Short-term Glucocorticoid Therapy Research Articles

Adult-onset Langerhans cell histiocytosis changing CNS lesion from pituitary to suprasellar extension.

SummaryLangerhans cell histiocytosis (LCH) is a rare disease characterized by the proliferation of abnormal Langerhans cells in various tissues and organs, including bone, skin, the lungs, and the pituitary gland. Hypothalamic–pituitary lesions in LCH often cause central diabetes insipidus (CDI), but the natural course of LCH in the CNS remains to be elucidated. In this study, we report an interesting case of altered LCH lesions in the CNS from the pituitary to the hypothalamus in a 45-year-old woman. She developed symptoms of polyuria and was diagnosed with CDI with lymphocytic hypophysitis due to an enlarged pituitary gland with stalk thickening shown on MRI. Short-term glucocorticoid therapy cured pituitary enlargement, but serum prolactin levels gradually increased. Six years later, the immunohistological findings of a skin biopsy revealed positive for leukocyte common antigen, S-100, and CD1a expression, indicating a diagnosis of LCH. MRI revealed a new lesion in the hypothalamus without pituitary involvement, likely due to LCH. Chemotherapy improved LCH lesions both in the skin and hypothalamus, but therapy was stopped on the patient’s request. Although adult-onset LCH is rare, it should be considered as a differential diagnosis in cases of CDI as the primary disease. The clinical course in the present case indicated that LCH lesion was altered from pituitary to suprasellar extension; where such changes were observed, the possibility of LCH should be considered.Learning pointsDiagnosing the primary disease of CDI is challenging; therefore, careful observation is necessary in pathologically unknown cases.Enhanced MRI should be performed in cases with suspected hypothalamic lesions, such as elevated serum prolactin.Although adult-onset LCH is rare, it should be considered a differential diagnosis in cases of CDI as the primary disease.The direction of changing CNS lesion from pituitary to suprasellar extension might be a unique MRI finding in LCH.

Treatment of Pneumocystis jirovecii pneumonia in non-human immunodeficiency virus-infected patients using a combination of trimethoprim-sulfamethoxazole and caspofungin.

BACKGROUND Pneumocystis jirovecii pneumonia (PJP) is an infectious disease common in immunocompromised hosts. However, the currently, the clinical characteristics of non-HIV patients with PJP infection have not been fully elucidated.AIMTo explore efficacy of trimethoprim–sulfamethoxazole (TMP-SMX) and caspofungin for treatment of non-human immunodeficiency virus (HIV)-infected PJP patients.METHODSA retrospective study enrolled 22 patients with non-HIV-infected PJP treated with TMP-SMX and caspofungin from 2019 to 2021. Clinical manifestations, treatment and prognosis of the patients were analyzed. RESULTSFive patients presented with comorbidity of autoimmune diseases, seven with lung cancer, four with lymphoma, two with organ transplantation and four with membranous nephropathy associated with use of immunosuppressive agents. The main clinical manifestations of patients were fever, dry cough, and progressive dyspnea. All patients presented with acute onset and respiratory failure. The most common imaging manifestation was ground glass opacity around the hilar, mainly in the upper lobe. All patients were diagnosed using next-generation sequencing, and were treated with a combination of TMP-SMX and caspofungin. Among them, 17 patients received short-term adjuvant glucocorticoid therapy. All patients recovered well and were discharged from hospital.CONCLUSIONNon-HIV-infected PJP have rapid disease progression, high risk of respiratory failure, and high mortality. Combination of TMP-SMX and caspofungin can effectively treat severe non-HIV-infected PJP patients with respiratory failure.

Thalidomide combined with short-term low-dose glucocorticoid therapy for the treatment of severe COVID-19: A case-series study

ObjectivesThe aim was to evaluate the safety and effectiveness of thalidomide, an immunomodulatory agent, in combination with glucocorticoid, for the treatment of COVID-19 patients with life-threatening symptoms. MethodsA nonrandomized comparative case series study was performed. Six patients received thalidomide 100 mg per day (with therapy lasting for ≥7 days) plus low-dose short-term dexamethasone, and 6 control patients matched with patients in the thalidomide group, received low-dose short-term treatment with dexamethasone alone. The main outcomes were: the duration of SARS-CoV-2 negative conversion from admission; length of hospital stay; and changes in inflammatory cytokine concentrations and lymphocyte subsets. ResultsThe median thalidomide treatment time was 12.0 days. The median duration of SARS-CoV-2 negative conversion from admission and hospital stay length were briefer in the thalidomide group compared to the control group (respectively, 11.0 vs 23.0 days, P = 0.043; 18.5 vs 30.0 days, P = 0.043). The mean reduction rates at 7–10 days after treatment for serum interleukin-6 and interferon-γ concentrations were greater in the thalidomide group compared to the control group. Alterations in lymphocyte numbers in the subsets between the 2 groups were similar. ConclusionsThalidomide plus short-term glucocorticoid therapy is an effective and safe regimen for the treatment of severely ill COVID-19 patients. The mechanism of action is most likely inhibition of inflammatory cytokine production.

