Overview]
Pituitary adenomas are common benign tumors with a general population occurrence word of 1 per 100,000. Some reports are as high as 7/100,000. Among intracranial tumors, it is only lower than glioblastosis and meningioma, accounting for about 10% of intracranial tumors, and the detection rate of them in autopsy is 20%-30%. There is a trend of increase in recent years.
Pituitary adenoma mainly harms human body from the following aspects.
(1) Excessive secretion of pituitary hormones causes a series of metabolic disorders and organ damage;
(2) Tumor compression makes other pituitary hormones low, causing the corresponding target gland’s low function;
(3) Compression of structures in the pterionic saddle area, such as optic cross, optic nerve, cavernous sinus, fundic artery, hypothalamus, III ventricle, even involving frontal lobe, frontal lobe, brain stem, etc., leading to serious impairment of corresponding functions. Since the late 19th century, people’s understanding of pituitary adenoma has been deepened, especially since the 1970s, with the rapid progress of modern science and technology, modern endocrinology, modern pathology, modern radiology, modern neuro-ophthalmology, modern microsurgery, and modern neurosurgery. The development of modern endocrinology, modern pathology, modern radiology, modern neuro-ophthalmology and modern microsurgery has led to many new advances in clinical and basic research on pituitary adenoma. This has deepened the understanding of the disease and improved the diagnosis and treatment level.
Clinical manifestations
Various endocrine cells in the pituitary gland can produce corresponding endocrine cell adenomas, causing endocrine function disorders. In the early stage of microadenoma, signs of endocrine hyperfunction can appear. As the adenoma grows and develops, it may compress and erode the pituitary tissue and its pituitary and peripituitary structures, resulting in hypoendocrine function, visual function and other cranial nerve and brain symptoms.
(1) Clinical manifestations of functional pituitary glands
(1) Prolactin adenoma: It is mainly characterized by amenorrhea, overflow of milk and infertility due to increased prolactin and decreased female hormone, also known as Forbis syndrome.
(2) Growth hormone adenoma: Due to excessive secretion of growth hormone, early microadenomas of a few millimeters can cause metabolic disorders, resulting in a series of changes in epiphysis, soft tissue and visceral overgrowth, etc. The course of the disease is slow and progressive.
(3) Adrenocorticotropic hormone adenoma: As the pituitary gland continues to secrete too much AcTH, it causes adrenocortical hyperplasia and excessive secretion of cortisol, i.e. Cushin8rsSyndrome. Resulting in a series of substance metabolism disorders and pathological changes, and many clinical symptoms and signs.
(4) Thyroid-stimulating hormone cell adenoma: Rare. Due to excessive TSH secretion, T2 and T. The clinical symptoms of hyperthyroidism are increased. There are also TsH adenomas caused by negative feedback secondary to hypothyroidism (e.g., thyroiditis, after homoeopathic treatment). The adenoma enlarges the butterfly saddle. Suprasellar development and visual dysfunction occur.
(5) Gonadotropin cell adenocarcinoma: Rare. Due to excessive secretion of FsH and LH, it may be asymptomatic in the early stage, but in the late stage, there is hypogonadism, amenorrhea, infertility, impotence, male IX atrophy and decrease in sperm count. Visual dysfunction may occur when the swelling grows. Some people divide into FsH cell adenoma and LH cell adenoma.
(6) Nonsecretory adenoma: Mostly seen in middle-aged men and postmenopausal women, it used to be called pituitary suspicious cell adenoma, which lacks plasma hormone levels and has no significant clinical symptoms. However, immunocytochemical and electron microscopic morphological studies have shown that FSH, ACTH, and H are still found in the tumor. -subunit, and also the presence of Bu LH, p-FSH, p-TSH. in cell culture studies with special oligonucleotide cDNAs hybridization techniques, can be produced. -subunit, B-LH subunit, etc. Since special glycoprotein subunits can be measured, it has been hypothesized that nonfunctional pituitary carpal tumors may be special glycoprotein tumors.
(2) Headache
In the early stage, about 2/3 of patients have headache, mainly located in the retro-orbital area, forehead and bilateral frontal areas, with mild and intermittent attacks, mostly caused by direct stimulation of tumor or increased intra-saddle pressure, resulting in pressure on pituitary dural sac and saddle diaphragm. When the tumor breaks through the saddle diaphragm and the intra-saddle pressure decreases, the pain can be reduced or disappeared. Late stage headache can be caused by the development of tumor to the saddle and invade the ridge membrane and blood vessels of skull base and compress the trigeminal nerve. In some cases, the suprasellar development of giant adenoma may cause obstruction of interventricular foramen or aqueduct. The headache is more severe when the intracranial pressure is increased. Or tumor necrosis or hemorrhage. The pressure inside the tumor increases sharply. If the tumor wall rupture causes pituitary stroke and subarachnoid hemorrhage, the headache will be sudden and severe with other neurological symptoms.
