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Purpose Little is known about the association between plasma adiponectin levels and nonalcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes mellitus (T2DM). We examined whether there is an association between lower plasma adiponectin levels and the presence/severity of NAFLD in people with T2DM. Methods We cross-sectionally recruited 79 men with non-insulin-treated T2DM and no known liver diseases, who had consecutively attended our diabetes outpatient service over a 6-month period and who underwent both ultrasonography and Fibroscan-measured liver stiffness (LSM). Nine single nucleotide polymorphisms (PNPLA3 rs738409 and other genetic variants) associated with NAFLD were investigated. Results Among the 79 participants included (mean age 67 ± 10 years, BMI 27.7 ± 4 kg/m2), 28 did not have NAFLD, 32 had steatosis alone, and 19 had NAFLD with coexisting significant fibrosis (LSM ≥ 7.0 kPa by Fibroscan®). Compared to those without NAFLD, patients with hepatic steatosis alone and those with hepatic steatosis and coexisting significant fibrosis had lower high-molecular-weight adiponectin levels (5.5 [IQR 2.3–7.6] vs. 2.4 [1.8–3.7] vs. 1.6 [1.0–2.9] µg/mL; p PNPLA3 rs738409 variant, lower plasma adiponectin levels were found to be associated with increased odds of both steatosis alone (adjusted-odds ratio [OR] 2.44, 95% CI 1.04–5.56, p = 0.042) and NAFLD with coexisting significant fibrosis (adjusted-OR 3.84, 95% CI 1.23–10.0, p = 0.020). Similar findings were observed after adjustment for the other eight genotyped NAFLD-related polymorphisms. Conclusion Lower plasma adiponectin levels are closely associated with the presence and severity of NAFLD in men with T2DM, pointing to a role of adiponectin in NAFLD development and progression.

We performed a cross-sectional study to investigate the prevalence of Diffuse Idiopathic Skeletal Hyperostosis (DISH) through Dual-Energy X-ray absorptiometry (DXA) Vertebral Fracture Assessment (VFA) in a group of post-menopausal women with Type 2 Diabetes Mellitus (T2DM). We also explored several biomarkers of bone turnover metabolism, including Wnt pathway modulators. DXA-VFA was performed to detect the presence of DISH. Serum samples were collected from all patients at the time of study recruitment. 16 different serum biomarkers were tested between the two subgroups. Given the exploratory nature of the study, we did not adjust for multiplicity. At VFA analysis, among 96 individuals enrolled in the study 20 (20.8%) showed features of DISH. No statistically significant difference was found for BMD values, between the DISH and NO-DISH subgroups. Concerning blood biomarkers, DISH patients showed a significant difference only in the sclerostin serum levels (32 vs 35.5 pmol/L, for the DISH and NO-DISH subgroup, respectively; p = 0.010). After adjustment for confounding factors, sclerostin serum levels remained significantly lower in DISH group (p = 0.002). We demonstrated a non-negligible prevalence of DISH in a population of post-menopausal women affected by T2DM and suggested low serum sclerostin as a possible key feature associated with DISH presence. In addition, we propose DXA-VFA analysis, whose radiation dose is considerably lower than conventional radiography, as a viable diagnostic and prognostic mean to obtain data not only on bone health, but also for the screening for DISH in subjects at risk.

La steatosi epatica non alcolica (NAFLD) e attualmente l’epatopatia cronica piu comune nella pratica clinica. La prevalenza della NAFLD e assai elevata nel diabete tipo 2 (T2D), essendo presente in oltre il 60–70% di tali pazienti. In questa breve rassegna discuteremo le evidenze clinico-epidemiologiche che suggeriscono una significativa associazione tra NAFLD e aumentato rischio di complicanze cardiovascolari nel T2D e i possibili meccanismi fisiopatologici che spiegano tale associazione.

Hyperuricemia/gout and atrial fibrillation (AF) are two pathological conditions that are highly prevalent in type 2 diabetes and share multiple cardiovascular risk factors. However, the relationship between elevated levels of serum uric acid and risk of AF in type 2 diabetes is currently poorly known.We studied a hospital-based sample of 842 (male/female = 463/379) patients with type 2 diabetes discharged from our Division of Endocrinology during 2007-2011. Hyperuricemia was defined as a serum uric acid level7 mg/dl for men and6 mg/dl for women or allopurinol use. The diagnosis of AF was confirmed in affected participants on the basis of ECGs and medical history by experienced cardiologists.Overall, 243 (28.9 %) patients had hyperuricemia and 91 (10.8 %) patients had persistent or permanent AF. Compared with those with normal serum uric acid levels, patients with hyperuricemia had a remarkably greater prevalence of AF (20.6 vs. 7.1 %; p0.001). Hyperuricemia was significantly associated with an increased risk of prevalent AF (odds ratio 3.41, 95 % CI 2.19-5.32; p0.001). Adjustments for age, sex, smoking, hemoglobin A1c, hypertension status, chronic kidney disease, chronic obstructive pulmonary disease and previous histories of hyperthyroidism, ischemic heart disease and valvular heart diseases did not weaken this association (adjusted-odds ratio 6.27, 95 % CI 1.82-21.5; p0.01).These results indicate that hyperuricemia is associated with an increased prevalence of AF in hospitalized patients with type 2 diabetes, independently of multiple risk factors and potential confounders.

