Secondary adrenal insufficiency

Introduction to secondary adrenal insufficiency Secondary adrenal insufficiency is due to a lack of adrenal dysfunction of ACTH. Secondary adrenal insufficiency can occur in patients with hypopituitarism, a single ACTH deficiency, and patients receiving corticosteroid therapy after discontinuation of corticosteroid therapy. Total pituitary dysfunction, most commonly seen in women with Shehan syndrome, but can also occur secondary to chromoblastoma, craniopharyngioma in a younger patient and a variety of tumors, granulomas, rare traumatic infection leading to pituitary Organizational destruction. After patients receive corticosteroids for more than 4 weeks or discontinue treatment for weeks to months, there is not enough ACTH secretory excitatory to produce sufficient corticosteroids during stress, or no response to ACTH due to adrenal cortical atrophy. This phenomenon can last for one year after the cessation of steroid treatment. During the long-term steroid treatment, the hypothalamic-pituitary-adrenal axis integrity can be determined by intravenous injection of teicokipeptide 5~250g intravenously. The plasma cortisol level should be >20g/dl (>552nmol/L) after 30 minutes. The lack of a single ACTH is idiopathic and extremely rare. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific people Mode of infection: non-infectious Complications: hypoglycemia, coma

Secondary adrenal insufficiency

(1) Insufficient corticotropin releasing hormone (CRH).

(B) pituitary insufficiency: postpartum pituitary necrosis (Sien syndrome), pituitary tumors, postoperative resection or hypoplasia, selective ACTH deficiency.

(C) the long-term increase in blood concentration of glucocorticosteroids or other steroid drugs, causing inhibition of the hypothalamus and pituitary.

1. After the removal of the energy adrenal tumor.

2. Excessive application of iatrogenic corticosteroids.

3. Oral contraceptives or immunosuppressive applications.

4. Long-term ACTH treatment.

Secondary adrenal insufficiency prevention

Active treatment of the primary disease is the key to preventive health care. The mission should enable the patient to fully understand the nature of the disease and recognize that the adrenal cortical hormone replacement therapy should be used for life. Once the diagnosis is clear, the appropriate amount should be explored and obtained, and under stress, the patient can be seen or the dose can be appropriately increased according to his actual situation. Basic treatment of chronic adrenal insufficiency requires long-term replacement therapy.

Secondary adrenal insufficiency complications Complications hypoglycemia coma

Complications include high fever, mental reactions and infections, and hypoglycemia and coma can also occur.

Symptoms of secondary adrenal insufficiency Common symptoms Intestinal dysfunction Loss of appetite Hypotension libido Decreased sleepiness Nausea adrenal crisis Salt corticosteroid secretion too little Cortical dysfunction Dizziness

The clinical manifestations of chronic adrenal insufficiency are due to a lack of cortisol and aldosterone.

(1) Weakness and weakness

For the main symptoms in the early stage, the degree of fatigue is directly proportional to the severity of the disease. In severe cases, it can reach the inability to turn over or reach out, and also can see severe muscle spasms, especially in the legs. These muscle lesions may be related to the sodium and potassium at the neuromuscular endplate. Related to balance disorders.

(two) weight loss

Due to cortisol deficiency, gastrointestinal dysfunction such as loss of appetite, nausea and vomiting, bloating and diarrhea, decreased fat storage and muscle wasting can lead to weight loss, and a progressively greater reduction may indicate an adrenal crisis.

(three) pigmentation

Due to the lack of cortisol, the feedback inhibition of melanocyte stimulating hormone (MSH) and lipoprotein (LPH) is weakened, and the secretion of these hormones is increased, and ACTH and LPH contain and -MSH structures, respectively. Therefore, skin, mucous membrane pigmentation, friction, palm print, areola, scars, etc. are particularly obvious, pigmentation is one of the main basis for the identification of primary and secondary adrenal insufficiency, sudden increase in pigment may indicate deterioration of the condition .

