I. Endocrine system diseases
(A) Hyperalgesia.
Chronic adrenocortical hypofunction is divided into two categories: primary and secondary. Primary hypofunction is also called Addison’s disease, while secondary hypofunction is caused by hypothalamic-pituitary lesions or surgery that leads to insufficient secretion of adrenocorticotropic hormone (ACTH), resulting in atrophy of the adrenal cortex.
Treatment principles
1.Basic treatment: including patient education, nutrition and correction of water-electrolyte disorders.
2.Glucocorticoid replacement therapy.
3.Prevent acute adrenal cortical crisis, if there is a precursor of crisis, it should be treated according to the crisis.
4.Treat for etiology: such as tuberculosis, infection, tumor, leukemia, etc. Also actively prevent and control secondary infection.
5.Chinese medicine treatment.
Application of glucocorticoid]
1. Determine a suitable basic amount according to height, weight, gender, age and physical work intensity, etc. Hydrocortisone is preferred for primary cases and prednisone for secondary cases.
The initial dose of hydrocortisone should be 0.3~0.5 mg kg-1 d-1, 2/3 of the total daily dose before 8:00 and 1/3 of the total daily dose from 14:00 to 15:00. A more convenient and commonly used dosing method is: 10~15mg of hydrocortisone in the morning after waking up, and 5~10mg in the afternoon (14:00~15:00). If salt loss is still present, small doses of salt corticosteroids such as 9α-fluorohydrocortisone 0.05-0.20mg daily or intramuscular injection of 125mg of desoxycorticosterone trimethylacetate per month may be added. The dose should be adjusted according to 24-hour urinary cortisol and clinical performance.
3.After bilateral adrenalectomy, hydrocortisone should be maintained at 20-30mg/d orally. And fludrocortisone should be supplemented. After removal of cortisol-secreting adrenal adenoma, prednisone can be used at an initial dose of 10 mg/d and then gradually reduced; after partial adrenalectomy, the hormone replacement dose should be appropriately reduced or even not supplemented to keep 24-hour urinary cortisol in the lower 1/3 of the normal range to facilitate the normal feedback of hypothalamic-pituitary-adrenal axis. Recovery.
4, with diabetes, the dose of hydrocortisone is generally not more than 30mg/d, otherwise it is necessary to increase the insulin dose and cause difficulties in glycemic control.
5. Patients with thyrotoxicosis should be replaced with glucocorticoids as soon as possible without waiting for the results of hyperthyroidism treatment.
6, with hypothyroidism, should be supplemented with sufficient amount of glucocorticoids before supplementing thyroxine, in order to avoid further aggravation of hyperaldosteronism due to increased thyroxine.
7. In case of stress, the dosage should be increased under the guidance of physicians. If there is a mild stress such as upper respiratory tract infection, tooth extraction, etc., increase the amount of glucocorticoid by one times until the disease is cured, which is usually controlled within 4 to 5 days. In case of severe stress, such as surgery, myocardial infarction, severe trauma and infection, hydrocortisone should be given to 200-300 mg/d. The glucocorticoid dosage should be increased several hours before the surgery. Those who cannot be given orally can be given intravenously by drip. After the stress is over, gradually reduce the dosage to the maintenance amount, which can be reduced by 1/3 to 1/2 every day for several days until the maintenance amount.
8. Whether primary or secondary, the replacement dose for patients with hyperalgesia needs to be combined with the clinical performance and urinary cortisol level of the patient, but in the case of dexamethasone, the urinary cortisol level does not reflect the level of glucocorticoids in the body, so it should be combined with the clinical performance.
(ii) Congenital adrenocortical hyperplasia.
Congenital adrenocortical hyperplasia (CAH) is a group of autosomal recessive disorders. Cortisol synthesis is partially or completely blocked due to related enzyme defects, and the secretion of adrenocorticotropin-releasing hormone (CRH) by the hypothalamus and ACTH by the pituitary gland increases, stimulating excessive adrenocortical hyperplasia. The biochemical changes and clinical manifestations of congenital adrenocortical hyperplasia are different depending on the type of congenital adrenocortical hyperplasia, but adrenocortical hyperplasia with adrenocortical hormone deficiency is a common feature of congenital adrenocortical hyperplasia, which is clinically manifested by different degrees of hyperalgesia.
Treatment principles
1, early diagnosis and treatment is very important.
