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Anatomical and functional imaging in endocrine hypertension.

Chaudhary V, Bano S - Indian J Endocrinol Metab (2012)

Bottom Line: In endocrine hypertension, hormonal excess results in clinically significant hypertension.The functional imaging (such as radionuclide imaging) complements anatomy-based imaging (such as ultrasound, computed tomography, and magnetic resonance imaging) to facilitate diagnostic localization of a lesion causing endocrine hypertension.The aim of this review article is to familiarize general radiologists, endocrinologists, and clinicians with various anatomical and functional imaging techniques used in patients with endocrine hypertension.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiodiagnosis, Employees' State Insurance Corporation (ESIC) Model Hospital, Gurgaon, Haryana, India.

ABSTRACT
In endocrine hypertension, hormonal excess results in clinically significant hypertension. The functional imaging (such as radionuclide imaging) complements anatomy-based imaging (such as ultrasound, computed tomography, and magnetic resonance imaging) to facilitate diagnostic localization of a lesion causing endocrine hypertension. The aim of this review article is to familiarize general radiologists, endocrinologists, and clinicians with various anatomical and functional imaging techniques used in patients with endocrine hypertension.

No MeSH data available.


Related in: MedlinePlus

Pituitary microadenoma. A 30-year-old male with features of Cushing's syndrome due to pituitary microadenoma. High-resolution dynamic contrast-enhanced T1-weighted coronal (a) and sagittal (b) images of brain (at 60 s) show a small nonenhancing (dark) microadenoma (arrow) lateralized to right side of the pituitary gland. The normal pituitary gland shows marked homogenous enhancement
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Figure 2: Pituitary microadenoma. A 30-year-old male with features of Cushing's syndrome due to pituitary microadenoma. High-resolution dynamic contrast-enhanced T1-weighted coronal (a) and sagittal (b) images of brain (at 60 s) show a small nonenhancing (dark) microadenoma (arrow) lateralized to right side of the pituitary gland. The normal pituitary gland shows marked homogenous enhancement

Mentions: Hypertension is one of the most distinguishing features of Cushing's syndrome. Cushing's syndrome (CS), a hormonal disorder of excess cortisol production can often be quite challenging to diagnose. The disease is broadly classified into two group, that is, ACTH-dependent or ACTH-independent Cushing's syndrome. In both ACTH-dependent and ACTH-independent CS patients, CT, and/or MRI is the primary imaging modality for localization of the lesion, while scintigraphy is a useful confirmatory imaging method. ACTH-dependent Cushing's syndrome accounts for about 80% of all cases and is either due to a ACTH secreting pituitary adenoma (common) or extrapituitary neoplasm with ectopic ACTH production (uncommon). Ectopic sources of ACTH derive from a diverse group of tumor types that are more common in men after age of 40-years. Among these small-cell lung carcinoma and carcinoid tumors (bronchial, pancreatic, thymic, and disseminated), medullary thyroid carcinoma and pheochromocytoma tend to predominate; other less common causes include pancreatic carcinoma, gall bladder carcinoma, colonic carcinoma, and mesothelioma. Imaging of pituitary is an important part of the investigation of ACTH-dependent Cushing's syndrome to identify a possible pituitary lesion. The pituitary tumors in CS are usually microadenomas, which are 10 mm or less in diameter. Macroadenomas (>10 mm) are uncommon in patients with CS. MRI is the method of choice for evaluation of pituitary tumors. Modern MRI techniques using T1-weighted spin echo and/or spoiled gradient recalled acquisition (SPGR) techniques will identify an adenoma in up to 80% of patients with Cushing's disease. On MRI, 95% of microadenomas exhibit a hypointense signal with no postgadolinium enhancement [Figure 2]; however, remaining 5% have an isointense signal on postgadolinium scan. CT scan is less sensitive (40–50%) and inferior to MRI in detecting pituitary microadenomas, and it should be therefore reserved for patients in whom MRI is contraindicated or unavailable. CT imaging typically shows a hypodense lesion that fails to enhance postcontrast.[17–19] Unfortunately, normal-appearing pituitary may occur in some patients with Cushing disease due to both diffuse hyperplasia of ACTH-producing cells and small microadenomas that are not detected on imaging studies. In the latter case, ACTH lateralization during an inferior petrosal sinus sampling (IPSS) study may be useful in lateralizing the occult lesion and in guiding surgical therapy.[20] In one study, IPSS could correctly localize the lesion in 23 of 34 patients of Cushing's disease, giving a sensitivity of 67.6%, and picked up all the four patients with ectopic Cushing's syndrome and one with adrenal carcinoma, thereby giving 100% specificity.[21] PET scanning helps to monitor the efficacy of treatment in patients with pituitary adenoma, particularly when the tumor size seems unchanged or there is need to decide on the course of a drug regimen. Chest and abdominal CT scans should be performed in patients with suspected ectopic ACTH production. Somatostatin scintigraphy may also be helpful in detecting ectopic ACTH tumors, as majority of ectopic ACTH secreting tumors are of neuroendocrine origin and typically have cell surface receptors for somatostatin.[22] Conversely, the ACTH-independent Cushing's syndrome (adrenal Cushing′s) is always caused by primary adrenal disease that secretes excess cortisol; it results from an adrenal adenoma (including adenoma within myelolipoma) and adrenal carcinoma accounting for 92% of cases, but rarely may be caused by bilateral adrenal hyperplasia (micronodular or macronodular).[171823] Cross-sectional imaging (CT and MRI) appearance of cortisol-secreting adrenal adenoma is similar to that of APA, being relatively small (<5 cm), homogenous, and ovoid, with features consistent with intracellular lipid. Adrenocortical carcinoma is a rare, highly malignant tumor affecting patients with a median age of about 43-years. Typical imaging features include large size at presentation, heterogeneous contrast enhancement, intratumoral calcification, hemorrhage, and necrosis. The majority of affected patients have metastatic disease (to lung and liver) at presentation; tumor invasion of IVC is also commonly reported.[2425] On scintigraphy, in adrenal carcinoma, adrenal glands are not visualized bilaterally. These neoplasms do not accumulate sufficient tracer for visualization on scintigraphy.[26] Bilateral micronodular and macronodular adrenal hyperplasia have characteristic imaging features. On cross-sectional imaging, bilateral micronodular adrenal hyperplasia, also known as primary pigmented nodular adrenal dysplasia (PPNAD) typically shows normal appearing adrenal glands with multiple small nodules of 2–5 mm size.[27] Whereas, in bilateral macronodular adrenal hyperplasia, also known as ACTH-independent macronodular adrenal hyperplasia (AIMAH), both glands are grossly enlarged and contains relatively larger nodules measuring up to 5 cm in diameter.[28] Iodine-131-labelled adrenal scintigraphy in patients with bilateral nodular adrenal hyperplasia (PPNAD and AIMAH) show bilateral increased uptake.[26] Most cases of PPNAD occur as part of the Carney complex (CNC). CNC is a familial multiple neoplasia and lentigines syndrome associated with (i) PPNAD, (ii) hyperpigmentation of skin, and (iii) a variety of nonendocrine (myxomas of the heart, skin or breast) and endocrine tumors (growth hormone producing pituitary adenoma, testicular Sertoli cell tumor, Leydig cell tumor, and adrenal rest tumors). Cushing's syndrome occurs in approximately 30% of cases of CNC.[29]