(four) cardiovascular symptoms

Due to the weakening of the catecholamines, the blood pressure is reduced, and the orthostatic hypotension is the most common. X-ray shows that the heart is reduced, the electrocardiogram shows low voltage, and the PR and QT intervals are prolonged. Patients often have dizziness, vertigo, and erectile fainting. .

(5) Low blood sugar

The patient's sensitivity to exogenous insulin is increased, and hypoglycemia is prone to occur in cases of starvation, gastrointestinal dysfunction, and infection.

(6) Neurological symptoms such as apathy, lethargy and even mental disorders.

(7) The resistance to various stresses such as infection and trauma is reduced , and the adrenal crisis is easily induced. It is extremely sensitive to anesthetics, sleeping sedatives and hypoglycemic drugs, and a small amount can cause coma.

(8) Sexual dysfunction

Both male and female patients may have sexual dysfunction. Female adrenal glands and androgen are related to maintenance hair and sexual desire. Therefore, female hair, pubic hair is scarce or shedding, menstrual disorders or amenorrhea, loss of libido, such as autoimmune etiology, may also have ovaries Premature failure of testicular function.

Secondary adrenal insufficiency test

(1) Blood routine examination

There may be mild positive cell dysplasia, occasional large cell or pernicious anemia, classification showing neutropenia, relative lymphocyte increase, eosinophils increased significantly, sometimes due to dehydration before treatment, hypovolemia The reason is that hemoglobin is normal.

(2) Electrolytes

Generally, there is blood sodium, and the ratio of blood to potassium is lowered, while low sodium and high potassium are rare. When the crisis is high, obvious low sodium and high potassium appear.

(three) disorders of glucose metabolism

In most patients, the fasting blood glucose was lower than normal. The oral glucose tolerance test (OGTT) showed a low-flat curve. Most patients had lower blood glucose levels after 3 hours of meal, indicating that they could not respond to hypoglycemia caused by endogenous insulin.

(4) Drainage water load test

In the simple water test, 90% of patients have a discharge of less than 10 ml per minute, and 50% of patients have less than 5 ml. When the cortisol water test is repeated, it can be corrected. This method is simple and easy, and the diagnostic value is large, but before the test. First test blood sodium, blood sodium drop is easy to cause water poisoning, not suitable.

(5) urinary 17-hydroxyl and 17-ketosteroid excretion

The normal value of urinary 17-hydroxycorticosteroid is 5. 5 ~ 28umol / 24h (2 ~ 10mg / 24h), the normal value of urinary 17-ketosteroid is 14 ~ 52umol / 24h (4 ~ 15mg / 24h), male is 22 ~ 88umol / 24h (7 ~ 25mg / 24h), most patients with adrenal insufficiency were lower than normal.

(6) Plasma cortisol

Plasma cortisol is pulsed and has obvious circadian rhythm changes. The blood concentration is the lowest from 1 hour to midnight after falling asleep at night, and starts to rise in the morning. Normal value: 8:220-660 nmol/L (8-24 ug/dl) in the afternoon. At 4:50 ~ 410nmol / L (2 ~ 15ug / dl), less than 140nmol / L at midnight (less than 5ug / dl), most patients with adrenal insufficiency were lower than normal, circadian rhythm disappeared.

(7) ACTH measurement

The plasma basic ACTH measurement of patients with this disease was significantly increased, exceeding 55pmol/L (250pg/ml), mostly between 88 and 440pmol/L (400-2000pg/ml), and normal people were lower than 11pmol/L (50pg/ml). However, in a small number of other diseases, plasma ACTH levels can be as high as 132 pmol/L (600 pg/ml) due to stress.

(8) ACTH Excitatory Test

The ACTH excitatory test has the most diagnostic value. No matter whether the basic urinary free cortisol excretion or cortisol is decreased, it is close to normal or normal. There is no obvious increase in ACTH excitability, and some patients are lower than before, even down to zero.