(3) Visual field impairment
Before the pituitary adenoma compresses the optic nerve, there is no visual field disturbance. Some scholars have studied that the blood supply microvessels in the middle part of the inferior optic cross are sparser than those in the lateral part, and the middle part is weaker than the posterior part, because the microadenoma with high perfusion state interferes with the normal blood supply of the optic cross by “stealing” the common supply vessels with the optic cross. The microadenoma “steals” the normal blood supply to the optic chiasm through its common supply vessel with the optic chiasm. As the tumor grows. About 60%-80% of the cases may have different parts of the visual pathway compressed. The tumor may cause different visual dysfunctions, typically bilateral temporal hemianopia. According to the arrangement of fibers in the visual pathway, the frontal superior quadrant is typically involved first, initially as a bundle defect, and then as a patch. The red visual field is affected first, followed by the white visual field. As the tumor increases in size, the inferior temporal, inferior nasal and superior nasal quadrants become involved in turn. This can lead to total blindness. If the tumor is deviated to one side, monocular partially blindness becomes total blindness. In a small number of cases, the tumor may develop in the posterior saddle. If the tumor develops to the posterior saddle and involves the third ventricle, there may be no visual field impairment. Most of the severe visual impairment is caused by advanced tumor optic nerve atrophy.
(4) Other neurological and brain damage
If the tumor develops posteriorly and superiorly and presses the pituitary stalk and hypothalamus, uveitis and hypothalamic dysfunction may occur; if the third ventricle, interventricular foramen and aqueduct are involved, intracranial pressure may increase. Anterior extension to the frontal lobe can cause psychiatric symptoms, epilepsy, and olfactory disturbance. Lateral invasion of the cavernous sinus may cause II, IV, V, VI cranial nerve palsy, and protrusion into the middle cranial fossa may cause frontal lobe epilepsy. If it grows backward into the interpeduncular sinus and slopes to compress the brainstem, crossed paralysis and coma may occur. Downward protrusion into the pterygoid sinus, nasal cavity and nasopharynx may cause epistaxis and cerebrospinal fluid leakage. Intracranial infection may occur.
Ancillary tests
Magnetic resonance F is the best test to diagnose this disease. Magnetic resonance imaging (MRI): MRI can distinguish small tissue differences and is good for imaging the pituitary gland and tumors, but is not sensitive to the dense bone of the pterygoid saddle. Because pituitary adenoma in the saddle, often short T1 and long T2, and cavernous sinus, large dL canal, optic nerve, optic cross, brain parenchyma and suprasellar pool, cerebrospinal fluid and other tissue structures are clearly visible. MRI (1.5Tesla) enhanced thin layer tomography, the detection rate of <5mm microglandular collapse is 50% a 60%. However, it is not as good as cT and x-ray to understand the bone changes in the pterygoid saddle area.
Treatment and prognosis
(1) Surgical treatment
Nowadays, for early stage pituitary microadenoma of only a few millimeters. Visual acuity and visual field can be diagnosed before they are affected. A large number of cases have been reported to achieve complete removal of the tumor and preservation of pituitary function under surgical visualization. With more experience, not only intra-saddle tumors but also large adenomas or even giant pituitary adenomas that extend suprasellarly can be safely removed. At present, transsphenoidal microsurgery for pituitary adenomas has been widely adopted by neurosurgeons in China and abroad and is constantly evolving. However, craniotomy is still required for pituitary tumors that develop paracranially or involve the middle cranial fossa. In order to eliminate the tumor, decompress the optic pathway and restore the function of the pituitary gland. Currently, there are two main types of surgery: transcranial surgery and transsphenoidal surgery. In addition, there are stereotactic surgery (transcranial or transsphenoidal), intracranial implantation of isotope gold 180, iridium 90, radiosurgery (Y-knife and x-knife), etc.
(2) Radiation therapy
Radiation therapy is suitable for pituitary adenoma and primary adenoidal wet or metastatic tumor cases where surgery is incomplete or may recur. Generally speaking, radiation therapy is more sensitive to those who have substantial changes than those who have cystic changes. It can control the tumor development, sometimes shrink the tumor and improve the visual field, but it cannot cure the tumor at all. It can be used for those who are too old and frail for surgery, or those whose surgical resection is not complete. During the course of radiation therapy, sometimes the tumor may become necrotic and bleeding, which may lead to a dramatic loss of vision or even blindness, so radiation therapy should be interrupted immediately and surgery should be performed to save vision. In late stage, the optic nerve of larger pituitary tumor is heavily compressed and its blood supply is very poor. Radiation therapy can sometimes cause the loss of only – point vision, but it can control the development of the tumor, which is still beneficial to the patient. Due to the different nature of pituitary tumors. The response of the tumor to pressure and endocrine function are different, and the impact of radiotherapy is also different.
(3)Drug therapy
Pharmacological treatment includes bromocriptine for PRL adenoma, GH adenoma and ACTH adenoma. Post-growth inhibitor or estrogen for GH adenoma. Cyproheptadine and biphenyldichloroethane, helium-based conductive sleep energy, mepivoxil, etomidate, and chlorophenylacetophenone for AcTH adenomas. Non-functioning adenomas and hypopituitarism. Various hormone replacement therapies are used.