Safety of repository corticotropin injection as an adjunctive therapy for the treatment of rheumatoid arthritis

ABSTRACT Introduction Disease-modifying antirheumatic drugs (DMARDs) have significantly improved clinical symptoms and quality of life with reduced disease progression in many patients with rheumatoid arthritis (RA). Short-term glucocorticoid therapy is often used initially in combination with DMARDs, but some patients still have difficulty reaching treatment goals. Repository corticotropin injection (RCI, Acthar® Gel) is approved as adjunctive therapy for short-term administration in patients with continued RA disease activity. Areas covered To determine the safety of RCI in the treatment of RA, adverse events (AEs) from a recent clinical trial of RCI as an adjunctive therapy along with DMARDs and glucocorticoids (ClinicalTrials.gov identifier NCT02919761) were compared with AEs reported in randomized clinical trials of DMARDs and glucocorticoids alone. A systematic review of the literature yielded 4 articles describing the detailed safety results of DMARD/glucocorticoid combination therapy used in the treatment of RA for comparison. Expert opinion There were no clinically significant differences between the AE profiles of RCI/DMARD/glucocorticoid treatment in the RCI clinical trial and those in the DMARD/glucocorticoid safety profile compiled from the reviewed clinical trials; this was supported by pharmacovigilance data. These results support the short-term safety of RCI as an adjunctive therapy for patients with persistently active RA.

Risk of Future Type 2 Diabetes Mellitus in Patients Developing Steroid-Induced Hyperglycemia During Hospitalization for Chronic Obstructive Pulmonary Disease Exacerbation.

We evaluated the future risk of developing impaired glucose tolerance and type 2 diabetes mellitus (T2DM) in patient without T2DM who develop hyperglycemia with short-term systemic glucocorticoid therapy during hospitalization. Retrospective analysis was performed on charts of non-diabetic patients admitted with COPD exacerbation and treated with a course of high dose systemic corticosteroid during hospitalization. Patients with BMI over 40kg/m2, endocrinopathy and on medications that could impair glucose tolerance were excluded. Patient data were collected for 1year after initial hospitalization. Diagnosis of T2DM or IGT was based on the ADA criteria. 311 charts were reviewed, of which 64 patients met our inclusion criteria. Depending on the blood glucose readings during hospitalization, the patients were categorized into two groups: hyperglycemic (> 140mg/dL; n = 42) and normoglycemic (≤ 140mg/dL; n = 22). In the hyperglycemic group, 17/42 (40%) patients developed prediabetes and 5/42 (12%) developed T2DM on follow-up. Interestingly, none of the patients developed IGT or T2DM in the normoglycemic group. Both the groups were well matched in terms of family history of DM, history of hypertension, hyperlipidemia, BMI > 25kg/m2, weight change, tobacco and alcohol use, corticosteroid therapy duration, and cumulative steroid dose. After adjusting for all these risk factors, on logistic regression analysis, hyperglycemic patients had 37 times higher chance of developing IGT, compared to normoglycemic patients (p = 0.003). Our study suggests that patients without T2DM with acute exacerbation of COPD who develop steroid-induced hyperglycemia in response to systemic corticosteroid treatment have an increased risk for developing future IGT or T2DM. Bigger studies are needed to support our findings since results drawn from our study have the limitations of smaller sample size (wider confidence interval) in a single center.

Effect of glucocorticoids on mortality in patients with acute respiratory distress syndrome: A meta-analysis.