2. Salt corticosteroids should be added promptly for salt loss, especially for infants and children.
3, with hypertension, hypokalemia, before the effect of glucocorticoid therapy, supplemented with potassium-preserving antihypertensive drugs.
4, with androgen excess and female masculinization or male precocious puberty should add anti-androgen if necessary to stop androgenization.
5, female clitoral hypertrophy or labial fusion, breast dysplasia can be plastic surgery.
6, female sexual infant or male pseudohermaphroditism, estrogen replacement therapy is needed at the same time.
Application of glucocorticoids
1.Therapeutic purpose: to correct acute hyperalgesia in newborns, to prevent and treat adrenocortical crisis, to inhibit excessive ACTH, to prevent excessive adrenocortical hyperplasia, and to reduce the adverse effects of excessive increase of intermediate metabolites on the organism.
2, cortisone acetate and hydrocortisone are more suitable for long-term replacement therapy for infants and children, but their half-life is short, requiring multiple doses, the inhibition of ACTH is not durable and stable enough, with the increase in age and weight, the corresponding adverse reactions are more obvious after the increase in dose, and are not suitable for use in adulthood. Prednisone and prednisolone have weaker sodium retention effects and are not suitable for patients with severe salt loss.
After 1 week, the adrenal cortex is maximally inhibited and then hydrocortisone is used to maintain the dose, or hydrocortisone can be used to maintain the dose at the beginning, but it takes longer to obtain complete inhibition. The maintenance dose of hydrocortisone is generally 0.5 mg?kg-1?d-1, divided into 3-4 doses. In order to achieve the maximum suppression of ACTH, the total amount of one day can be divided into 4-5 portions, 1/4 in the morning, 1/4 in the middle, 1/2 in the evening, or 1/5, 1/5, 1/5, 2/5, given on time.
4, neonatal acute adrenocortical (hypofunction) crisis treatment: loss of salt type children 3 to 15 days after birth often appear acute hyperalgesia, that is, adrenocortical crisis: anorexia, severe nausea, vomiting, acidosis, circulatory failure. If not diagnosed and treated in time, it often leads to premature death. When the diagnosis is suspicious, urine and blood should be collected immediately for further clarification of the diagnosis, but do not wait for the results, start treatment at the first opportunity: rehydration + hydrocortisone (give 5% glucose saline 20 ml/kg + hydrocortisone 25 mg intravenously in the first hour), if there is improvement, continue rehydration (dose of 5% glucose saline 60 ml?kg-1?d-1), if there is acidosis, use 1/6 mol sodium lactate was added to the rehydration solution as a drip. If no improvement is seen after the first hour, the sodium retention hormone deoxycorticosterone acetate (DOCA) 1 to 2 mg, twice/d, should be administered intramuscularly or 9α-fluhydrocortisone 0.1 mg, orally, and changed to maintenance dose when symptoms improve.
5, adult patients can choose dexamethasone (or prednisone) treatment, the initial dose of prednisone 1.5-2.25 mg/d, if changed from prednisone to dexamethasone, can start from 0.75mg/d, after stabilization to maintenance amount of 0.25-0.75mg/d, the time to take the drug to bedtime every night is better, in order to maximize the suppression of ACTH, but if the excitement and insomnia after taking the drug, you can take the drug But if you get excited and insomnia after taking the drug, you can advance the time of taking the drug.
6. Glucocorticoid dose adjustment should be based on ACTH, steroid hormone intermediate metabolites, testosterone, electrolytes, plasma renin activity, etc., combined with growth curve, bone age and pubertal development. It is recommended to check ACTH and electrolytes at 8:00 every 3 months. 17-hydroxyprogesterone (17-OHP), testosterone, free testosterone, dehydroepiandrosterone sulfate should be added for CAH with androgen increase, and progesterone for sex hormone deficiency. Plasma renin activity is optional. Patients treated with cortisone or prednisone should have 24-hour urine cortisol checked to see if the cortisol replacement dose is appropriate, which is highly accurate and can be used as a basis for dose adjustment. Plasma cortisol levels before and 2 hours after dosing are for reference only and should not be used as a basis for glucocorticoid adjustment. For those who take dexamethasone, blood and urine cortisol levels cannot reflect the actual hormone level and cannot be used as the basis for dose adjustment.
7. Glucocorticoid replacement patients should routinely take calcium supplements, and infants and adolescents in the growth period should also take zinc supplements, and maintain appropriate physical exercise, especially longitudinal exercise, to facilitate bone growth.
