Hydrocortisone Acetate Tablets are a commonly-used synthetic glucocorticoid in clinical practice. Possessing potent pharmacological effects including anti-inflammatory, anti-allergic and immunosuppressive activities, they are widely applied in the treatment of adrenocortical insufficiency, autoimmune diseases, severe allergic disorders and other conditions. Nevertheless, as a prescription-only hormonal agent with broad-spectrum yet poorly-targeted pharmacological actions, long-term continuous administration can interfere with normal human metabolism and organ function, trigger multi-system adverse reactions and even cause irreversible physical damage. This article elaborates on the core hazards associated with its long-term oral use.
I. Metabolic disorders and induced somatic lesions
The most-frequently-encountered adverse effect of long-term Hydrocortisone Acetate Tablets is systemic metabolic disturbance, which alters the normal metabolism of glucose, lipids and proteins. In terms of glucose metabolism, the drug inhibits glucose uptake and utilization in peripheral tissues and promotes hepatic gluconeogenesis, resulting in sustained hyperglycaemia and steroid-induced diabetes mellitus. The risk is especially high among patients with impaired glucose tolerance.
Disturbed lipid metabolism leads to fat redistribution and the typical "hormone-induced body habitus" characterized by centripetal obesity with fat accumulation over the trunk, face and abdomen, manifesting as moon-shaped face and buffalo hump, alongside progressive muscle wasting of the extremities. Accelerated protein catabolism and suppressed protein synthesis cause skin thinning, muscle atrophy, fatigue and emaciation, reduced skin elasticity, striae, ecchymoses and markedly delayed wound healing. In addition, the drug can induce sodium-water retention, giving rise to oedema, elevated blood pressure and an increased risk of hypertension.
II. Skeletal damage and elevated fracture risk
Glucocorticoids constitute a major risk factor for bone health. Long-term intake of Hydrocortisone Acetate Tablets severely disrupts bone metabolic homeostasis. The medication suppresses osteoblast activity and bone matrix synthesis while accelerating osteoclast proliferation and bone loss, eventually leading to glucocorticoid-induced osteoporosis after prolonged accumulation.
Such bone damage presents no obvious symptoms at the early stage. As treatment continues, patients may experience bone pain in the lumbodorsal region and limbs, accompanied by substantially reduced weight-bearing capacity of bones. Middle-aged and elderly patients as well as postmenopausal women carry higher risks and are highly susceptible to fragility fractures such as vertebral compression fractures and rib fractures. Meanwhile, the drug inhibits intestinal calcium absorption and increases renal calcium excretion, lowering serum calcium levels. Avascular necrosis of the femoral head may also be triggered, resulting in joint dysfunction and severely impaired limb mobility.
III. Immune-system suppression and reduced host resistance
Immunosuppression is one of the primary pharmacological actions of Hydrocortisone Acetate Tablets. While short-term administration can curb inflammatory injury caused by over-activated immune responses, prolonged use comprehensively impairs the body's normal immune defence. The drug inhibits the proliferation and activity of immune cells such as lymphocytes and macrophages, diminishing the body's capacity to recognise and eliminate bacteria, viruses and fungi.
Patients on long-term therapy remain in a state of persistent immunodeficiency and are highly prone to recurrent infections of the respiratory tract, urinary tract, skin and other sites. Once infected, their conditions are harder to control with prolonged and recurrent courses; a common cold may progress to pneumonia, and minor skin wounds could develop into severe infections. Furthermore, impaired immune surveillance weakens the clearance of abnormal cells, which slightly raises the potential risk of tumour development.
IV. Adverse reactions in the gastrointestinal and endocrine systems
Gastrointestinally, long-term medication stimulates excessive secretion of gastric acid and pepsin while impairing gastric mucosal repair and breaking down the gastric mucosal protective barrier. This predisposes patients to gastritis, gastric ulcers and duodenal ulcers. Severe complications including gastric mucosal erosion, haemorrhage and perforation may occur, often accompanied by epigastric pain, acid regurgitation, belching and other discomforts.
Endocrine disturbance is another prominent concern. Long-term exogenous hormone supplementation suppresses endogenous adrenocortical function, leading to adrenal atrophy and hypofunction. Hormone withdrawal syndrome, presenting with fatigue, low-grade fever, nausea, hypotension and other symptoms, is likely to occur after drug discontinuation. In paediatric patients, growth-hormone secretion is inhibited, skeletal development is retarded and growth delay may arise. Females may suffer from menstrual irregularities or amenorrhoea, whereas males could develop hypogonadism and reduced sexual function.
