample Size: Sample size was calculated at a 95% confidence interval with an expected 54–55% proportion of patients presenting with neurological manifestations as reported by Zargar et al., allowing a 20% error. Using the formula n = (Z¹⁻ᵅ⁄²)² × P(1−P) / E², the minimum sample size was 24, rounded to 25–30 patients due to the rarity of pituitary adenomas.

Inclusion Criteria: Patients of either gender aged above 18 years with a confirmed diagnosis of pituitary adenoma based on radiological imaging and hormonal assay findings.

Exclusion Criteria: Patients unwilling to provide informed consent and those diagnosed with multiple endocrine neoplasia type I or type II (MEN-I and MEN-II)

Data were collected from case records and hormonal assays, with demographic details, clinical features and biochemical parameters documented in a structured case report form. Baseline investigations included routine hematological and biochemical tests, contrast MRI pituitary, comprehensive hormonal assays by electrochemiluminescence, and specialized tests such as OGTT, dexamethasone suppression and dehydration tests when indicated. Data were analyzed using SPSS version 23. Categorical variables were expressed as percentages, and continuous variables as mean ± SD. Chi-square and t-tests were applied. A p-value <0.05 was considered significant.

Ethical Consideration: Ethical clearance and written informed consent were obtained prior to the study.

In this study, most patients were aged 41–50 years (56.6%), with a female predominance (53.3%). Headache (83.3%) was the commonest symptom, followed by vomiting and visual disturbances. Non-functioning adenomas predominated (60%). Mean biochemical values were within expected ranges. MRI was used in all patients, with macroadenomas (90%) being more common than microadenomas.

Table 1: Distribution of cases according to clinical presentation, neurological manifestations and cardiovascular abnormalities in patients with pituitary adenoma.

In this study, cardiovascular abnormalities (43.3%) were most common, followed by neurological manifestations (36.6%) and sexual disturbances (20%). Acromegalic features were seen in 23.3%. Headache predominated neurologically (76.9%), while carotid intima-media thickness (27.27%) was the commonest cardiovascular abnormality.

Figure 1: Distribution of cases according to Signs.

Here we found that 50% patients with visual Disturbance followed by 20% with paresis.

Table 2: Correlation of symptoms with type of adenomas.

Here we classified adenoma with symptoms. We found that headache and vomiting was seen majorly in growth hormone, NFPA and prolactinoma patients.

Table 3: Correlation of signs with type of adenoma.

Here we found that fatigue was most commonly seen in all the subtype of adenomas i.e 83.3% in growth hormone, 100% in NFPA and 100% in prolactinoma patients.

Table 4: Correlation of clinical and hormonal investigations with the type of pituitary adenoma.

In this study, clinical and hormonal investigations were correlated with different types of pituitary adenomas, including growth hormone–secreting adenomas, non-functioning pituitary adenomas, and prolactinomas, to assess variations in presentation and biochemical profiles

Pituitary tumors are common intracranial neoplasms with a prevalence of 1/1000, though clinically overt cases are rare.7 Autopsy studies reveal higher occult prevalence. Prolactinomas are most frequent.8 This study presents our clinical, biochemical, radiological and ophthalmological experience to aid improved management.

In the present study, cardiovascular abnormalities (43.3%) were the most frequent clinical presentation, followed by neurological manifestations (36.6%) and sexual disturbances (20%); acromegalic features were observed in 23.3% patients. Headache was the commonest neurological symptom. Asadi Lari et al.9 reported lower acromegaly prevalence, whereas Zerehpoosh et al.10 observed significantly higher rates, highlighting clinical variability.

In distribution of signs, Zargar A H et al11 reported elevated post-prandial glucose levels and macroadenomas in all patients, indicating metabolic and mass-effect signs. Modi et al12 observed that growth hormone–secreting tumors were usually large, with hormone levels correlating with tumor size, emphasizing tumor-related clinical and biochemical signs.

Correlation of signs with adenoma type showed that non-functioning pituitary adenomas commonly presented with mass-related signs. Cury Licia M et al.13 reported hypopituitarism and neuro-ophthalmological signs in 89% patients, with headache and visual field defects in 68%. Similarly, Abbara A et al.14 observed visual abnormalities and ocular palsies as predominant signs, reflecting pressure effects of larger adenomas.

Correlation of symptoms with adenoma type showed that non-functioning pituitary adenomas commonly presented with mass-related symptoms. Cury Licia M et al.13 reported hypopituitarism, headache (68%) and visual field defects (68%) as predominant features. Similarly, Ferrante et al.15 found headache (41.4%) and visual deficits (67.8%) to be the most frequent symptoms in NFPAs.