The usual method of this test is intravenous infusion of ACTH 25u, maintaining the infusion for 8 hours at a balanced rate. If the disease is highly suspected in clinical practice, dexamethasone 1 mg should be taken before the test, which will not affect the measurement and prevent the occurrence of crisis.

In order to identify primary or secondary adrenal insufficiency, a 3-day ACTH stimulation test is required, or a synthetic ACTH 24 peptide 25 ug can be administered intravenously, plasma cortisol is measured before injection and 30 minutes after injection, or intramuscular injection. Plasma cortisol was measured before the same dose and 60 minutes after injection, and normal human plasma cortisol could be increased by 276-552 nmol/L (10-20 ug/dl).

(9) Image inspection

Imaging examination has a higher value in tuberculous patients. X-ray renal plain film can have the following signs: adrenal density is evenly increased, showing fine granularity, accompanied by coarse granular adrenal calcification.

Adrenal tuberculosis is easier to display in B-ultrasound and CT examination. Circular or elliptical shadows can be seen on CT examination, which is a heterogeneous low-density shadow with granular calcification shadows.

Frequent serum electrolyte levels including low sodium (<130 mEq/L), high potassium (>5 mEq/L), low HCO3- (15-20 mEq/L) and high BUN together with characteristic clinical manifestations suggest Eddie's disease. Plasma renin activity and ACTH levels increase. When adrenal failure is due to insufficient production of pituitary ACTH, electrolyte levels are generally normal.

Adrenal insufficiency test Cocoon peptide (cosyntropin, synthetic 24 peptide corticotropin) 5 ~ 25g intravenous bolus. Normal plasma cortisol before injection was between 5~25g/dl (138~690nmol/L), which was doubled in 30~90 minutes, with the lowest value being 20g/dl (552nmol/L). Edison is at a low or normal value and does not rise after excitement.

Diagnosis and diagnosis of secondary adrenal insufficiency

diagnosis

Determination of hypothalamic-pituitary-adrenal axis integrity can be administered intravenously via tecocopeptide 5~250g. After 30 minutes, plasma cortisol should be >20g/dl (>552nmol/L), and pituitary mass or pituitary atrophy strongly suggest secondary adrenal insufficiency.

Differential diagnosis

Secondary adrenal insufficiency is mainly distinguished from primary adrenal insufficiency: most secondary adrenal insufficiency is due to pituitary destruction, so the sella CT or MRI helps to exclude tumors and atrophy. Saddle syndrome is not always associated with hypopituitarism. When pituitary shadows change, functional tests must be performed. Patients with primary adrenal disease have elevated plasma ACTH levels (50 pg/ml). Pituitary failure or ACTH levels in patients with single ACTH deficiency Low. If ACTH cannot be determined, it should be tested with metyrapone. Since metyrapone blocks the hydroxylation of cortisol precursor 11 and plasma cortisol is reduced. Normal human cortisol reduces excitatory ACTH secretion, resulting in increased cortisol precursor synthesis. , especially 11-deoxycortisol (compound S), excreted as a metabolite in the urine (tetrahydro-S). The best and easiest way is to take oral metyrapone 30mg/kg in the middle of the night, while eating a small amount of food to avoid the stomach Stimulation. At 8 o'clock in the morning, plasma cortisol should be <10g/dl (<276nmol/L), and 11-deoxycortisol should be between 7~22g/dl (0.2~0.6mol/L). No reaction to metyrapone. The patient must be tested for the ketol peptide.

Patients with primary adrenal insufficiency have low levels of both compounds and do not respond to tekok peptide. Patients with hypopituitarism respond to synthetic ACTH and do not respond to metyrapone. It is necessary to muscle the patient 3 days before the test. Intravenous injection of long-acting ACTH20u, 2 times a day, to prevent adrenal atrophy in patients with pituitary failure. Insufficient response to metyrapone, but there is a positive response, you need to make this preparation.

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