Pathophysiology
P-I-9. Endocrine disorder, Case 1
内分泌疾患 症例1
A 41-year-old male patient presented at the hospital emergency department accompanied by his wife. His right leg was bleeding. According to his wife, he was preparing for a gastroreality show of a commercial television program and injured his leg on an oven door that was left open. The patient seemed mildly confused. After acute treatment he was oriented to time and space, but according to his wife his behavior had changed significantly in the last couple of years; sometimes he was in an extremely elevated mood and talked continuously, at other times he seemed depressed. The medical history revealed that the patient has been taking steroids for the last 10 years for rheumatoid arthritis. After the treatment of the leg injury the following findings were collected:
Physical examination: Male patient in normal general state and obese nutritional condition. Obesity is abdominal. Extremities are thin. The physical examination shows extreme thinness of the skin, there are prominently livid stretch marks on the protuberant abdomen. Significant supraclavicular fat pads, thick neck. Several hematomas on the lower extremities, based on their color they were not formed at the same time.
Chest: normal respiratory and heart sounds. Abdomen: no abnormalities apart from the significant protrusion and skin alteration. Dorsalis pedis arteries palpable. Blood pressure: 166/104 mmHg, pulse at rest 68/min. Respiratory rate: 16/min.
Medication: apart from the above-mentioned steroids the patient takes analgesics almost daily. The patient receives antihypertensive treatment for hypertension (ACE inhibitors, aldosterone antagonists), and he is on statins for known hypercholesterolemia. No known drug intolerance.
Laboratory findings: The below results should be highlighted: Sedimentation: 38 mm/h, results show significant lymphocytopenia. Blood glucose: 7.1 mmol/l. Total serum cholesterol: 5.8 mmol/l. Serum sodium: 140 mmol/l. Serum potassium: 3.2 mmol/l.
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “taking steroids for the last 10 years for rheumatoid arthritis” | Chronic exogenous glucocorticoids → the cause (iatrogenic Cushing’s syndrome) |
| “Obesity is abdominal. Extremities are thin”; supraclavicular fat pads, thick neck | Central fat redistribution — truncal obesity, buffalo hump, moon facies (glucocorticoid effect) |
| “extreme thinness of the skin”; “livid stretch marks on the protuberant abdomen” | Catabolic glucocorticoid action on skin/collagen → thin skin and purple striae |
| “Several hematomas … not formed at the same time” | Easy bruising from capillary fragility (glucocorticoid effect) |
| BP 166/104 mmHg; blood glucose 7.1 mmol/L | Glucocorticoid-induced hypertension and hyperglycaemia (steroid diabetes tendency) |
| K⁺ 3.2 mmol/L (low) | Hypokalaemia from the mineralocorticoid activity of excess steroid |
| “significant lymphocytopenia” | Glucocorticoid-induced redistribution/suppression of lymphocytes |
| “extremely elevated mood … at other times … depressed” | Steroid-induced neuropsychiatric mood changes |
Key Points
- Diagnosis: Iatrogenic (exogenous) Cushing’s syndrome from 10 years of glucocorticoid therapy for rheumatoid arthritis.
- Pathophysiology: Sustained excess glucocorticoid → central obesity, protein catabolism (thin skin, striae, bruising), hypertension, hyperglycaemia, hypokalaemia, and immune suppression.
- Endocrine axis: Exogenous steroid suppresses ACTH and the hypothalamic–pituitary–adrenal axis (in contrast to ACTH-driven endogenous Cushing’s).
- Caution: Steroids must never be stopped abruptly — risk of adrenal crisis from suppressed adrenal function.
- Complications: Hypertension, glucose intolerance, osteoporosis, infection risk, and mood disturbance.
一問一答
▶Why does Cushing's cause thin skin and purple striae?
Glucocorticoids inhibit collagen and protein synthesis (catabolic action), thinning the skin so dermal vessels show through as livid striae.
▶What is the cause of Cushing's syndrome in this patient?
Chronic exogenous glucocorticoids taken for rheumatoid arthritis.
▶What is the diagnosis in a patient on 10 years of steroids with central obesity, thin skin, purple striae, and easy bruising?
Iatrogenic (exogenous) Cushing's syndrome.
▶Why does this patient bruise easily with hematomas of different ages?
Glucocorticoids weaken capillary support and connective tissue, causing capillary fragility and easy bruising.
▶Why is fat redistributed centrally (truncal obesity, buffalo hump, moon face) in Cushing's?
Excess glucocorticoid promotes central/visceral fat deposition while causing peripheral lipolysis and muscle wasting.
▶Why does glucocorticoid excess cause hyperglycaemia?
Glucocorticoids stimulate gluconeogenesis and induce insulin resistance, raising blood glucose ('steroid diabetes').
▶Why does this patient have hypertension?
Glucocorticoids (and their mineralocorticoid activity) promote sodium/water retention and vascular sensitivity to vasoconstrictors.
▶Why is potassium low (3.2 mmol/L) in this patient?
The mineralocorticoid activity of excess steroid increases renal K⁺ excretion, causing hypokalaemia.
▶Why does this patient have lymphocytopenia?
Glucocorticoids redistribute and suppress lymphocytes, lowering the circulating lymphocyte count.
▶How does exogenous glucocorticoid affect the HPA axis?
It suppresses pituitary ACTH and the hypothalamic–pituitary–adrenal axis, causing adrenal atrophy.
▶How does iatrogenic Cushing's differ from endogenous ACTH-driven Cushing's in terms of ACTH?
Exogenous steroid suppresses ACTH (low ACTH), whereas endogenous Cushing's disease is driven by high ACTH.
▶Why must chronic steroids never be stopped abruptly?
The suppressed adrenal cortex cannot produce enough cortisol acutely, risking a life-threatening adrenal crisis.
▶Why are the limbs thin while the trunk is obese in Cushing's?
Glucocorticoids cause peripheral muscle protein catabolism (wasting) while promoting central fat deposition.
▶What neuropsychiatric effects can glucocorticoids cause, as seen here?
Mood disturbances such as alternating elevated/manic and depressed states.
▶Why are patients with Cushing's syndrome prone to infections?
Glucocorticoids suppress immune function (e.g., lymphocytes), increasing susceptibility to infection.
▶What skeletal complication results from long-term glucocorticoid use?
Osteoporosis (with increased fracture risk).
▶Why does glucocorticoid-induced osteoporosis occur?
Glucocorticoids reduce bone formation and intestinal calcium absorption while increasing bone resorption.
▶Why was this patient already on ACE inhibitors and aldosterone antagonists?
To treat the steroid-induced hypertension (and counter mineralocorticoid effects).
▶What overall metabolic effect does chronic glucocorticoid excess have on protein?
A catabolic effect — protein breakdown exceeds synthesis, causing muscle wasting, thin skin, and poor healing.
▶Why is this patient's bleeding/poor wound healing relevant to glucocorticoid therapy?
Glucocorticoids impair collagen synthesis and immune/inflammatory responses, delaying wound healing.