Anatomical and functional imaging in endocrine hypertension.

Chaudhary V, Bano S - Indian J Endocrinol Metab (2012)

Pituitary microadenoma. A 30-year-old male with features of Cushing's syndrome due to pituitary microadenoma. High-resolution dynamic contrast-enhanced T1-weighted coronal (a) and sagittal (b) images of brain (at 60 s) show a small nonenhancing (dark) microadenoma (arrow) lateralized to right side of the pituitary gland. The normal pituitary gland shows marked homogenous enhancement
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3475894&req=5

Figure 2: Pituitary microadenoma. A 30-year-old male with features of Cushing's syndrome due to pituitary microadenoma. High-resolution dynamic contrast-enhanced T1-weighted coronal (a) and sagittal (b) images of brain (at 60 s) show a small nonenhancing (dark) microadenoma (arrow) lateralized to right side of the pituitary gland. The normal pituitary gland shows marked homogenous enhancement
Mentions: Hypertension is one of the most distinguishing features of Cushing's syndrome. Cushing's syndrome (CS), a hormonal disorder of excess cortisol production can often be quite challenging to diagnose. The disease is broadly classified into two group, that is, ACTH-dependent or ACTH-independent Cushing's syndrome. In both ACTH-dependent and ACTH-independent CS patients, CT, and/or MRI is the primary imaging modality for localization of the lesion, while scintigraphy is a useful confirmatory imaging method. ACTH-dependent Cushing's syndrome accounts for about 80% of all cases and is either due to a ACTH secreting pituitary adenoma (common) or extrapituitary neoplasm with ectopic ACTH production (uncommon). Ectopic sources of ACTH derive from a diverse group of tumor types that are more common in men after age of 40-years. Among these small-cell lung carcinoma and carcinoid tumors (bronchial, pancreatic, thymic, and disseminated), medullary thyroid carcinoma and pheochromocytoma tend to predominate; other less common causes include pancreatic carcinoma, gall bladder carcinoma, colonic carcinoma, and mesothelioma. Imaging of pituitary is an important part of the investigation of ACTH-dependent Cushing's syndrome to identify a possible pituitary lesion. The pituitary tumors in CS are usually microadenomas, which are 10 mm or less in diameter. Macroadenomas (>10 mm) are uncommon in patients with CS. MRI is the method of choice for evaluation of pituitary tumors. Modern MRI techniques using T1-weighted spin echo and/or spoiled gradient recalled acquisition (SPGR) techniques will identify an adenoma in up to 80% of patients with Cushing's disease. On MRI, 95% of microadenomas exhibit a hypointense signal with no postgadolinium enhancement [Figure 2]; however, remaining 5% have an isointense signal on postgadolinium scan. CT scan is less sensitive (40–50%) and inferior to MRI in detecting pituitary microadenomas, and it should be therefore reserved for patients in whom MRI is contraindicated or unavailable. CT imaging typically shows a hypodense lesion that fails to enhance postcontrast.[17–19] Unfortunately, normal-appearing pituitary may occur in some patients with Cushing disease due to both diffuse hyperplasia of ACTH-producing cells and small microadenomas that are not detected on imaging studies. In the latter case, ACTH lateralization during an inferior petrosal sinus sampling (IPSS) study may be useful in lateralizing the occult lesion and in guiding surgical therapy.[20] In one study, IPSS could correctly localize the lesion in 23 of 34 patients of Cushing's disease, giving a sensitivity of 67.6%, and picked up all the four patients with ectopic Cushing's syndrome and one with adrenal carcinoma, thereby giving 100% specificity.