Increased Risk of Vertebral Fractures in Patients With Mild Autonomous Cortisol Secretion.

CONTEXT: The risk of vertebral fractures (VFx) in patients with adrenal incidentalomas (AI) and mild autonomous cortisol secretion (MACS) is debated. OBJECTIVE: To evaluate the VFx prevalence and incidence in patients with AI and MACS. METHODS: This cross-sectional and longitudinal study using retrospective data from 4 Italian endocrinology units included 444 patients (cross-sectional arm) and 126 patients (longitudinal arm, 24.9 ± 5.3 months follow-up) to evaluate prevalent and incident VFx, respectively, in patients with MACS (MACS-yes) and without MACS (MACS-no). The main outcome measures were serum cortisol after a 1-mg dexamethasone test (F-1mgDST), bone mineral density (BMD) by dual-energy x-ray absorptiometry at spine (LS) and femur (FN), and VFx presence by x-ray. RESULTS: Cross-sectional arm: 214 and 230 patients were MACS-yes and MACS-no, respectively, based on F-1mgDST >1.8 µg/dL (50 nmol/L). Patients with MACS had higher VFx prevalence (62.6%) than those without MACS (22.9%, P < .001); MACS was associated with prevalent VFx (odds ratio, 5.203; 95% CI, 3.361-8.055; P < .001; relative risk [RR] 2.07), regardless of age, body mass index, gender distribution, LS-BMD, and presence of type 2 diabetes mellitus (T2D). Longitudinal arm: 66 and 60 patients were MACS-no and MACS-yes, respectively. Patients without MACS showed higher number of incident VFx (36.4%) than patients without MACS (10.0%, P < .001); MACS was associated with the presence of an incident VFx (RR 4.561; 95% CI, 1.600-13.003; P = .005) regardless of age, LS-BMD, gender distribution, presence of prevalent VFx, and T2D. Results were confirmed in women and men when separately evaluated. CONCLUSION: Women and men with AI and MACS are at higher risk of VFx.

Chronic low-dose glucocorticoid inhalatory therapy as a cause of bone loss in a young man: case report.

Osteoporosis in men is less frequent than in women and is more often due to an underlying cause, such as nutritional deficiencies or lifestyle factors, endocrinological or systemic affections, long-term specific therapies. The growing attention on male osteoporosis is mainly explained by the increasing use of some drugs producing bone loss as frequent side effect, like gonadotropin-releasing hormone (GnRH) agonists for prostate cancer, immunosuppressive agents, or glucocorticoids. Glucocorticoids are largely used for the cure of lots of haematological, rheumatological, dermatological, pneumological, and other systemic diseases. It is well known glucocorticoid-induced osteoporosis (GIOP) develops rapidly at prednisone > 5mg/d or equivalent levels but recurrence is recently also observed in patients receiving low dose and intermittent therapy. However, the possible side effects of corticosteroids at low dose on bone are not completely understood and rightly prevented. We present the case of a young man with precocious bone loss. His improper and irregular use of corticosteroids at low dose was finally recognized as the underlying cause of his unexplainable bone demineralization. The following short review about effects of glucocorticoids on bone suggests fracture incidence and bone mineral density should be assessed even in young people and men perceiving glucocorticoids at undefined dose for long period.

Low bone mineral density in a growth hormone deficient (GHD) adolescent.

It is largely recognized that Growth Hormone (GH) plays an important role in linear growth during childhood and subsequent completion of appropriate height in early adulthood. It has also significant influence on a variety of metabolic activities, as well as the cardiovascular system and quality of life (QoL) in adults. GH is involved in the attainment of optimal Bone Mineral Density (BMD), the most important predictor of osteoporotic fractures, during the transition from paediatric to adult age. The time interval between paediatric and adult age is a critical period of life to clinically assess persistence of GHD in patients affected by childhood onset GHD (COGHD) and determine the need for continuing treatment with recombinant human Growth Hormone (rhGH) even in the face of closure of epiphyseal growth plates. It has been reported GHD is associated with higher fracture's risk in COGHD patients and GH therapy should minimize, if not prevent, osteoporosis in adulthood. We report the case of a COGHD young man, rhGH treated until final height completion, presenting a wrist fracture and precocious bone density loss.

Severe spinal deformity and multiple vertebral collapses in juvenile Cushing Syndrome: a case report.

Cushing's Syndrome (CS) is rare in adolescence but the pathological effects of excessive circulating glucocorticoids concentration on bone during the developmental age still represent a challenge for orthopedists. Only few reports describe the gravity of early developed damages of spine in young affected by CS. A 18-years-old woman suffering from Cushing's Disease presented after many years treatment of the primary disease referring severe back pain and worsening back deformity. Radiological investigations showed vertebral collapses a devastating thoraco-lumbar scoliosis of 80° Cobb. Lumbar dual X-ray absorptiometry Z-score values were very low and consistent with severe osteoporosis. The patient was treated with bracing, antiresorptive therapy, calcium and vitamin D supplementation, and followed-up with imaging investigations to screen for further fractures. The bone mineral density will be monitored until its normalization will allow to plane surgical treatment in case of progression of spinal deformity and collapses. Early diagnosis and treatment of hypercortisolism, periodical clinical and radiographic follow-up, and treatment for the bone damage are mandatory to prevent the devastating sequelae of secondary osteoporosis.

Basedow-Graves' disease in a pediatric patient with Sticlker syndrome, a new endocrine finding to improve personalized treatment.

BACKGROUND: Stickler syndrome is a connective tissue disorder with predominantly autosomal dominant inheritance, with ocular, auditory and joint involvement. Thyroid dysfunction was not described as part of alterations in Stickler syndrome and in particular, the association between Stickler's syndrome and Graves' disease has never been previously reported in literature. Moreover, the presence of Graves' disease is uncommon in the pediatric age (especially in children younger than 6 years old). CASE PRESENTATION: We report the case of a 5-years old child affected by Stickler syndrome who received the diagnosis of Graves's disease, in absence of suggestive symptoms, during health supervision. CONCLUSIONS: This is the first evidence of thyroid dysfunction and autoimmune pattern for Sticker syndrome. Further clinical reports are expected before suggesting the implementation of new clinical skills for Stickler syndrome, but this paper may contribute to improve personalized management of this rare disorder.