To date, the efficacy of glucocorticoid therapy to reduce mortality in patients with acute respiratory distress syndrome (ARDS) has remained controversial among the studies available. The present meta-analysis study aimed to further clarify the impact of glucocorticoid therapy on mortality in patients with ARDS by performing a pooled analysis of the previous data. The PubMed, Chinese Knowledge Infrastructure, Wanfang and Cochrane trials databases were searched for relevant studies published between 1966 and 2016. Randomized controlled trials (RCTs) that included the use of glucocorticoids in patients with ARDS and had reported on mortality were included. Odds ratios (OR) and 95% confidence intervals (CI) for mortality were calculated. A total of 10 RCTs were included in the meta-analysis. Of these, 4 studies used high-dose glucocorticoid therapy, while 6 used low-dose glucocorticoid therapy. In the pooled analysis, glucocorticoids were indicated to significantly reduce ARDS-associated mortality (OR=0.64, 95% CI: 0.48-0.85, P=0.002). Further subgroup analysis indicated the following: i) Long-term low-dose glucocorticoid therapy reduced ARDS-associated mortality compared with that in the control group (OR=0.60, 95% CI: 0.44-0.82, P=0.001), whereas high-dose short-term glucocorticoid therapy did not reduce mortality (OR=0.82, 95% CI: 0.43-1.57, P=0.55). ii) Early initiation of glucocorticoid therapy was associated with reduced mortality compared with that in the control group (OR=0.60, 95% CI: 0.44-0.83, P=0.002); however, late initiation did not reduce mortality (OR=0.36, 95% CI: 0.03-3.76, P=0.39). iii) Therapeutic rather than preventive use of glucocorticoids reduced mortality (OR=0.65, 95% CI: 0.49-0.86, P=0.003). Overall, the present meta-analysis suggests that early initiation of long-term low-dose glucocorticoid therapy reduces mortality of patients with ARDS.

Serum Biomarkers Related to Glucocorticoid-Induced Osteonecrosis of the Femoral Head: A Prospective Nested Case-Control Study.

Early diagnosis and prevention of glucocorticoid (GC)-induced osteonecrosis of the femoral head (ONFH) continues to be a challenging problem for clinicians and researchers. However, the role of circulating biomarkers for GC-induced ONFH, which may reveal individual susceptibility and facilitate earlier diagnosis, remains to be determined. The aim of this study was to identify potential biomarkers that may predict early GC-induced ONFH. A total of 123 patients scheduled for initial systemic GC therapy were enrolled in this prospective nested case-control study. The serum concentrations of 13 potential biomarkers were measured in seven patients with GC-induced ONFH, diagnosed instantly after short-term use of GCs and in 20 controls who did not develop osteonecrosis despite similar GC therapy. Biomarkers were measured both before and after taking GCs to identify any differences in marker levels and the changes during GC therapy between two groups. Type I collagen cross-linked C-telopeptide (β-CTX; p = 0.000) was significantly lower, high-density lipoprotein cholesterol (p = 0.092) and apolipoprotein (apo)-B/apo-A1 (p = 0.085) tended to be lower and higher, respectively, before GC treatment in osteonecrosis group. After GC therapy, β-CTX (p = 0.014) was significantly lower and amino terminal telopeptide of procollagen type I (PINP; p = 0.068) tended to be lower in the osteonecrosis group. As secondary outcomes, we observed remarkable changes in nine potential biomarkers following short-term GC therapy in both groups. In conclusion, we found that β-CTX, could potentially be used to predict GC-induced ONFH before GC therapy. Lower β-CTX and PINP are promising biomarkers for the early diagnosis of GC-induced ONFH. These findings need to be confirmed in large-scale prospective studies. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:2348-2357, 2019.

Treatment of primary Sjögren syndrome.

Primary Sjögren syndrome (pSS) is a progressive autoimmune disease characterized by sicca and systemic manifestations. In this Review, we summarize the available data on topical and systemic medications, according to clinical signs and disease activity, and we describe the ongoing studies using biologic drugs in the treatment of pSS. Expanding knowledge about the epidemiology, classification criteria, systemic activity scoring (ESSDAI) and patient-reported outcomes (ESSPRI) is driving active research. Treatment decisions are based on the evaluation of symptoms and extraglandular manifestations. Symptomatic treatment is usually appropriate, whereas systemic treatment is reserved for systemic manifestations. Sicca is managed by education, environment modification, elimination of contingent offending drugs, artificial tears, secretagogues and treatments for complications. Mild systemic signs such as fatigue are treated by exercise. Pain can require short-term moderate-dose glucocorticoid therapy and, in some cases, disease-modifying drugs. Severe and acute systemic manifestations indicate treatment with glucocorticoids and/or immunosuppressant drugs. The role for biologic agents is promising, but no double-blind randomized controlled trials (RCTs) proving the efficacy of these drugs are available. Targets for new treatments directed against the immunopathological mechanisms of pSS include epithelial cells, T cells, B-cell overactivity, the interferon signature, proinflammatory cytokines, ectopic germinal centre formation, chemokines involved in lymphoid cell homing, and epigenetic modifications.