[21] PET scanning helps to monitor the efficacy of treatment in patients with pituitary adenoma, particularly when the tumor size seems unchanged or there is need to decide on the course of a drug regimen. Chest and abdominal CT scans should be performed in patients with suspected ectopic ACTH production. Somatostatin scintigraphy may also be helpful in detecting ectopic ACTH tumors, as majority of ectopic ACTH secreting tumors are of neuroendocrine origin and typically have cell surface receptors for somatostatin.[22] Conversely, the ACTH-independent Cushing's syndrome (adrenal Cushing′s) is always caused by primary adrenal disease that secretes excess cortisol; it results from an adrenal adenoma (including adenoma within myelolipoma) and adrenal carcinoma accounting for 92% of cases, but rarely may be caused by bilateral adrenal hyperplasia (micronodular or macronodular).[171823] Cross-sectional imaging (CT and MRI) appearance of cortisol-secreting adrenal adenoma is similar to that of APA, being relatively small (<5 cm), homogenous, and ovoid, with features consistent with intracellular lipid. Adrenocortical carcinoma is a rare, highly malignant tumor affecting patients with a median age of about 43-years. Typical imaging features include large size at presentation, heterogeneous contrast enhancement, intratumoral calcification, hemorrhage, and necrosis. The majority of affected patients have metastatic disease (to lung and liver) at presentation; tumor invasion of IVC is also commonly reported.[2425] On scintigraphy, in adrenal carcinoma, adrenal glands are not visualized bilaterally. These neoplasms do not accumulate sufficient tracer for visualization on scintigraphy.[26] Bilateral micronodular and macronodular adrenal hyperplasia have characteristic imaging features. On cross-sectional imaging, bilateral micronodular adrenal hyperplasia, also known as primary pigmented nodular adrenal dysplasia (PPNAD) typically shows normal appearing adrenal glands with multiple small nodules of 2–5 mm size.[27] Whereas, in bilateral macronodular adrenal hyperplasia, also known as ACTH-independent macronodular adrenal hyperplasia (AIMAH), both glands are grossly enlarged and contains relatively larger nodules measuring up to 5 cm in diameter.[28] Iodine-131-labelled adrenal scintigraphy in patients with bilateral nodular adrenal hyperplasia (PPNAD and AIMAH) show bilateral increased uptake.[26] Most cases of PPNAD occur as part of the Carney complex (CNC). CNC is a familial multiple neoplasia and lentigines syndrome associated with (i) PPNAD, (ii) hyperpigmentation of skin, and (iii) a variety of nonendocrine (myxomas of the heart, skin or breast) and endocrine tumors (growth hormone producing pituitary adenoma, testicular Sertoli cell tumor, Leydig cell tumor, and adrenal rest tumors). Cushing's syndrome occurs in approximately 30% of cases of CNC.[29]

Bottom Line: In endocrine hypertension, hormonal excess results in clinically significant hypertension.The functional imaging (such as radionuclide imaging) complements anatomy-based imaging (such as ultrasound, computed tomography, and magnetic resonance imaging) to facilitate diagnostic localization of a lesion causing endocrine hypertension.The aim of this review article is to familiarize general radiologists, endocrinologists, and clinicians with various anatomical and functional imaging techniques used in patients with endocrine hypertension.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiodiagnosis, Employees' State Insurance Corporation (ESIC) Model Hospital, Gurgaon, Haryana, India.

ABSTRACT
In endocrine hypertension, hormonal excess results in clinically significant hypertension. The functional imaging (such as radionuclide imaging) complements anatomy-based imaging (such as ultrasound, computed tomography, and magnetic resonance imaging) to facilitate diagnostic localization of a lesion causing endocrine hypertension. The aim of this review article is to familiarize general radiologists, endocrinologists, and clinicians with various anatomical and functional imaging techniques used in patients with endocrine hypertension.

No MeSH data available.


Related in: MedlinePlus