8.During glucocorticoid replacement, in case of fever, infection, surgery, mood swings and other stressful conditions, glucocorticoid dosage should be increased to prevent adrenal cortical crisis.
9. Heavy and all female patients should be treated with lifelong replacement therapy. In males with androgenic symptoms (simple masculine type), treatment can be stopped when they reach adulthood and have sufficient height. However, ACTH level, adrenal gland morphology and spermatogenic ability should be closely monitored, and treatment should be resumed if ACTH continues to rise, adrenal hyperplasia worsens, and infertility increases.
(iii) Adrenocortical crisis.
In primary or secondary acute or chronic hyperalgesia, cortisol cannot be produced in normal amount, and the secretion of cortisol cannot be increased correspondingly in stress, so acute clinical manifestations of adrenocortical hormone deficiency may appear: high fever, gastrointestinal disturbance, circulatory deficiency, indifference, depression or agitation, delirium or even coma, which is called adrenocortical crisis. The patient’s life will be delayed.
Treatment principles
1, adrenal cortical crisis should be actively rescued. When this disease is suspected without waiting for the results of laboratory tests, immediate treatment should be given and blood specimens should be taken to detect cortisol and ACTH.
2.Intravenous glucocorticoid injection.
3.Correct dehydration and electrolyte disturbance.
4.Prevent and treat hypoglycemia.
5.Treat the causative factors: actively treat the presence of a certain stress state such as infection and other causative factors.
6.The care should be strengthened during the dangerous period of the disease. Hypoadrenocortical patients are particularly sensitive to morphine and barbiturates, which should be disabled before the start of glucocorticoid therapy.
7. Prevention: Glucocorticosteroids should not be stopped or reduced without authorization, and should be increased in a timely and appropriate manner.
Application of glucocorticosteroids
1. The dose of glucocorticosteroids depends on the severity of the disease and treatment response. If there is impaired consciousness and shock, immediately inject intravenous hydrocortisone phosphate or succinyl hydrocortisone 100mg to make the blood cortisol concentration reach the level of normal people in the event of severe stress. Subsequently, 100 mg is added to the rehydration solution every 6 hours intravenously for a total of about 400 mg for the first 24 hours, which can be reduced to 300 mg intravenously in divided doses on the second to third day. If the condition improves, continue to reduce to 200mg and then 100mg daily. if vomiting stops and food can be eaten, the dose can be changed to oral. When the oral dose is reduced to less than 50-60mg per day, 9α-fluorohydrocortisone should be added.
2. Supplementary salt corticosteroids: If the systolic blood pressure cannot be raised to 100 mm Hg (13.3kPa) after using hydrocortisone sodium succinate or hydrocortisone, or if there is hyponatremia, DOCA 1~3mg can be injected intramuscularly at the same time, once or twice a day, or 9α-fluorohydrocortisone 0.05~0.2mg/d can be changed when the condition improves and food can be taken. severe chronic adrenal Cortical hypocorticism or double adrenalectomy patients need to take long-term maintenance amount.
3. Prevent stress ulcers, give gastric mucosal protective agents and proton pump inhibitors, and pay attention to the side effects of sodium retention and water retention drug overdose such as edema, hypertension and hypernatremia during the application of salt corticosteroids.
(iv) Graves’ ophthalmopathy.
Graves’ ophthalmopathy is a common organ-specific autoimmune disease associated with the thyroid gland. It can occur in different states of thyroid function: hyperthyroidism (hyperthyroidism), hypothyroidism (hypothyroidism), and normal thyroid function. The main manifestations are eyelid contracture, protrusion of the eyeball, bulbar conjunctival edema, periorbital edema, and impaired eye movement. In severe cases, corneal exposure, diplopia, and compressive optic neuropathy, which can lead to blindness, may occur.
Principles of treatment
1, mild Graves’ ophthalmopathy treatment: according to the European Group of Experts on Graves’ Ophthalmopathy (EUGOGO) severity assessment for mild cases to control hyperthyroidism or hypothyroidism, while giving local treatment, and quit smoking or avoid passive smoking, pay attention to eye hygiene, the risk of using glucocorticoids is greater than the efficacy, can observe the development of the disease, such as progressive aggravation can be considered glucocorticoid treatment.
