Partial Clinical Remission Reduces Lipid-Based Cardiovascular Risk in Adult Patients With Type 1 Diabetes.

Importance: Risk factors for atherosclerotic cardiovascular disease (ASCVD) are well established in type 2 diabetes (T2D), but not in type 1 diabetes (T1D). The impact of partial clinical remission (PR) on short-term ASCVD risk in T1D is unclear. Aim: To investigate the impact of PR on the earliest ASCVD risk phenotype in adult T1D using factor analysis to compare the lipid phenotypes of T1D, T2D and controls after stratifying the T1D cohort into remitters and non-remitters. Subjects and Methods: A study of 203 adults subjects consisting of 86 T2D subjects, and 77 T1D subjects stratified into remitters (n=49), and non-remitters (n=28). PR was defined as insulin-dose adjusted HbA1c of ≤9, and obesity as a BMI ≥30 kg/m2. Factor analysis was used to stratify the groups by ASCVD risk by factorizing seven lipid parameters (TC, LDL, HDL, non-HDL, TC/HDL, TG, TG/HDL) into 2 orthogonal factors (factor 1: TC*LDL; factor 2: HDL*TG) that explained 90% of the variance in the original seven parameters. Results: The analysis of individual lipid parameters showed that TC/HDL was similar between the controls and remitters (p=NS) but was significantly higher in the non-remitters compared to the remitters (p=0.026). TG/HDL was equally similar between the controls and remitters (p=NS) but was lower in the remitters compared to the non-remitters (p=0.007). TG was significantly lower in the remitters compared to T2D subjects (p<0.0001) but was similar between T2D subjects and non-remitters (p=NS). Non-HDL was significantly lower in the controls versus non-remitters (p=0.0003) but was similar between the controls and remitters (p=NS). Factor analysis showed that the means of factor 1 and factor 2 composite scores for dyslipidemia increased linearly from the controls, remitters, non-remitters to T2D, p value 0.0042 for factor 1, and <0.0001 for factor 2, with remitters having similar lipid phenotype as controls, while non-remitters were similar to T2D. Conclusions: Partial clinical remission of T1D is associated with a favorable early lipid phenotype which could translate to reduced long-term CVD risk in adults.

CLINICALLY SILENT ADRENOCORTICOTROPIC HORMONE-SECRETING CROOKE CELL ADENOMA PRESENTING AS UNILATERAL EAR PAIN.

OBJECTIVE: Crooke cell adenoma (CCA) is a rare tumor of the anterior pituitary. It is highly aggressive and carries significant risk of morbidity and mortality. METHODS: This report focuses on the presentation of this disease process and review diagnosis and treatment. The patient is a 64-year-old male with a history of resected pituitary adenoma of unknown pathology. RESULTS: The patient underwent serial magnetic resonance imaging surveillance for numerous years without recurrence of tumor, however eventually developed symptoms of worsening left ear pain over 3 weeks that rapidly evolved to include ptosis. Imaging revealed a new pituitary macroadenoma. Urgent surgical resection revealed histopathological diagnosis of CCA. Corticotroph adenomas represent a rare subset of pituitary tumors. Clinically silent pituitary tumors demonstrate relatively higher rates of cavernous sinus invasion (30% versus 18%) and progression or recurrence (34% versus 6%) when compared to nonfunctioning adenomas. In CCA, only 65% of patients have clinical features of Cushing disease at presentation. Twenty-four-hour urinary free cortisol is discussed in the literature as a potential tool, where a value 4 times the upper limit of normal was predictive of higher risk of having Crooke cell changes. With a recurrence rate of up to 60%, multimodal treatment (surgery and radiation) is preferred. CONCLUSION: This case highlights early detection and treatment as keys to reducing the risk of morbidity and mortality from CCA. Currently, there are limited tools for identifying patients who are high risk for developing Crooke cell changes. Treatment modalities classically include surgery and radiotherapy. Adjuvant and novel chemotherapies are being explored.