Diabetes in HIV‐infected persons in Cameroon?

In the past, the increased prevalence of diabetes in HIV infection has been attributed to antiretroviral drugs. In this study, Cameroonians with HIV infection were shown in a paper in this issue of the Journal to be more likely to have diabetes if they were not on therapy. Future research should examine if the diabetes is related to the host response to infection or to socioeconomic factors that might both contribute to not being on anti‐retroviral therapy and predispose to diabetes. Copyright © 2016 John Wiley & Sons, Ltd.     

Emphysema in α<Subscript>1</Subscript>-Antitrypsin Deficiency

Severe alpha(1)-antitrypsin (AAT) deficiency is an inherited disorder that leads to the development of emphysema in smokers at a relatively young age; most are disabled in their forties. Emphysema is caused by the protease-antiprotease imbalance when smoking-induced release of neutrophil elastase in the lung is inadequately inhibited by the deficient levels of AAT, the major inhibitor of neutrophil elastase. This protease-antiprotease imbalance leads to proteolytic damage to lung connective tissue (primarily elastic fibers), and the development of panacinar emphysema. AAT replacement therapy, most often applied by weekly intravenous infusions of AAT purified from human plasma, has been used to partially correct the biochemical defect and raise the serum AAT level above a theoretically protective threshold level of 0.8 g/L. A randomized controlled clinical trial was not considered feasible when purified antitrypsin was released for clinical use. However, AAT replacement therapy has not yet been proven to be clinically effective in reducing the progression of disease in AAT-deficient patients. There was a suggestion of a slower progression of emphysema by computed tomography (CT) scan in a small randomized trial. Two nonrandomized studies comparing AAT-deficient patients already receiving replacement therapy with those not receiving it, and a retrospective study evaluating a decline in FEV(1) before and after replacement therapy, suggested a possible benefit for selected patients. Because of the lack of definitive proof of the clinical effectiveness of AAT replacement therapy and its cost, we recommend reserving AAT replacement therapy for deficient patients with impaired FEV(1) (35-65% of predicted value), who have quit smoking and are on optimal medical therapy but continue to show a rapid decline in FEV(1) after a period of observation of at least 18 months. A randomized placebo-controlled trial using CT scan as the primary outcome measure is required. Screening for AAT deficiency is recommended in patients with chronic irreversible airflow obstruction with atypical features such as early onset of disease or disability in their forties or fifties, or positive family history, and in immediate family members of patients with AAT deficiency.     

What's in a name? Renaming ‘NAFLD’ to ‘MAFLD’

In medicine, language matters and the words used to name and describe a disease can have a profound impact on patients and their families. Over the last two decades, many criticisms have been voiced about the nomenclature and definition of non‐alcoholic fatty liver disease (NAFLD) in regards not only to the prominent role that alcohol plays in the definition but also on the negative impacts of the nomenclature including trivialization, stigmatization and less consideration of the disease in health policy. Recently, a consensus of international experts proposed that the disease acronym be changed from NAFLD to metabolic (dysfunction) associated fatty liver disease or ‘MAFLD’. This change goes far beyond a mere semantic revision and may be the first step that catalyses the process to better conceptualize the disease for health promotion, patient orientation, case identification, ongoing clinical trials and for health services delivery. Here we review the history of, and definitions of MAFLD in the context of advancing our understanding of the pathogenesis of the disease. We also address the reasons, signals, promises, challenges and the way going forward from the name change from various stakeholder perspectives.     

Val/Leu<Superscript>247</Superscript> and Trp/Ser<Superscript>316</Superscript> polymorphisms in β<Subscript>2</Subscript> glycoprotein I and their association with thrombosis in unselected Chilean patients

It is known that polymorphisms of β ₂-glycoprotein I (β ₂GPI) in exon 7 affect interaction between the phospholipid binding site and the antibodies, and that other polymorphisms in exon 8 increase the generation of antibodies. In this study, we analyzed genetic polymorphisms of β ₂GPI in unselected Chilean patients to determine the prevalence of β ₂GPI polymorphisms in the phospholipid domain in patients with venous and arterial thrombosis and the clinical correlation with thromboembolic complications. This study comprised 149 patients with venous and arterial thrombosis (62 with venous thrombosis and 87 with arterial thrombosis) and 160 healthy controls with no previous history of thrombosis. Polymorphisms of exons 7 and 8 of β ₂GPI, which encode for its fifth domain, were determined by PCR-RFLP. The presence of aPL or anti-β ₂GPI in the patients was detected by ELISA. Anti-β ₂GPI were present in 8/149 patients (5.4%); of these, five had aCL antibodies of low titer. The allele containing Val/Leu²⁴⁷ and Trp/Ser³¹⁶ was significantly more frequent in patients with thrombosis than in the control group (OR=3.1, CI 1.6–6.0, p=0.0003; OR=2.9, CI 1.1–8.6, p=0.027, respectively). These polymorphisms did not correlate with aPL or anti-β ₂GPI but significant differences were observed with venous thrombosis (p=<0.0001) and arterial thrombosis (p=0.026). In conclusion, the β ₂GPI polymorphisms Val/Leu²⁴⁷ and Trp/Ser³¹⁶ are not related to the presence of anti-β ₂GPI antibodies in unselected Chilean patients with venous and arterial thrombosis, but they are significantly associated with venous and arterial thrombosis.     

<Emphasis Type="Italic">Clostridium Difficile</Emphasis> Infection in Non–HIV-Immunocompromised Patients and in HIV-Infected Patients

Clostridium difficile infection is a common cause of morbidity in patients with HIV infection and in patients with non-HIV immune deficiency. The frequency of C. difficile–associated diarrhea (CDAD) seen in these two patient populations has been attributed to immune deficiency, as well as to increased exposure to hospital environments and antibiotic therapy, both of which are major risk factors for CDAD. This article reviews recent data useful in the evaluation, treatment, and prevention of C. difficile infection in these patient groups. Recent publications relating to C. difficile infection in specific immunocompromised conditions are also discussed.