2.Treatment of moderate to severe Graves’ ophthalmopathy: For moderate to severe patients in the active stage (activity score ≥3), the classical treatment plan is based on intravenous or oral glucocorticoid therapy, which can also be combined with orbital radiotherapy. In the inactive stage (activity score <3/7), rehabilitation surgery is feasible if the disease is stable for a long time.
3. Treatment of vision-threatening Graves’ ophthalmopathy: mostly due to thyroid disease-related optic neuropathy and/or corneal injury, requiring immediate treatment. Glucocorticoid therapy and intraorbital decompression surgery are effective methods for treating thyroid disease-related optic neuropathy, but if glucocorticoid therapy is not effective after 1 to 2 weeks or if significant side effects occur, intraorbital decompression surgery should be performed promptly.
Application of glucocorticoids
1.Oral administration: Prednisone (Long) or equivalent dose of methylprednisolone can be chosen, the dose of prednisone as an example: the starting dose of 80-100mg/d can be improved in 48 hours, the dose is maintained for 2-8 weeks and then gradually reduced, glucocorticoid therapy generally needs to be maintained for 3 months, at which time cyclosporine is added. If patients with Graves’ ophthalmopathy in active stage need 131I treatment, glucocorticoids should be applied prophylactically, i.e., 0.3~0.5 mg?kg-1?d-1 of prednisone should be given orally 1~3 days after 131I treatment, and the dose should be gradually reduced and discontinued after 2 months.
2, intravenous drug delivery: intravenous drug delivery methods are various, commonly used methods are methylprednisolone 500mg, 48 hours can be repeated. Severe patients can be given methylprednisolone 500-1000mg intravenous shock treatment, every other day once, for three times. However, methylprednisolone can cause serious toxic liver injury or even death due to dose accumulation, the incidence is 0.8%, the cumulative dose of less than 8g is relatively safe.
3.Postball injection: not recommended as routine.
4. Although hypertension and diabetes mellitus are not contraindications to glucocorticoid therapy for Graves’ ophthalmopathy, they should be monitored regularly and the treatment plan should be adjusted in a timely manner.
(E) The application of glucocorticoids in the diagnosis of endocrine system diseases.
1.Small dose dexamethasone suppression test (LDDST): including standard 48-hour small dose dexamethasone suppression test and overnight dexamethasone suppression test. The standard 48-hour dexamethasone suppression test is performed by administering 0.5 mg of dexamethasone orally every 6 hours for 2 days and measuring the blood cortisol level 48 hours after the first dexamethasone administration. The overnight dexamethasone suppression test is performed by a single oral dose of dexamethasone 0.5-2 mg (commonly 1 mg) at 23:00 midnight, and blood cortisol levels are measured at 8:00 or 9:00 a.m. the next morning. The domestic dexamethasone single dose is 0.75 mg, in practice 1.125 mg (1½ tablets) can be given in the overnight method and 0.75 mg every 8 hours for two days in the classical method. Overnight dexamethasone suppression test blood cortisol level suppression to 138nmol/L (5μg/dl ) can basically exclude Cushing’s syndrome, if this threshold down to 50nmol/L (1.8μg/dl ) can significantly improve the sensitivity of the test up to 98%, especially in people with moderate cortisolism, occasionally normal people are not suppressed to that level. The overnight 1 mg dexamethasone suppression test is mostly used in outpatients because of its simplicity and low cost. The classic 2-day method can be used as a first-line screening test. Dexamethasone suppression tests can produce false positive results due to missed doses of dexamethasone, decreased dexamethasone absorption or accelerated hepatic enzyme metabolism (most commonly seen with hepatic enzyme inducers such as phenytoin sodium, carbamazepine, phenobarbital, amiloride, rifampin) and/or increased plasma concentrations of cortisol-binding globulin (CBG) (in pregnancy or with oral estrogen). False-positive results may also occur in patients with moderate or severe depression.
2. High-dose dexamethasone suppression test (HDDST): HDDST is the most classical method to identify Cushing’s disease from adrenal adenoma. The standard HDDST is 2 mg of oral dexamethasone every 6 hours for 2 days over 48 hours. The single domestic dose of dexamethasone is 0.75 mg, which in practice can be given as 2½-3 tablets-2½-3 tablets every 6 hours (total daily dose of 8.25 mg) for two consecutive days. Observe the degree of cortisol suppression after dexamethasone administration. The 24-hour urinary cortisol level or blood cortisol level can be used, and Cushing’s disease is considered to be suppressed by 50% or more, whereas adrenal tumors, cortical carcinoma or ectopic ACTH syndrome are mostly not suppressed by 50% or more, and pituitary Cushing’s disease cannot be excluded if the suppression rate does not reach 50%. However, about 10% of ectopic ACTH syndromes can also be suppressed to less than 50%.
