Mechanisms Linking COPD to Type 1 and 2 Diabetes Mellitus: Is There a Relationship between Diabetes and COPD?

Chronic obstructive pulmonary disease (COPD) patients frequently suffer from multiple comorbidities, resulting in poor outcomes for these patients. Diabetes is observed at a higher frequency in COPD patients than in the general population. Both type 1 and 2 diabetes mellitus are associated with pulmonary complications, and similar therapeutic strategies are proposed to treat these conditions. Epidemiological studies and disease models have increased our knowledge of these clinical associations. Several recent genome-wide association studies have identified positive genetic correlations between lung function and obesity, possibly due to alterations in genes linked to cell proliferation; embryo, skeletal, and tissue development; and regulation of gene expression. These studies suggest that genetic predisposition, in addition to weight gain, can influence lung function. Cigarette smoke exposure can also influence the differential methylation of CpG sites in genes linked to diabetes and COPD, and smoke-related single nucleotide polymorphisms are associated with resting heart rate and coronary artery disease. Despite the vast literature on clinical disease association, little direct mechanistic evidence is currently available demonstrating that either disease influences the progression of the other, but common pharmacological approaches could slow the progression of these diseases. Here, we review the clinical and scientific literature to discuss whether mechanisms beyond preexisting conditions, lifestyle, and weight gain contribute to the development of COPD associated with diabetes. Specifically, we outline environmental and genetic confounders linked with these diseases.

Therapeutic Potential of Alpha-1 Antitrypsin in Type 1 and Type 2 Diabetes Mellitus.

Alpha-1 antitrypsin (AAT) has established anti-inflammatory and immunomodulatory effects in chronic obstructive pulmonary disease but there is increasing evidence of its role in other inflammatory and immune-mediated conditions, like diabetes mellitus (DM). AAT activity is altered in both developing and established type 1 diabetes mellitus (T1DM) as well in established type 2 DM (T2DM). Augmentation therapy with AAT appears to favorably impact T1DM development in mice models and to affect ß-cell function and inflammation in humans with T1DM. The role of AAT in T2DM is less clear, but AAT activity appears to be reduced in T2DM. This article reviews these associations and emerging therapeutic strategies using AAT to treat DM.

Novel oral anticoagulants in intracardiac thrombosis resolution: a case series.

BACKGROUND: Vitamin K antagonists (VKAs) have been regarded as the therapy of choice for intracardiac thrombosis for decades based mostly on observational data. The advent of direct oral anticoagulants (DOACs) has displaced VKAs as the first-line therapy for multiple thrombotic disorders but not for intracardiac thrombosis. Although limited, there is growing evidence that DOACs are effective for intracardiac thrombosis and some data suggest that thrombus resolution might be superior to that with warfarin. CASE SUMMARY: Here, we present a series of six patients with left atrial appendage thrombi were treated with a venous thromboembolic dose of DOACs with resolution within 2-6 months with no reported complications. DISCUSSION: This case series adds to the accumulating evidence supporting the efficacy of DOACs in the treatment of intracardiac thrombi.

Jerky Movement with Ceftazidime: A Case of Ceftazidime-Induced Neurotoxicity with a Review of the Literature.

Neurotoxicity manifested as confusion and seizures has been recognized as a side effect of multiple cephalosporins including ceftazidime. Renal impairment and inappropriate dosing are the most common contributors to the development of neurological abnormalities in patients receiving these antibiotics. The presence of baseline neurological abnormalities likely contributes to the frequency of these adverse events. Here, we present a case of a 78-year-old man that developed altered mental status and myoclonic movement after initiation of ceftazidime in the setting of mild renal dysfunction. Resolution of clinical picture was evident after 48 hours of discontinuation of the antibiotic without additional interventions.