Is porto sinusoidal vascular disease to be actively searched in patients with portal vein thrombosis?

Porto sinusoidal vascular liver disease(PSVD) and portal vein thrombosis(PVT)are distinct vascular liver diseases characterized, respectively, by an intrahepatic and a prehepatic obstacle to the flow in the liver portal system. PVT may also occur as a complication of the natural history of PSVD, especially if a prothrombotic condition coexists. In other cases, it is associated to local and systemic pro-thrombotic conditions, even if its cause remains unknown in up to25% despite an active search. In our opinion, the presence of PSVD should be suspected in patients with PVT especially in those with PVT "sine causa" and the active search of this condition should be included in their diagnostic work-out.However, sometimes the diagnosis of pre-existing PSVD is very hard. Biopsy cannot be fully discriminant as similar histological data have been described in both conditions. Liver stiffness may help as it has been shown to be higher in PSVD than in "pure" PVT, due to the presence of sclerosis in the portal venous radicles observable in PSVD patients. Nevertheless, comparing liver stiffness between PVT and PSVD has until now been restricted to very limited series of patients. In conclusion, even if it is still totally hypothetical, our point of view may have clinical consequences, especially when deciding to perform a liver biopsy in patients with a higher liver stiffness and suspending the anticoagulation in patients with PVT and no detectable prothrombotic factors.     

Suppressive Effects of 24,25-Dihydroxycholecalciferol on Bone Resorption Induced by Acute Bilateral Nephrectomy in Rats

The possible suppressive effects of 24,25-dihydroxycholecalciferol on secondary hyperparathyroidism and increased bone resorption were investigated in adult rats raised on a diet normal in calcium, phosphorus, and vitamin D, and subjected to acute bilateral nephrectomy. The animals had received subcutaneous radiocalcium 4 wk before the experiment. 5 h after nephrectomy an increase in serum total calcium, ⁴⁵Ca-specific activity, citrate, phosphorus, and magnesium concentrations were observed. Serum immunoreactive parathyroid hormone increased, while serum calcitonin decreased. The osteoclast count in the tibial metaphyses was augmented. The biochemical and histological changes observed were partly parathyroid hormone and calcitonin independent, as they also occurred in parathyroidectomized hypocalcemic rats. Pretreatment with 650 pmol of 24,25-dihydroxycholecalciferol 16 h before nephrectomy prevented bone calcium mobilization and diminished the rise in serum total calcium and citrate both in parathyroid-intact and in parathyroidectomized animals. In parathyroid-intact rats, serum immunoreactive parathyroid hormone and calcitonin remained normal in spite of the fall in serum-ionized calcium, and the number of osteoclasts did not increase. In parathyroidectomized rats, 24,25-dihydroxycholecalciferol did not prevent the postnephrectomy rise in the osteoclast count. This latter observation suggests that this metabolite exerts its effect on bone either by acting on cells other than osteoclasts, i.e., the osteocytes, or by inhibiting cell activity. At equimolar dosage 1,25-dihydroxycholecalciferol had a potent stimulatory effect on bone resorption. This effect of 1,25-dihydroxycholecalciferol was partly blocked by the simultaneous administration of 24,25-dihydroxycholecalciferol.     

Dentoskeletal effects of a removable appliance for expansion of the maxillary arch: a postero-anterior cephalometric study

The aim of this study was to evaluate the dentoskeletal effects of early treatment in the primary or early mixed dentition with a removable appliance with expansion springs, assessed on postero-anterior (PA) cephalograms, in patients with a unilateral posterior crossbite when compared with untreated subjects. The treatment group consisted of 23 subjects, 8 males, and 15 females treated with a removable appliance for the expansion of the maxillary arch. The mean age at the start of expansion (T1) was 6 years 2 +/- 17 months, and 8 years +/- 18 months at the end of active therapy and after 1 year of retention (T2), with an observation interval of 22 +/- 7 months. The control group comprised 20 subjects (9 males and 11 females) with an untreated unilateral posterior crossbite. Their mean age was 5 years 9 +/- 15 months at the first observation and 7 years and 4 +/- 16 months at the second examination. The interval between the two observations was 18 +/- 7 months. Nine skeletal and two dental measurements on the transverse plane were assessed. The data from the two groups were compared by means of a Student's t-test for independent samples (P < 0.05). Positive dental and skeletal effects induced by the therapy were observed at T2. The width of the upper dental arch and that of the skeletal maxillary transverse dimension were significantly greater (P < 0.001) in the treatment group when compared with the controls.     

Endocrine care of transpeople part II. A review of cross‐sex hormonal treatments,outcomes and adverse effects in transwomen

The treatment of transwomen relies on the combined administration of anti‐androgens or GnRH analogues to suppress androgen production and thereby reduce male phenotypic characteristics together with oestrogens to develop female characteristics. In transwomen, synthetic oestrogens such as ethinyl oestradiol, as well as conjugated equine oestrogens (CEE), should be avoided to minimize thromboembolic risks especially in older transwomen and in those with risk factors. Currently, available short‐ and long‐term safety studies suggest that cross‐sex hormonal therapy (CHT) can be considered safe in transwomen improving the well‐being and quality of life of these individuals. Long‐term monitoring should aim to decrease cardiovascular risks and should include prostate and breast cancer screenings.     

Antioxidant treatment of hindlimb-unloaded mouse counteracts fiber type transition but not atrophy of disused muscles

Oxidative stress was proposed as a trigger of muscle impairment in various muscle diseases. The hindlimb-unloaded (HU) rodent is a model of disuse inducing atrophy and slow-to-fast transition of postural muscles. Here, mice unloaded for 14 days were chronically treated with the selective antioxidant trolox. After HU, atrophy was more pronounced in the slow-twitch soleus muscle (Sol) than in the fast-twitch gastrocnemius and tibialis anterior muscles, and was absent in extensor digitorum longus muscle. In accord with the phenotype transition, HU Sol showed a reduced expression of myosin heavy chain type 2A (MHC-2A) and increase in MHC-2X and MHC-2B isoforms. In parallel, HU Sol displayed an increased sarcolemma chloride conductance related to an increased expression of ClC-1 channels, changes in excitability parameters, a positive shift of the mechanical threshold, and a decrease of the resting cytosolic calcium concentration. Moreover, the level of lipoperoxidation increased proportionally to the degree of atrophy of each muscle type. As expected, trolox treatment fully prevented oxidative stress in HU mice. Atrophy was not prevented but the drug significantly attenuated Sol phenotypic transition and excitability changes. Trolox treatment had no effect on control mice. These results suggest possible benefits of antioxidants in protecting muscle against disuse.