II. Respiratory diseases
(i) Asthma (adults).
Bronchial asthma is a chronic inflammatory disorder of the airways involving a variety of cells including inflammatory and structural cells of the airways (e.g., eosinophils, mast cells, T lymphocytes, neutrophils, smooth muscle cells, airway epithelial cells, etc.) and cellular components. This chronic inflammation leads to airway hyperresponsiveness, usually with widespread and variable reversible airflow limitation, and causes recurrent episodes of wheezing, shortness of breath, chest tightness, or coughing, often at night and/or early in the morning, or exacerbated by treatment.
Principles of treatment
1.Glucocorticoids are currently the most effective drugs for controlling airway inflammation.
2.The goal of asthma treatment is to achieve and maintain asthma control.
3.The long-term asthma treatment plan is divided into 5 levels. Patients should be followed up, evaluated and monitored regularly for the degree of asthma control, and the treatment plan should be revised in a timely manner according to changes in the condition.
4.Allergens and triggers should be avoided and patient education should be enhanced.
5.Antibiotics should be used only when there is an indication of infection.
6.If the acute attack of critical asthma does not improve or even continues to deteriorate after standard drug treatment, respiratory support therapy should be given promptly.
Application of glucocorticoids
1.Inhaled glucocorticoid is the drug of choice for long-term treatment of asthma. Acute asthma attacks can be treated with systemic glucocorticoids.
2. The routes of administration include inhalation, oral and intravenous application. Inhalation is the preferred route for non-emergency treatment.
3.Most patients with chronic persistent asthma can be better controlled by inhaling small doses of glucocorticoids (equivalent to 400μg of budesonide per day). A combination of inhaled glucocorticoids and long-acting β2-agonists can be used for moderate to severe persistent asthma. When asthma is controlled and maintained for at least 3 months, the dose is gradually reduced until the minimum effective dose of inhaled glucocorticosteroids is reached. In case of unsatisfactory asthma control, timely assessment and up-regulation of treatment are required. For acute worsening of symptoms, inhaled glucocorticoids can be increased by 4 times and applied continuously for 7 to 14 days.
4. Oral glucocorticosteroids can be given for mild to moderate acute attacks of asthma. The reference dose is: prednisone or prednisolone 20～40mg/d for 5～7 days, gradually reduce the dose to discontinue after the symptoms are relieved, the dose and the course of treatment can be adjusted appropriately according to the severity of the disease, or nebulized inhalation budesonide suspension 2～4mg/d for treatment. In severe acute asthma attacks, hydrocortisone succinate (200-1000mg/d) or methylprednisolone (40-160mg/d) should be given intravenously in a timely manner. Those without glucocorticoid-dependent tendency can stop the drug within a short period of time, while those with glucocorticoid-dependent tendency can extend the dosing time appropriately and gradually reduce the dose after controlling asthma symptoms. Long-term use of dexamethasone is not recommended. For patients with uncontrolled and acutely exacerbated refractory asthma, a higher dose of glucocorticoids can be given to control symptoms first, and then the dose can be gradually reduced and maintained with the lowest dose. In addition, high-dose inhaled glucocorticosteroids should be given at the same time to reduce the maintenance dose of oral glucocorticosteroids.
5. The adverse effects of inhaled glucocorticosteroids in the oropharynx include hoarseness, pharyngeal discomfort, Candida colonization and infection. The oropharynx should be rinsed with water in time after inhalation. Long-term use of higher doses of inhaled glucocorticosteroids may also lead to medical manifestations of Cushing’s syndrome.
(B) Idiopathic interstitial pneumonia.
IIP is a group of respiratory diseases of unknown origin, mainly manifested by interstitial inflammation and fibrosis of the lung. The response and prognosis of the seven types of IIP to glucocorticoid therapy vary greatly. The types of IIP that are currently considered to be more effective for glucocorticoid therapy include COP and NSIP, while most IPF do not respond well to glucocorticoid therapy.