In the present study, headache, vomiting and visual disturbances were common across growth hormone–secreting, prolactinoma and non-functioning pituitary adenomas, reflecting mass effects, while hormonal abnormalities varied by adenoma type. Zerehpoosh F B et al.10 similarly reported pressure-related symptoms and hormone-specific features, and Modi et al.12 demonstrated that growth hormone levels correlated with tumor size in GH-producing adenomas.

Our findings corroborate demographic, clinical, biochemical features, risk factors and tumor types reported in large pituitary apoplexy series. Headache was the predominant symptom, often lasting over one day, and many patients had preceding endocrine dysfunction. These observations highlight the need for prospective randomized trials to determine optimal timing between surgical and conservative management strategies

1. Coire CI, Horvath E, Kovacs K, Smyth HS, Ezzat S. Cushing’s syndrome from an ectopic pituitary adenoma with peliosis: A histological, immunohistochemical, and ultrastructural study and review of the literature. Endocr Pathol 1997;8:65‑74.
2. Laws ER, Ebersold MJ, Piepgras DG, et al. The results of transsphenoidal surgery in specific clinical entities. In: Laws ER, Randall RV, Kern EB, et al. Management of Pituitary Adenomas and Related Lesions with Emphasis on Transsphenoidal Microsurgery. New York: AppletonCentury- Crofts, 1982: 277-305.
3. Rajasekaran S, Vanderpump M, Baldeweg S, Drake W, Reddy N, Lanyon M, Markey A, Plant G, Powell M, Sinha S, et al. UK guidelines for the management of pituitary apoplexy Pituitary Apoplexy Guidelines Development Group: May 2010. Clinical Endocrinology 2011 74 9–20.
4. Lloyd RV, Kovacs K, Young WF Jr, Farrell WE, Asa SL, Troillas J, et al. Pituitary tumours’: introduction. In: DeLellis RA, Lloyd RV, Heinz PU, Eng C (eds). Wolrd Health Organization Classifcation of tumours. Pathology and genetics: Tumours of endocrine organs. IARC Press, Lyon. 2004. P. 24-5.
5. Möller-Goede DL, Brändle M, Landau K, Bernays RL & Schmid C. Pituitary apoplexy: re-evaluation of risk factors for bleeding into pituitary adenomas and impact on outcome. European Journal of Endocrinology 2011 164 37–43.
6. Randeva HS, Schoebel J, Byrne J, Esiri M, Adams CB & Wass J. Classical pituitary apoplexy: clinical features, management and outcome. Clinical Endocrinology 1999 51 181–188.
7. Daly AF, Rixhon M, Adam C, Dempegioti A, Tichomirowa MA, Beckers A. High prevalence of pituitary adenomas: A cross‑sectional study in the province of Liege, Belgium. J Clin Endocrinol Metab 2006;91:4769‑75.
8. Thorner MO, Vance ML, Horvath E, Kovacs K. The anterior pituitary. In: Wilson JD, Foster DW, editors. William’s Text book of Endocrinology. 8th ed. Philadelphia (PA): WB Saunders; 1995. p. 221-220.
9. Asadi-Lari M, Sadeghipour AR, Mahouzi L, Solaimani Dodaran M, Fallah A. Assessment of the demographic characteristics and the quality of life in patients with pituitary adenoma in a referral pituitary center in Tehran in 2011. J Rafsanjan Univ Med Sci 2015;13:695-704.
10. Zerehpoosh FB, Sabeti S, Sharifi G, Shakeri H, Alipour S, Arman F. Demographic study of pituitary adenomas undergone trans-sphenoidal surgery in Loghman Hakim Hospital, Tehran, Iran 2001–2013. Indian J Endocr Metab 2015;19:791-6.
11. Zargar A H, Laway B A, Masoodi S R, Salahuddin M. Clinical and endocrine aspects of pituitary tumor. Saudi Med J 2004;25 (10): 1428-1432.
12. Modi KD, Mithal A, Banerji D, Kumar D, Shah P, Jain VK, et al. Growth hormone-producing pituitary tumors: Clinical profile and results of surgery. National Medical Journal of India 1996; 9: 262-265.
13. Cury M L C, Fernandes J C, Machado H R, Elias L L et al. Non-functioning pituitary adenomas: clinical feature, laboratorial and imaging assessment, therapeutic management and outcome. Arq Bras Endocrinol Metab(2009);53/1.
14. Abbara A, Clarke S, Eng P C, Milburn J et al. Clinical and biochemical characteristics of patients presenting with pituitary apoplexy. Endocrine Connections (2018);7:1058–1066.
15. Ferrante E, Ferraroni M, Castrignanò T, Menicatti L, Anagni M, Reimondo G, et al. Non‑functioning pituitary adenoma database: A useful resource to improve the clinical management of pituitary tumors. Eur J Endocrinol 2006;155:823‑9.