To report the case of a patient initially diagnosed with acute posterior multifocal placoid pigment epitheliopathy (APMPPE), characterized by relentless evolution despite high-dose steroid therapy. An interferon-gamma release assay (IGRA) indicated a diagnosis of suspected tuberculous choriocapillaritis and the disease responded only to massive inflammation suppressive therapy and antibiotic therapy. Case report. Review of clinical features and investigational procedures. Smoldering relentless evolution and subsequent arrest of progression could be precisely monitored by indocyanine green angiography (ICGA). The patient did not recover after standard anti-tubercolosis (TB) therapy combined with corticosteroid. A fourth antibiotic had to be added in order to stop the progression of the retinal disease. In each case of choriocapillaritis such as APMPPE an infectious cause including TB has to be excluded making IGRA tests unavoidable. As the main structure involved is the choriocapillaris the most precise follow-up or monitoring is obtained with ICGA.

Purpose: In its typical form and when seen at onset, Vogt-Koyanagi-Harada (VKH) is characterized by easily recognizable signs that allow diagnosis without difficulty. In cases that do not have acute onset, that are seen at a later stage or that do not show the complete set of signs, appraisal is more difficult and diagnosis may cause difficulties. We present here a case of bilateral granulomatous uveitis compatible with VKH disease in order to allow several experts to give their opinion on the most appropriate manner to confirm or reject the diagnosis and their approach to the management of the case. Case presentation: A 17-year-old female patient consulted her ophthalmologist for blurred vision OU following an episode of a flu-like disease with malaise, fever and headaches. A bilateral anterior granulomatous uveitis with a right papillitis was diagnosed and the patient presented with a bilateral acute myopization. Fluorescein angiography showed right disc hyperfluorescence with late leakage and slight left disc hyperfluorescence. The patient was given a course of one week of peroral corticosteroid therapy followed by an intramuscular injection of Bentelan® twice weekly. In the absence of significant improvement the patient was sent sixweeks later to a specialized center where a complete work-up was performed. Expert opinion: The diagnostic work-up, investigational tests, and differential diagnosis to confirm or reject the diagnosis of VKH as well as the management of the case will be described by the experts

Purpose Firstly, to give a review of characteristic indocyanine green angiographic (ICGA) signs in Vogt–Koyanagi–Harada (VKH) disease and, secondly, to determine the utility of ICG angiography in the assessment and follow-up of choroidal inflammatory activity during initial high-dose inflammation suppressive therapy and during the tapering of therapy. Methods We have first reviewed characteristic ICGA signs in VKH. This is followed by a study of four patients with an acute initial VKH uveitis episode who received regular initial and follow-up angiographic examinations for at least 9 months. Classical ICGA signs were recorded at onset and followed for at least 9 months and were correlated with treatment levels. The treatment consisted of high-dose oral corticosteroids (0.8–1.5 mg/kg) preceded by pulse intravenous methylprednisolone (500–1000 mg) for 3 days in hyperacute cases and followed by very slow tapering with the addition of an immunosuppressive agent in cases of insufficient response. Results The major ICGA signs that were both consistently present and easy to record in the four VKH patients having an acute initial uveitis episode with a pre-treatment angiography and an angiographic follow-up for a minimum of 9 months include (1) early choroidal stromal vessel hyperfluorescence and leakage, (2) hypofluorescent dark dots, (3) fuzzy vascular pattern of large stromal vessels and (4) disc hyperfluorescence. All patients were treated with high-dose inflammation suppressive therapy: in two patients, within 14 and 21 days after initial symptoms, respectively, and in the other two patients, within 6 weeks. Hypofluorescent dark dots, the most constant and easily recordable sign, was very prominent in all cases at presentation. A 90% to complete resolution of dark dots was noted in all four patients after 4 months of therapy. The other three major angiographic signs, early choroidal stromal vessel hyperfluorescence and leakage, indistinct fuzzy vessels at the intermediate angiographic phase and disc hyperfluorescence resolved in all cases within 8 weeks or less of high-dose inflammation suppressive therapy. In three of the four patients, dark dots reappeared after a mean of 7.8 ± 2.8 months after onset of therapy when the patients were under a mean corticosteroid dose of 13.2 ± 6.3 mg per day without any significant clinical or fluorescein angiographic signs, indicating subclinical recurrence. An increase in the inflammation suppressive therapy again brought about angiographic resolution of choroidal subclinical disease in all cases. Conclusion Choroidal inflammation shown by ICG angiography can be suppressed completely by initial high-dose inflammation suppressive therapy. However, recurrent subclinical choroidal inflammation is detected at the end of the tapering period in a high proportion of cases. This indicates that, in the absence of an ICGA follow-up, undetected smoldering subclinical disease may persist, thereby explaining the frequently reported evolution towards sunset glow fundus despite an apparently controlled disease. This is a clear indication that VKH disease should be followed by ICG angiography and, in the case of choroidal subclinical reactivation, a reversal of therapy tapering and an extension of therapy duration should be considered.