Principles of treatment
1, IPF: There is no real and effective treatment for IPF. For typical IPF diagnosed by pathology and typical IPF with foveal-like changes as the main lesion shown by high-resolution chest CT (HRCT), glucocorticoid therapy is basically ineffective and is not recommended. Treatment with glucocorticoids combined with immunosuppressive agents (e.g., azathioprine) may be considered in patients with early inflammatory exudate in IPF (chest CT showing ground glass lesions). It is recommended that the decision to treat with glucocorticoids and immunosuppressive agents should be discussed with the patient and family and informed consent should be signed. aggressive glucocorticoid therapy should be given during acute exacerbations of IPF. Optimal supportive therapy such as oxygen therapy and pulmonary rehabilitation should be given to all IPF patients. Lung transplantation is the main means of treatment for end-stage IPF.
2. NSIP: Recently, it is believed that NSIP is not a single disease and may exist in mixture with other IIP. Pathology classifies NSIP into cellular, mixed and fibrotic types. Cellular and mixed type NSIP are satisfactory for glucocorticoid treatment, while fibrotic type is less effective. Some patients may need glucocorticoid combined with immunosuppressive therapy.
3.COP: Most patients with COP have good results with glucocorticoid therapy. A small number of COP may have acute onset and may die from acute respiratory failure within a short period of time after the onset of symptoms. Severe cases or relapsing patients may require higher doses of glucocorticoids in combination with immunosuppressive systems.
4, AIP: Most patients with AIP have poor glucocorticoid therapy. For early AIP glucocorticoid shock therapy may be effective.
5.DIP: Because DIP has obvious lung function impairment and rapid disease progression, glucocorticoid therapy may be required in general, and some patients may need combined immunosuppressive system.
6.RBILD: The effect of glucocorticosteroid treatment is not clear. There are reports that glucocorticoid therapy can be used for those whose condition does not improve after smoking cessation or continues to deteriorate, and some patients’ condition improves.
7.LIP: There are individual differences in response to glucocorticoid therapy, some patients have better efficacy, but some patients have poor efficacy and may die within a few months due to disease progression or lung infection.
Application of glucocorticoids
1. IPF: It is clear that high-dose glucocorticosteroid (0.5-1 mg?kg-1?d-1) treatment cannot improve survival and is associated with a high mortality rate. For some IPF, lower doses of glucocorticoids (prednisone 0.5 mg?kg-1?d-1) combined with N-acetylcysteine and azathioprine can be considered and the efficacy should be evaluated after 4-8 weeks of treatment. There is no sufficient evidence for the above dose and duration of treatment.
2. COP and NSIP: There is no sufficient evidence-based evidence on the ideal dose and duration of glucocorticoid therapy. The recommended starting dose is prednisone 0.75-1 mg?kg-1?d-1 (or equivalent dose of methylprednisolone or prednisolone), and the disease and efficacy will be evaluated in about 4-12 weeks, and the dose will be gradually reduced to maintenance dose. If the treatment effect is not good, the drug should be stopped or changed to other drugs.
3.AIP: There is no sufficient evidence-based medical evidence on the dose and duration of glucocorticoid therapy. Early AIP glucocorticoid shock therapy may be effective. If glucocorticoid shock is ineffective, the combination of immunosuppressive drugs can be considered.
4.DIP: The ideal dose and duration of glucocorticoid therapy is not clear, and there is no sufficient evidence-based medical evidence. Recommended treatment regimen: starting dose of prednisone (or equivalent dose of methylprednisolone/prednisolone) 20-60 mg/d, gradually reducing to maintenance dose.
5.RBILD: There is no sufficient evidence-based medical evidence. The effect of glucocorticoid treatment is not clear. Some patients may improve with glucocorticoid treatment.
6.LIP: There is no sufficient evidence-based medical evidence. The recommended starting dose is prednisone (or equivalent dose of methylprednisolone/prednisolone) 0.75-1 mg?kg-1?d-1, gradually reduced to maintenance dose.
(iii) Allergic bronchopulmonary aspergillosis.
ABPA is a disease caused by the body’s metabolic reaction to the antigen of Aspergillus parasiticus in the bronchus, which is characterized by wheezing, fever, cough, sputum and hemoptysis in the acute phase and pulmonary fibrosis and bronchodilation in the chronic phase.
Treatment principles
1.Glucocorticoid therapy is preferred, with adjuvant antifungal drugs (such as itraconazole).
2.The treatment plan should be decided according to the stage of the disease.
3.Exposure to high concentration of Aspergillus environment should be avoided.
4.Treat concomitant other diseases, such as allergic rhinitis, gastroesophageal reflux disease, etc.
