Crutches in Cushing's disease
Avascular necrosis of bone can be almost silent until it comes under unusual strain. We report a case in point and lessons learned.
Sunday, August 26, 2012
Hip Pain: Another Cushing's Symptom
Cushing's Disease Presenting with Avascular Necrosis of the Hip: An Orthopedic Emergency
ABSTRACT
Nontraumatic avascular necrosis (AVN) of the hip is commonly caused by exogenous glucocorticoid administration, whereas it has rarely been associated with endogenous hypercortisolism. We report a 30-yr-old woman with Cushing's disease whose presenting manifestation was early AVN of the hip. Although plain x-ray was negative, magnetic resonance imaging (MRI) of the hip showed stage 2 AVN. Her orthopedic disease was considered an emergency, and thus, it was treated with core decompression before the diagnosis of Cushing's syndrome (CS) was pursued further. The femur recovered fully, as demonstrated by her improved clinical picture and a subsequent MRI. AVN carries a poor prognosis, if not treated early. The diagnostic procedure of choice is MRI, because plain radiographs are falsely negative in early stages. This case illustrates that AVN can be the presenting manifestation of CS; to prevent irreversible effects on the femoral head, core decompression should not be delayed for the purpose of evaluation and treatment of CS.Read article in full here:
Yup, Your Ticker Could Go, Too!!
Cushing's Patients Must Be Screened for Heart Disease
By Piriya Mahendra, MedWire Reporter
Published August 12, 2012
Individuals who use glucocorticoids and exhibit iatrogenic Cushing's syndrome should be "aggressively" targeted for early screening of cardiovascular (CV) risk factors, say researchers.
Laurence Fardet (University College London, UK) and colleagues found that individuals with iatrogenic Cushing's syndrome who were prescribed glucocorticoids had a significantly higher incidence of CV events (including coronary heart disease, heart failure, or ischemic cerebrovascular events) than individuals prescribed glucocorticoids without iatrogenic Cushing's syndrome, or those not prescribed glucocorticoids.
Indeed, Cushing's syndrome patients prescribed glucocorticoids had a CV incidence rate per 100 person-years at risk of 15.1 compared with 6.4 and 4.1 in those without Cushing's but who were prescribed glucocorticoids and those not prescribed glucocorticoids, respectively.
Multivariate analysis revealed that iatrogenic Cushing's patients had a 2.27-fold increased risk for coronary heart disease, a 3.77-fold increased risk for heart failure, and a 2.23-fold increased risk for ischemic cerebrovascular events.
Compared with individuals prescribed glucocorticoids without iatrogenic Cushing's syndrome, those with Cushing's and glucocorticoids had a 2.74-fold increased risk for CV events.
Cushing's patients prescribed glucocorticoids also had a 4.16 higher risk for CV events than individuals not prescribed glucocorticoids.
"These results raise the question of whether glucocorticoids increase the risk of CV events in all patients or only in those who develop iatrogenic Cushing's syndrome," remark the authors.
Iatrogenic Cushing's syndrome is characterized by a cushingoid adiposity, with hypertrophy of adipose tissue in the face (giving the appearance of a "moon face"), dorsocervical region ("buffalo hump," double chin), and abdomen, and thinning of the subcutaneous adipose tissue of the limbs.
The authors say that a glucocorticoid-induced cushingoid appearance must no longer be considered as a minor adverse event of glucocorticoid treatment and point out that it has been associated with some features of the metabolic syndrome.
"It is therefore essential that patients prescribed glucocorticoids who develop iatrogenic Cushing's syndrome are assessed for CV risk and monitored regularly in both primary care and secondary care for early prevention of CV disease," they conclude in the British Medical Journal.
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