Adult panhypopituitarism

Introduction to adult hypopituitarism Endocrine deficiency syndrome due to loss of partial or complete anterior pituitary function. The most common cause of pituitary decline. Note that decreased LH and FSH secretion may be caused by excessive PRL secretion and lead to secondary hypogonadism. Pituitary apoplexy, if there is a visual field disorder or sudden numbness of the oculomotor nerve, or if the hypothalamic oppression, lethargy gradually dizzy, should be treated immediately. Although high-dose corticosteroid medical treatment and general support are sufficient for a small number of cases, routine decompression of the butterfly as a hemorrhagic tumor should be performed immediately. basic knowledge The proportion of illness: 0.03% Susceptible people: no specific people Mode of infection: non-infectious Complications: amenorrhea

Adult total pituitary dysfunction

Endocrine deficiency syndrome due to loss of partial or complete anterior pituitary function. The most common cause of pituitary decline. Note that decreased secretion of LH and FSH may be caused by excessive PRL secretion and lead to secondary hypogonadism.

Adult total pituitary dysfunction prevention

The etiology of this disease is not clear, and may have certain correlation with environmental factors, genetic factors, dietary factors, and mood and nutrition during pregnancy. Therefore, it is impossible to directly prevent the disease against the cause. Early detection, early diagnosis, and early treatment are important for indirect prevention of this disease, and can also reduce complications such as short stature and short stature.

Adult total pituitary dysfunction complications Complications amenorrhea

Women lack LH and FSH, often complicated by amenorrhea, secondary sexual deterioration, infertility, castration or menopausal female symptoms are typical manifestations of gonads. Men lack gonadotropin, often with impotence, testicular atrophy, secondary sexual deterioration And sperm production reduces infertility.

Symptoms of hypopituitarism in adults Common symptoms Postpartum pituitary necrosis tachycardia Adult growth hormone secretion deficiency Drowsiness pituitary dysfunction palpitations loss of consciousness Blood pressure decline Cortical dysfunction

Before the treatment of life-long hormone replacement therapy, the diagnosis of pituitary dysfunction must be established. There should be pituitary morphological abnormalities and hormone deficiency. The skull X-ray and visual field measurement of the sella will prove the presence of tumors. High-resolution CT or MRI (enhanced when needed) Agent) is the preferred method. When there is no high-resolution CT, the multi-layered slide of the saddle can be used. The stratified radiograph of the positron flow is used as a research tool in a few special centers. The cerebral angiography is only when the X-ray examination prompts An indication of an abnormality in the parasagittal vascular or hemangioma. When there is no modern neuroradiation device, a simple low-conduit pituitary axon is a reasonable preferred method for pituitary adenomas >10 mm in diameter.

When suspected of hypopituitarism, first assess the need to check for TSH and ACTH deficiency, because these two diseases may be life-threatening.

Thyroid function assessment Radioimmunoassay can measure T4, T3 and TSH. It should be all levels lower, due to increased TSH, indicating primary thyroid dysfunction. Using synthetic TRH200~500g intravenous bolus can identify hypothalamic lesions or pituitary lesions. The peak of TSH response to TRH is generally seen 30 minutes after injection, and the TSH of hypothalamic disease is elevated. Unfortunately, some patients with primary pituitary disease also have this type of reaction. In other pituitary diseases, TSH can respond to TRH. Any TSH increases.

Assessment of ACTH secretion in some patients with adrenal insufficiency basal blood cortisol in the normal range, but reduced storage function, low response to one or more ACTH-adrenal axis stimulation test. Evaluation of the most ACTH (and GH and PRL) stocks A reliable method is insulin tolerance test, the dose is regular insulin 0.1u / kg body weight, intravenous bolus injection within 15 ~ 30 seconds, zero time (before insulin injection), then 20, 30, 45, 60 and 90 minutes to collect venous blood Determination of GH cortisol and glucose levels. If serum glucose decreased slightly by 50% to <40mg/dl (2.22mmol/L), the test should be repeated. (Note: This test may have severe total pituitary dysfunction or DM and elderly patients may have Accidents, contraindications for patients with ischemic heart disease and epilepsy. During the test, there should be medical staff next to it. Usually only transient hyperhidrosis, tachycardia, neuroticism. Such as patients complained of palpitations, loss of consciousness, epilepsy Onset, the test should be terminated immediately, with a 50% glucose bolus.

The insulin tolerance test does not distinguish between primary (Addison's disease) and secondary (pituitary dysfunction) adrenal insufficiency. This distinction and assessment of the hypothalamic-pituitary-adrenal axis test in Section 9 Addison's Laboratory Description in the inspection.

PRL assessment of patients with total pituitary decline, PRL is not always inhibited. In fact, in the hypothalamic disease due to loss of dopamine inhibition of PRL, there may be increased PRL. Hyperprolactinemia results, often accompanied by gonadotropin hypoxia and succession Hair loss.

GH assessment adults do not advocate the lack of routine screening for GH, because even if GH deficiency is found, it is customary to not treat, unless the skeleton is not closed, the short stature patient. Adult insulin-like growth factor-1 (IGF-1) normally indicates the absence of GH deficiency However, the low value does not prove GH deficiency.