Application of glucocorticoids
1. Preferred oral glucocorticoid therapy: (1) The recommended dose in the acute stage: general prednisone 0.5 mg?kg-1?d-1, changed to 0.5 mg/kg orally every other day after 2 weeks, the general course of treatment is about 3 months, the glucocorticoid dose and the course of treatment can be adjusted according to the condition. The dose of prednisone can be increased to 40-60 mg/d in the first 2 weeks for those with severe symptoms in the acute phase, and the course of treatment can be extended according to the condition. Dose reduction should be determined according to symptoms, chest imaging and total IgE level. (2) Patients in chronic glucocorticoid-dependent stage and pulmonary fibrosis stage may need long-term application of glucocorticoids, and alternate day dosing is advocated to reduce adverse drug reactions.
(2) Inhaled glucocorticoids can improve asthma symptoms without affecting the absorption of pulmonary infiltrates.
(iv) Nodular disease.
Nodular disease is a systemic disease of unknown cause, characterized by non-caseating necrotizing granulomas. It often invades the lungs and bilateral hilar lymph nodes, and clinically more than 90% have pulmonary changes, followed by skin and ocular lesions, and almost every organ of the body, such as superficial lymph nodes, liver, spleen, kidney, bone marrow, nervous system, and heart, can be involved.
Principles of treatment
1. Individual assessment is required before treatment plan is formulated, including the scope and severity of the involved organs, staging and expected treatment effect.
2. Glucocorticoid therapy is preferred for: (1) patients with obvious respiratory symptoms (such as cough, shortness of breath, chest pain) or progressive stage II and stage III disease; (2) progressive deterioration of chest imaging or progressive pulmonary impairment; (3) invasion of extra-pulmonary organs, such as cardiac or central nervous system involvement, or ocular involvement with visual impairment, or persistent hypercalcemia.
3. If advanced pulmonary fibrosis is already present, its treatment should focus on strengthening supportive therapy and symptomatic management. If indicated, lung transplantation may be considered.
4. Asymptomatic stage I patients do not need glucocorticoid therapy. Asymptomatic stage II or III patients with only mild abnormalities in pulmonary function and stable disease are not recommended to apply glucocorticoid therapy too aggressively, but to maintain dynamic follow-up, and should be applied promptly when there are obvious indications.
Application of glucocorticosteroids
1. Oral glucocorticoid therapy is preferred: the reference initial dose is prednisone (or equivalent dose of methylprednisolone or prednisolone) 20-40 mg/d (or 0.5 mg?kg-1?d-1). The efficacy of treatment was evaluated after 4 weeks, and if effective, the dose was gradually reduced to the maintenance dose. The duration of treatment is 6 to 24 months, usually at least 1 year.
2.If the disease relapses after discontinuation, glucocorticoid treatment again remains effective and immunosuppressive drugs are added when necessary.
3.Inhaled glucocorticosteroids have no significant benefit, but may be effective for patients with airway mucosal involvement.
(E) Chronic obstructive pulmonary disease (COPD).
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease characterized by airflow limitation, which is not completely reversible, progressive and associated with abnormal inflammatory response of the lungs to harmful gases or particles such as cigarette smoke. COPD mainly involves the lungs, but can also cause systemic (or extra-pulmonary) adverse effects.
Treatment principles
1, according to the stage and severity grading to determine the treatment plan.
2.Stable COPD: including patient education and management, avoidance of risk factors, bronchodilators and inhaled glucocorticoids and other drug therapy, as well as oxygen therapy and rehabilitation treatment.
3.Out-of-hospital treatment during acute exacerbation of COPD: First, determine the cause and severity evaluation of acute exacerbation of COPD. In addition to bronchodilators, oral glucocorticoids can be considered.
4, COPD acute exacerbation hospitalization: controlled oxygen therapy, anti-infection, bronchodilator, systemic glucocorticoid and respiratory support therapy, etc.
Application of glucocorticosteroids
1.Inhaled glucocorticosteroids are suitable for (1) COPD patients with stable stage 1-second force expiratory volume (FEV1) < 50% of the expected value (grade III and IV COPD) and with clinical symptoms; (2) COPD patients with repeated acute exacerbations.
2. The combination of inhaled glucocorticoids and long-acting β2-agonists is more effective than inhaled glucocorticoids alone. Some patients with acute exacerbation of COPD can choose glucocorticoids combined with β2-agonists for nebulized inhalation.
