Glucocorticoid (GC)-induced osteoporosis is the leading form of secondary osteoporosis. Bone loss can be rapid. However, longitudinal studies at the very beginning of treatment are scarce. Patients relapsing from multiple sclerosis are treated with high-dose, short-term iv GCs. A number of them are young, without concomitant disease affecting bone and with no substantial impairment of mobility. Such patients were selected for the present study. Thirteen patients suffering from multiple sclerosis [11 females, two males; age 32 +/- 2 yr (mean +/- se)] and receiving iv methylprednisolone 15 mg/kg daily for 10 d completed the study. We measured serum osteocalcin (OC), aminoterminal propeptide of type I collagen (PINP), bone isoform of alkaline phosphatase (bALP), carboxyterminal telopeptide of type I collagen (CTX), and urinary calcium/creatinine ratio (uCa/Cr) during the 10-d cycle and 3 months later. Dual-energy x-ray absorptiometry and calcaneal quantitative ultrasonometry were performed before and 6 months after therapy. We found an immediate, impressive fall of OC and PINP (-80 +/- 3 and -54 +/- 5% at d 2, respectively), which persisted throughout the whole treatment period (P < 0.0001 for both markers). bALP levels showed only a modest decrease at d 6 (-19 +/- 7%, P < 0.05), with subsequent return to baseline in d 7-10. After 3 months, OC, PINP, and bALP levels rose to +51 +/- 22, +37 +/- 16 (not significant), and +61 +/- 17% (P < 0.01) with respect to baseline, respectively. uCa/Cr and CTX showed a progressive, marked increase during treatment, peaking at d 7-9 (+92 +/- 44 and +149 +/- 63%, respectively), with subsequent decrement at d 10 (P < 0.01 and P < 0.05, respectively) despite continuing GC administration. After 3 months, uCa/Cr and CTX levels were also higher than baseline. No change in quantitative ultrasonometry parameters and bone mineral density was observed 6 months after therapy. In conclusion, high-dose, short-term iv GC regimens cause an immediate and persistent decrease in bone formation and a rapid and transient increase of bone resorption. Our data also support the concept that discontinuation of such regimens is followed by a high bone turnover phase.

Objective: Glucocorticoids (GCs) at pharmacological doses stimulate bone resorption. Mechanisms of this action are unclear. The osteoclastogenic cytokine interleukin (IL)-6 acts through an oligomeric receptor consisting of two subunits, gp80 (or IL-6 receptor a, IL-6Ra) and gp130; both exist in membrane and soluble forms. Soluble IL-6Ra (sIL-6Ra) enhances, while sgp130 inhibits IL-6 signalling. In vitro, GCs enhance many effects of IL-6 by up-regulation of IL-6Ra. The aim of the present study was to assess acute changes of IL-6 system in the peripheral blood of patients given high-dose GCs. Subjects and methods: Serum levels of IL-6, sIL-6Ra, sgp130 and bone turnover markers were assessed before and each day during treatment in 24 multiple sclerosis (MS) patients undergoing high-dose (prednisolone, 15 mg/kg per day), short-term (3 to 5 days) intravenous GC therapy for relapse at the Regional Multiple Sclerosis Centre. Results: An immediate and marked fall of osteocalcin and an early increase of C-terminal telopeptide of type I collagen were already noticed at day 2 (P , 0.001 and P , 0.02, respectively); both became more apparent in the subsequent days. IL-6 was always below or near the detection limit of our ELISA. sgp130 showed a slight increase. sIL-6Ra significantly increased, peaking at day 4 (P , 0.01). However, inter-individual variability of response was noticed. Four patients showed a slight decrease, while no change was observed in one patient and an increase was noticed in the remaining nineteen (maximum change ranging from þ10% to þ67% with respect to baseline). In these patients, a significant increase of sIL-6Ra/sgp130 ratio was apparent. No correlation was found between bone turnover markers and any measured component of the IL-6 system. Conclusions: sIL-6Ra and sIL-6Ra/sgp130 ratio are precociously increased in the peripheral blood of the vast majority of patients given high-dose, intravenous GCs. The increase of systemically available sIL-6Ra conceivably results in the enhancement of IL-6-dependent osteoclastogenesis. The role of such a mechanism in the bone loss observed in inflammatory and immune-mediated diseases (where abundancy of IL-6 in the bone microenvironment is expected) requires further investigation. European Journal of Endocrinology 154 745-751

The article illustrates the case report of a patient, an elderly woman, admitted in the Emergency Department (ED) with acute pulmonary edema, which was quickly solved through a well-timed application of the therapeutic protocols. At first, the course of the treatment was positive, but some complications developed because of the long stay in the hospital, specifically a decubitus ulcer; this condition quickly evolved regardless of the proper treatment, and caused a progressive fall of the general clinical status of the patient. Within the ER, some state-of-the-art clinical apparatus (protocols, unintrusive ventilation) are available for even the treatment of the worst conditions. ED overcrowding – with full occupancy of beds and long waits of patients – is related to greater risk of poor outcomes. One of the risks is to expose the patient to serious complications, that are note related to the reason of admission in hospital, but, paradoxically, are caused by the prolonged hospitalization in ED.

A 53-year-old man arrives in emergency room for fever, asthenia and weight loss. Few days before the visit, he was treated with amoxicillin/clavulanic acid for a hard and not much sore submandibular swelling, with no result. Both ultrasound and CT showed the presence of colliquative multiple nodes, as well as multiple areas of hypoechoic nodules in the liver and spleen, granulomas related to pathognomonics of the hepatosplenic form of disease. In spite of a silent medical history and the lack of exposure to animal or insects, he resulted positive to IgM anti-Bartonella, and the diagnosis of cat scratch disease was confirmed by biopsy. We decided to treat with an association of ertapenem 1g/day and teicoplanin 600 mg/day for 3 weeks, and thus we obtained the recovery. The case report is of particular interest because of the lack of guidelines, the unusual manifestation of the disease and the singular associations of drugs administered.

We present a case report of a 52-year-old man who was hospitalized for right leg pain due to a relevant hemorrhagic effusion. He was on dual antiplatelet therapy (DAPT): acetylsalicylic acid and ticagrelor, a reversible P2Y12 receptor antagonist. Signs, symptoms, and laboratory blood tests led to the diagnosis of acquired hemophilia A (AHA). Ticagrelor therapy-associated AHA was hypothesized due to the fact that, before adding this drug, all laboratory and clinical examinations were repeatedly normal. Prednisone and cyclophosphamide treatment was started without DAPT interruption due to the high risk of stent thrombosis. After 10 days, prolonged activated partial thromboplastin time dropped from 107 to 49 seconds, the patient’s factor VIII (FVIII) levels gradually normalized over the following few weeks, and FVIII inhibitor titer was negative. Recently, some reports have established a link between the development of AHA and treatment with clopidogrel, an irreversible P2Y12 receptor antagonist. However, to the best of our knowledge, this is the first time that a link between AHA and ticagrelor has been reported.