GH determination in children is generally helpful, but only after the stimulation test. The GH response is generally abnormal due to thyroid and adrenal insufficiency. The stimulation test must be performed after sufficient hormone replacement therapy. The insulin tolerance test can be most effective. GH release. Less risky and less reliable is the arginine GH release test (500mg/kg, intravenous infusion for 30 minutes), levodopa oral (500mg for adults, 10mg/kg for children), sleep or 20 minutes After strenuous exercise, clonidine (4 g/kg orally) is another powerful stimulant for GH release, which is a promising alternative to insulin. The side effects are only lethargy and mild blood pressure drop. In general, GH > 10 ng / ml or excitement The post-GH response >5 ng/ml is sufficient to rule out GH deficiency. The increase in GH is <5 ng/ml or <10 ng/ml after excitation, which is difficult to explain.

The standard for normal response is artificially determined. All GH secretion tests can occasionally produce misleading results. Because there is no single test that is 100% effective in stimulating GH release, at least two different tests should be performed in the absence of GH response. Insulin and sulphur After acid, the peak of GH is between 30 and 90 minutes. After oral administration of levodopa, the peak of GH is between 30 and 120 minutes. It begins to fall asleep. After 20 minutes of clonidine and strenuous exercise, the peak of GH is between 60 and 120 minutes.

Exogenous GHRH assessment of GH secretion value has not been determined. Normal people, GHRH1g / kg, intravenous bolus injection 11 ~ 30 seconds can lead to the largest, but there is a change in GH release. Typically peaked about 60 minutes after GHRH bolus. The change in pituitary GHRH response is consistent with the hypothesis that intermittent . . . . . . The hypothalamic and pituitary lesions are still unclear. Children with GH deficiency may be secondary to GHRH deficiency. The highly variable response of GH to GH-RH has been reported.

It is known that the challenge test does not detect mild defects that regulate the release of GH. For example, in short stature children secondary to GH secretion dysfunction, the GH release challenge test is usually normal. However, a series of GH measurements are performed 12 to 24 hours, indicating these The total GH secretion in children 12 to 24 hours is lower than normal.

Evaluation of serum LH and FSH without the use of exogenous estrogen in menopausal women, the determination of these hormones in the basal state is most helpful in assessing pituitary dysfunction. These menopausal women, usually GnH is high (>30mIU/ml). And FSH is rarely helpful to others. Although the whole pituitary function is reduced, GnH is low, but it overlaps with the normal values of LH and FSH. Synthetic GnRH 100g intravenously, LH and FSH should have increased reactivity. The peak of LH after GnRH injection is about At 30 minutes, the peak of FSH was 40 minutes. However, the response to GnRH was normal, low, and lacking in hypothalamic-pituitary dysfunction. LH and FSH had large changes in the normal increase in GnRH response, and were helpless with exogenous GnRH. Identification of primary hypothalamic and primary pituitary disease.

Evaluation of multiple hormones Simultaneous determination of several pituitary hormone stores is the most effective method for assessing pituitary function. Insulin (regular insulin 0.1 u / kg), TRH (200 g), GnRH (100 g) together with intravenous bolus injection within 15 to 30 seconds Blood glucose, cortisol, GH, TSH, PRL, LH, FSH and ACTH were measured multiple times in 180 minutes. Another method was insulin alone, and TRH and GnRH were given simultaneously after 120 minutes. According to the recommended GHRH (1 g/kg), CRH (1g/kg) and TRH, GnRH together with intravenous bolus, insulin is not necessary as a part of the combined pre-pituitary function test, the application of these release hormones in the pituitary test remains to be established. In any case, the normal response is the same as before Said.

Adult full pituitary dysfunction check

1. Skull X-ray and visual field measurement of the sella will prove the presence of tumor;

2. High resolution CT or MRI (using a fortifier when needed) is the preferred method;

3. Cerebral angiography: only when X-ray examination indicates an abnormality of the parasagittal vascular or hemangioma;

4. Check TSH and ACTH;

Diagnosis and differentiation of adult total pituitary dysfunction

Total pituitary dysfunction must also be differentiated from certain other diseases, including anorexia nervosa, chronic liver disease, myotonic dystrophy, multi-gland autoimmune disease. Clinical features of anorexia nervosa (generally found in women) can usually be diagnosed Symptoms include cachexia, abnormal food and body shape, although amenorrhea, but secondary sexual characteristics still exist, basal levels of GH and cortisol generally increase. Because hypothalamic lesions can control appetite central disorders, suspected anorexia nervosa, X-ray saddle inspection should be done.

Alcoholic cirrhosis or hemochromatosis, when there is testicular atrophy with general weakness, often suspected pituitary dysfunction. However, in most cases, potential primary disease can be found, laboratory tests can rule out pituitary dysfunction. Rarely have a broad morphological basis for pituitary dysfunction.

Patients with myotonic dystrophy complain of progressive muscle weakness, early baldness, cataract, suggesting premature aging face; men may have testicular atrophy. Endocrine examination can rule out pituitary dysfunction.

Multi-gland autoimmune disease, usually with two or more endocrine hormone deficiency. If these are pituitary gland hormones, it should be considered pituitary. Determination of pituitary hormones will prove normal pituitary function, unless lymphocytic pituititis is Part of the syndrome.

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