Recommendations of the French Society for Rheumatology for managing rheumatoid arthritis

IntroductionThis article reports the latest recommendations of the French Society for Rheumatology (SFR) regarding the management of rheumatoid arthritis (RA). MethodsNew recommendations were developed by hospital- and community-based rheumatologists having extensive experience with RA and a patient self-help organization representative. They rest on the recently issued EULAR recommendations and a literature review. ResultsPoints emphasized in the 15 recommendations include the need to share treatment decisions between the rheumatologist and the patient, the acquisition by patients of self-management skills, remission or minimal disease activity as the treatment target, the need for initiating disease-modifying drugs as early as possible, and the usefulness of regular disease activity assessments to allow rapid treatment adjustments if needed (i.e., tight disease control). First-line methotrexate monotherapy is recommended, with concomitant short-term glucocorticoid therapy if indicated by the risk/benefit ratio. Patients who fail this approach (no response after 3months or target not achieved after 6months) can be considered for another synthetic disease-modifying antirheumatic drug (DMARD: leflunomide or sulfasalazine), combined synthetic DMARD therapy, or methotrexate plus a biologic, depending on the prognostic factors and patient characteristics. If the first biologic fails, switching to a second biologic is recommended. In the event of a sustained remission, cautious dosage reduction of the biological and/after synthetic DMARDs is in order. ConclusionThese recommendations are designed to improve the management of patients with RA.

Short-term vs Conventional Glucocorticoid Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Leuppi, Jörg D.*; Schuetz, Philipp†; Bingisser, Roland‡; Bodmer, Michael‡; Briel, Matthias§; Drescher, Tilman*∥; Duerring, Ursula∥; Henzen, Christoph¶; Leibbrandt, Yolanda#; Maier, Sabrina*; Miedinger, David*; Müller, Beat†; Scherr, Andreas*; Schindler, Christian**; Stoeckli, Rolf∥; Viatte, Sebastien#††; Von Garnier, Christophe‡‡; Tamm, Michael§§; Rutishauser, Jonas#∥∥ Author Information

A Clinical Prediction Tool for Prognosis in Patients with Cystic Fibrosis, Short-Term Glucocorticoid Therapy for Chronic Obstructive Pulmonary Disease, and Laryngeal Ultrasound for Prediction of Postextubation Laryngeal Edema

A Clinical Prediction Tool for Prognosis in Patients with Cystic Fibrosis, Short-Term Glucocorticoid Therapy for Chronic Obstructive Pulmonary Disease, and Laryngeal Ultrasound for Prediction of Postextubation Laryngeal Edema

Therapeutic glucocorticoid administration alters the diurnal pattern of dehydroepiandrosterone

Significant alteration in hypothalamic-pituitary-adrenal function has been demonstrated in patients after short-term glucocorticoid therapy, but its impact on the circadian rhythm of steroid hormones has never been investigated. This study examined the effects of short-term prednisone administration on the diurnal patterns of dehydroepiandrosterone (DHEA) and testosterone. Saliva samples were collected from 11 healthy, physically active, male volunteers for DHEA and testosterone analysis, as follows: every 4 h from 0800 to 2000 h on 2 control days without medication, and after 1 week of oral therapeutic prednisone treatment (60 mg daily) (days 0-3). Overall, a diurnal decline in the two steroid hormones was observed on the control days. After short-term glucocorticoid administration, DHEA concentrations were significantly decreased with a complete disappearance of the DHEA diurnal pattern, which lasted 2 days post-treatment. No glucocorticoid effect was observed for testosterone. The results indicate that short-term prednisone treatment affects the circadian pattern of saliva DHEA but not testosterone in healthy active volunteers. Further studies are necessary to determine whether this alteration in DHEA circadian pattern has clinical consequences in patients with chronic glucocorticoid therapy.

Ulcerative Tracheobronchitis Due to Aspergillus

Aspergillus ulcerative tracheobronchitis is a life-threatening form of invasive aspergillosis and is seldom seen in patients without underlying an immunocompromised state. Bronchoscopists must be familiar with this entity and consider Aspergillus ulcerative tracheobronchitis whenever mucosal erosions are seen, especially when unconventional risk factors such as intensive care unit admission and short-term glucocorticoid therapy are present. We present a case of invasive Aspergillus causing widespread ulcerative tracheobronchitis in a 39-year-old man with an asthma exacerbation requiring intensive care unit admission.

