ABSTRACT
BACKGROUND: Chronic pruritus is common in patients with diabetes though its pathophysiology is unknown and difficult to pinpoint given the multi-system manifestations of diabetes. Herein, we aim to evaluate the severity of chronic itch in patients with diabetes and its association with glycaemic control, microvascular complications and quality of life. METHODS: We conducted a retrospective study of 105 adults with diabetes evaluated by a dermatologist at a tertiary care centre in Mexico City. Degree of chronic pruritus and its impact on quality of life as well as laboratory, clinical and demographic data were collected. Patients without chronic pruritus (n = 62) were compared to those with chronic pruritus (n = 43). The latter cohort was further stratified by itch severity, and characteristics of their itch were quantified. RESULTS: Neuropathy and loss of protective sensation were more common in patients with chronic pruritus, compared to those without chronic pruritus (p = 0.007 and p = 0.001, respectively). Anxiety and depression were more common in individuals with chronic pruritus (p = 0.009), and these group reported higher effect of pruritus on their quality of life (p < 0.0001). The most common sites of itch were the head, back and arms. Among patients with chronic itch, increasing itch severity was associated with decreasing eGFR (p = 0.080). CONCLUSIONS: The underlying cause of chronic itch in patients with diabetes is likely multifactorial and owing to microvascular complications such as neuropathy and nephropathy. Better understanding of the causes of itch in these patients can allow for more targeted treatment, leading to improved quality of life.
Subject(s)
Diabetes Mellitus , Peripheral Nervous System Diseases , Adult , Humans , Quality of Life , Retrospective Studies , Pruritus/drug therapy , Severity of Illness IndexABSTRACT
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is a global health threat with the potential to cause severe disease manifestations in the lungs. Although COVID-19 has been extensively characterized clinically, the factors distinguishing SARS-CoV-2 from other respiratory viruses are unknown. Here, we compared the clinical, histopathological, and immunological characteristics of patients with COVID-19 and pandemic influenza A(H1N1). We observed a higher frequency of respiratory symptoms, increased tissue injury markers, and a histological pattern of alveolar pneumonia in pandemic influenza A(H1N1) patients. Conversely, dry cough, gastrointestinal symptoms and interstitial lung pathology were observed in COVID-19 cases. Pandemic influenza A(H1N1) was characterized by higher levels of IL-1RA, TNF-α, CCL3, G-CSF, APRIL, sTNF-R1, sTNF-R2, sCD30, and sCD163. Meanwhile, COVID-19 displayed an immune profile distinguished by increased Th1 (IL-12, IFN-γ) and Th2 (IL-4, IL-5, IL-10, IL-13) cytokine levels, along with IL-1ß, IL-6, CCL11, VEGF, TWEAK, TSLP, MMP-1, and MMP-3. Our data suggest that SARS-CoV-2 induces a dysbalanced polyfunctional inflammatory response that is different from the immune response against pandemic influenza A(H1N1). Furthermore, we demonstrated the diagnostic potential of some clinical and immune factors to differentiate both diseases. These findings might be relevant for the ongoing and future influenza seasons in the Northern Hemisphere, which are historically unique due to their convergence with the COVID-19 pandemic.
