Obstructive sleep apnea (OSA) is frequently associated with obesity and metabolic syndrome. Also frequently associated with metabolic syndrome is type 2 diabetes mellitus (T2DM). Therefore, it is common to find OSA and T2DM together in individuals with metabolic syndrome. Additionally, both OSA and T2DM have a common pathophysiological link with development of insulin resistance. Individuals with severe insulin resistance are likely to have inadequate glycemic control. Long standing poorly controlled T2DM is associated with debilitating microvascular complications such as retinopathy, nephropathy, neuropathy and macrovascular complications such as coronary artery and cerebrovascular disease. There is extensively published literature exploring the cause-effect relationship between OSA and T2DM. In this article we provide an in-depth review of the complex pathophysiological mechanisms linking OSA to T2DM. Specifically, this review focusses on the effect of OSA on the microvascular complications of T2DM such as retinopathy, nephropathy and neuropathy. Additionally, we review the current literature on the effect of continuous positive airway pressure use in individuals with T2DM and OSA.
Noise is a significant contributor to sleep disruption in the intensive care unit (ICU) that may result in increased patient morbidity such as delirium and prolonged length of stay in ICU. We conducted a pre-post intervention study in a 24-bed tertiary care academic medical ICU to reduce the mean noise levels. Baseline dosimeter recordings of ICU noise levels demonstrated a mean noise level of 54.2 A-weighted decibels (dBA) and peak noise levels of 109.9 dBA, well above the Environmental Protection Agency's recommended levels. There were 1735 episodes of "defects" (maximum noise levels > 60 dBA). Following implementation of multipronged interventions, although the mean noise levels did not change significantly between pre- and post-intervention (54.2 vs 53.8 dBA; p = 0.96), there was a significant reduction in the number of "defects" post-intervention (1735 vs 1289, p ≤ 0.000), and the providers felt that the patients were sleeping longer in the ICU post-intervention.
Case Description: - A 76 year old lady was diagnosed with Chronic Lymphocytic Leukemia (CLL) with 11 q deletion after she presented with generalized lymphadenopathy and anemia. She was treated with rituximab 375mg/m2 day1 and bendamustine 60mg/m2 on day 1 and day 2 and completed six cycles of treatment. After the sixth cycle she developed multiple itchy, papular lesions with bleeding on both lower extremities. She was evaluated multiple times by vascular surgery and dermatology without a definitive diagnosis. She underwent a biopsy with staining for HHV-8, CD31 and CD34 which was positive confirming the diagnosis of Kaposi sarcoma. ELISA test for HIV was negative. She was started on treatment with Doxorubicin 20 mg/m2every 3 weeks and with 3 cycles there was significant regression of the lesions.
Discussion-: We describe a case of CLL which was initially started on treatment with rituximab and bendamustine. She tolerated the treatment well, but a few months later presented with skin lesions which on biopsy was diagnosed as Kaposi sarcoma. It is very uncommon for Kaposi sarcoma to develop in a HIV negative patient. This patient was immunocompromised with recent chemotherapy. Rituximab specifically depletes B cells and leads to impaired T cell mediated immunity. This case illustrates the importance of a high index of suspicion in patients treated with rituximab as it is used for a number of hematologic malignancies like leukemia, lymphoma as well as non-malignant conditions like autoimmune disorders. While infusion reactions and reactivation of hepatitis B are side effects physicians are aware of and cautious of while using rituximab, Kaposi’s Sarcoma remains a less known side effect. Awareness of this possibility is important in physicians prescribing rituximab.
Footnotes
* Asterisk with author names denotes non-ASH members.
Disclosures
No relevant conflicts of interest to declare.
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