5 days of prednisone was noninferior to 14 days in patients with acute COPD exacerbation

Source Citation Leuppi JD, Schuetz P, Bingisser R, et al. Short-term vs conventional glucocorticoid therapy in acute exacerbations of chronic obstructive pulmonary disease: the REDUCE Randomized Cl...

Short-term vs Conventional Glucocorticoid Therapy in Acute Exacerbations of Chronic Obstructive Pulmonary Disease

International guidelines advocate a 7- to 14-day course of systemic glucocorticoid therapy in acute exacerbations of chronic obstructive pulmonary disease (COPD). However, the optimal dose and duration are unknown. To investigate whether a short-term (5 days) systemic glucocorticoid treatment in patients with COPD exacerbation is noninferior to conventional (14 days) treatment in clinical outcome and whether it decreases the exposure to steroids. DESIGN, SETTING, AND PATIENTS REDUCE: (Reduction in the Use of Corticosteroids in Exacerbated COPD), a randomized, noninferiority multicenter trial in 5 Swiss teaching hospitals, enrolling 314 patients presenting to the emergency department with acute COPD exacerbation, past or present smokers (≥20 pack-years) without a history of asthma, from March 2006 through February 2011. Treatment with 40 mg of prednisone daily for either 5 or 14 days in a placebo-controlled, double-blind fashion. The predefined noninferiority criterion was an absolute increase in exacerbations of at most 15%, translating to a critical hazard ratio of 1.515 for a reference event rate of 50%. Time to next exacerbation within 180 days. Of 314 randomized patients, 289 (92%) of whom were admitted to the hospital, 311 were included in the intention-to-treat analysis and 296 in the per-protocol analysis. Hazard ratios for the short-term vs conventional treatment group were 0.95 (90% CI, 0.70 to 1.29; P = .006 for noninferiority) in the intention-to-treat analysis and 0.93 (90% CI, 0.68 to 1.26; P = .005 for noninferiority) in the per-protocol analysis, meeting our noninferiority criterion. In the short-term group, 56 patients (35.9%) reached the primary end point; 57 (36.8%) in the conventional group. Estimates of reexacerbation rates within 180 days were 37.2% (95% CI, 29.5% to 44.9%) in the short-term; 38.4% (95% CI, 30.6% to 46.3%) in the conventional, with a difference of -1.2% (95% CI, -12.2% to 9.8%) between the short-term and the conventional. Among patients with a reexacerbation, the median time to event was 43.5 days (interquartile range [IQR], 13 to 118) in the short-term and 29 days (IQR, 16 to 85) in the conventional. There was no difference between groups in time to death, the combined end point of exacerbation, death, or both and recovery of lung function. In the conventional group, mean cumulative prednisone dose was significantly higher (793 mg [95% CI, 710 to 876 mg] vs 379 mg [95% CI, 311 to 446 mg], P < .001), but treatment-associated adverse reactions, including hyperglycemia and hypertension, did not occur more frequently. In patients presenting to the emergency department with acute exacerbations of COPD, 5-day treatment with systemic glucocorticoids was noninferior to 14-day treatment with regard to reexacerbation within 6 months of follow-up but significantly reduced glucocorticoid exposure. These findings support the use of a 5-day glucocorticoid treatment in acute exacerbations of COPD. isrctn.org Identifier: ISRCTN19646069.

Short term vs conventional glucocorticoid therapy in acute exacerbations of COPD

Short term vs conventional glucocorticoid therapy in acute exacerbations of COPD

Short versus conventional term glucocorticoid therapy in acute exacerbation of chronic obstructive pulmonary disease - THe "REDUCE" trial

International guidelines advocate a 10 to 14-day course of systemic glucocorticoid therapy in the management of COPD exacerbations. The optimal duration of therapy is unknown and glucocorticoids have serious adverse effects. The aim of this trial is to demonstrate non-inferiority of a five-day compared to a 14-day course of systemic glucocorticoids with respect to COPD outcome, thereby significantly reducing steroid exposure and side effects in patients with COPD exacerbations. This is a randomised, placebo-controlled, non-inferiority multicentre trial. Patients with acute COPD exacerbation are randomised to receive 40 mg of prednisone-equivalent daily for 14 days (conventional arm) or glucocorticoid treatment for 5 days, followed by placebo for another 9 days (intervention arm). Follow-up is 180 days. The primary endpoint is time to next exacerbation. Secondary endpoints include cumulative glucocorticoid dose, time to open-label glucocorticoid therapy, glucocorticoid-associated side effects and complications, duration of hospital stay, death, change in FEV1, need for assisted ventilation, clinical outcome assessed by standardised questionnaires, and suppression of the hypothalamic-pituitary-adrenal axis. Mean age (± SD) of patients who finished the study was 70 ± 11 years. 12% had mild or moderate disease, whereas severe and very severe stages were found in 30 and 58%, respectively. At the time of inclusion, 20% of patients were under treatment with systemic glucocorticoids. If the strategy of significantly reducing cumulative exposure to glucocorticoids while taking advantage of their beneficial short-term effects proves to be successful, it will warrant a change in common glucocorticoid prescription practice, thereby improving the management of COPD.