3. Systemic glucocorticoids are beneficial for the treatment of acute exacerbation of COPD. Short-acting β2-agonists are more suitable for the treatment of acute exacerbation of COPD, and anticholinergic drugs can be added; more serious patients can also consider intravenous infusion of theophylline drugs. inpatients with exacerbation of COPD are recommended to apply bronchodilators on the basis of oral or intravenous glucocorticoids. The dosage should be decided on the basis of efficacy and safety. Reference dose: Prednisone or prednisolone 20-40 mg/d orally for 5-10 days and then gradually reduce the dose and stop. Or give intravenous methylprednisolone 40 mg/d orally after 2-5 days, and adjust the dose and duration of glucocorticoids according to the condition. Long-term oral glucocorticoid therapy is not recommended for COPD patients.
4. For COPD patients, the local adverse effects of inhaled glucocorticoids in the oropharynx include hoarseness, pharyngeal discomfort and Candida colonization and infection. After inhalation, the oropharynx should be rinsed with water in a timely manner.
(vi) Allergic rhinitis.
Allergic rhinitis is a chronic inflammatory disease of the nasal mucosa mediated by IgE after exposure to allergens. The main clinical symptoms are runny nose, nasal congestion, nasal itching and sneezing, which are self-limiting or can be relieved by treatment. Allergic rhinitis can be classified as intermittent or persistent according to the duration of symptoms; mild or moderate-severe according to the severity of symptoms and the impact on life.
Treatment principles
1, mainly including avoidance of allergen exposure, drug therapy, immunotherapy and patient education.
2.Intranasal glucocorticoid is the most effective drug for the treatment of allergic rhinitis.
3. A stepwise drug treatment program is used according to the severity and duration of symptoms. For patients with persistent allergic rhinitis, clinical follow-up and efficacy evaluation should be adhered to, and the treatment plan should be adjusted accordingly, and the intensity of treatment should be increased or decreased.
Application of glucocorticoids
1. Intranasal glucocorticoids are the first-line treatment for moderate-to-severe persistent allergic rhinitis. It can also be used for moderate-to-severe intermittent allergic rhinitis and mild persistent allergic rhinitis.
2. Reference treatment options.
(1) Moderate-to-severe persistent allergic rhinitis: intranasal glucocorticoids (beclomethasone 300-400 μg/d or equivalent doses of other intranasal glucocorticoids) are preferred. If symptoms are severe, oral H1 antihistamines and/or short-term oral glucocorticoids may be added at the beginning of treatment.
(2) Moderate-severe intermittent allergic rhinitis: intranasal glucocorticoids (beclomethasone 300-400 μg/d or equivalent doses of other intranasal glucocorticoids). If necessary, oral H1 antihistamines and/or short-term oral glucocorticoids may be added after 1 week of treatment.
(3) Mild persistent allergic rhinitis: oral H1 antihistamine or low-dose intranasal glucocorticoid (beclomethasone 100-200 μg/d or equivalent dose of other intranasal glucocorticoid). The intranasal glucocorticoid dose can be adjusted appropriately according to the condition.
3. Intramuscular injection and long-term oral glucocorticosteroids are not recommended.
4. Intranasal glucocorticosteroids have certain stimulating effects on the mucous membrane of the nasal cavity and may cause side effects such as nasal dryness, nasal crusting and nasal bleeding, etc. Long-term users should stop using them and give appropriate treatment if local fungal infection occurs in the nose.
(vii) Eosinophilic bronchitis.
Eosinophilic bronchitis is a non-asthmatic bronchitis characterized by airway eosinophil infiltration. The clinical manifestations are chronic cough, induced sputum eosinophil ratio ≥2.5%, no airway hyperresponsiveness, ineffective bronchodilator therapy, and good response to glucocorticoid therapy.
Principles of treatment
1.Avoid contact with allergens.
2. Inhaled glucocorticoids are currently the main drug for the treatment of eosinophilic bronchitis.
Application of glucocorticoids
1.Glucocorticoids are the first-line treatment for eosinophilic bronchitis.
2. Reference treatment plan: (1) Usually treated with inhaled glucocorticoids at a dose of 250-500 μg/dose of beclomethasone or equivalent dose of other glucocorticoids, twice daily, for more than 4 weeks. (2) Initial treatment can be combined with the application of short-term oral glucocorticoids, prednisone 10-20 mg per day for 3-5 d.