Glucocorticoids Alter Craniofacial Development and Increase Expression and Activity of Matrix Metalloproteinases in Developing Zebrafish (Danio rerio)

Teratogenic effects are observed following long-term administration of glucocorticoids, although short-term glucocorticoid therapy is still utilized to reduce fetal mortality, respiratory distress syndrome, and intraventricular hemorrhage in preterm infants. However, the mechanism of glucocorticoid-induced teratogenicity is unknown. We hypothesize that glucocorticoid-induced teratogenesis is mediated through the glucocorticoid receptor (GR) and results from altering the expression and activity of the matrix metalloproteinases (MMPs). During embryogenesis, degradation of the extracellular matrix to allow for proper cellular migration and tissue organization is a tightly regulated process requiring appropriate temporal and spatial expression and activity of the MMPs. Studies have demonstrated that MMP gene expression can be either inhibited or induced by glucocorticoids in a variety of model systems. Using the zebrafish (Danio rerio) as a model of development, the data presented here demonstrate that embryonic exposure to the glucocorticoids dexamethasone or hydrocortisone increased expression of two gelatinases, MMP-2 ( approximately 1.5-fold) and MMP-9 (7.6- to 9.0-fold), at 72 h postfertilization (hpf). Further, gelatinase activity was increased approximately threefold at 72 hpf following glucocorticoid treatment, and changes in craniofacial morphogenesis were also observed. Cotreatment of zebrafish embryos with each glucocorticoid and the GR antagonist RU486 resulted in attenuation of glucocorticoid-induced increases in MMP expression (52-84% decrease) and activity (41-94% decrease). Furthermore, the abnormal craniofacial phenotype observed following glucocorticoid exposure was less severe following RU486 cotreatment. These studies demonstrate that in the embryonic zebrafish, dexamethasone, and hydrocortisone alter expression and activity of MMP-2 and -9, and suggest that these increases may be mediated through the GR.

Current management of reflex sympathetic dystrophy syndrome (complex regional pain syndrome type I)

Although no major advances have occurred in the curative treatment of reflex sympathetic dystrophy syndrome (RSDS), new pathogenic insights may soon lead to innovative approaches, which may also prove effective in alleviating some forms of neuropathic pain. Preventing nerve compression and ischemia-reperfusion injury constitute valuable measures for preventing RSDS. Vitamin C administration can also prevent RSDS, together with clonidine in high-risk patients. Short-term glucocorticoid therapy has been found effective in preventing RSDS after stroke but has not been evaluated in other situations. Beneficial effects of bisphosphonates have been documented in several placebo-controlled trials. Placebo-controlled trials of ketamine and spinal cord stimulation are in order to confirm or refute the promising results obtained in open-label studies. Mirror visual feedback was introduced recently for the rehabilitation of patients with RSDS but needs to be evaluated in randomized controlled trials.

Spinal epidural lipomatosis following haploidentical allogeneic bone marrow transplantation for non‐Hodgkin lymphoma

Spinal epidural lipomatosis, is a very rare condition, usually seen as an uncommon complication of Cushing's syndrome secondary to chronic steroid therapy leading to increased fat deposits in the epidural space. We report the first documented case of acute symptomatic spinal epidural lipomatosis in a patient with relapsed non-Hodgkin lymphoma. The patient underwent an allogeneic bone marrow transplantation (BMT) and a month of steroid treatment for acute graft vs. host disease (GvHD). He presented with a mild to moderate Cushing's syndrome and minimal obesity. He progressed rapidly to paraparesis, sensory deficit, urinary incontinence and finally respiratory arrest complicated with staphylococcal sepsis. Epidural lipomatosis, with subacute thecal sac compression, is a possible life-threatening complication of relatively short-term systemic glucocorticoid therapy for GvHD in BMT setting.