scTox is associated with lower muscle mass and mid-thigh girth and more fatigue. Physical activity training can partially ameliorate these characteristics. More studies are needed to determine what training program would be optimum, both in terms of beneficial effects and for avoiding potential adverse responses.

The SCH patients had worse muscle function, regarding HS (25.19 ± 7.00 vs. 30.45 ± 9.98 kgf in EU, P = 0.009) and functional capacity of the shoulder (41.28 ± 48.36 vs. 56.68 ± 37.44 s in EU, P = 0.004). The self-perception of fatigue by Chalder questionnaire (23.91 ± 5.39 vs. 29.77 ± 7.03, P = 0.000) and the QoL in terms of functional capacity (70.20 ± 21.57 vs. 56.25 ± 28.79, P = 0.025), physical aspects (71.42 ± 36.44 vs. 45.83 ± 42.88, P = 0.004), pain (62.48 ± 22.20 vs. 50.05 ± 24.80, P = 0.035), and emotional aspects (70.74 ± 38.26 vs. 46.29 ± 44.56, P = 0.008) were also worse in SCH. In conclusion, the SCH was associated with alterations in the QoL, reduction in the muscle function of upper limbs, and higher degree of fatigue.

Introduction Pituitary abscess is a rare condition, representing 0.2-0.6% of all pituitary lesions. The presentation can be non-specific, and imaging can mimic a pituitary adenoma, often making the diagnosis challenging. We present a case of a pituitary abscess from Staphylococcus epidermidis and Corynebacterium propinquum with resulting hypopituitarism and central diabetes insipidus (DI). Clinical case A 42-year-old man with a history of hypothyroidism secondary to thyroiditis presented to the emergency room with sudden onset headache, nausea, and emesis. There were associated symptoms of fatigue, weight loss, and sexual hypofunction for approximately six months. He did not have fever or leukocytosis. Brain MRI revealed a 2.5×1.8×1.6 cm sellar and suprasellar mass with rim enhancement and compression of the optic chiasm. Pre-operative pituitary hormonal evaluation showed central hypogonadism, growth hormone deficiency and secondary adrenal insufficiency: FSH 0.4 mIU/mL (n < 15mIU/mL), LH <0.2mIU/mL (n < 10 mIU/mL), AM Testosterone 8 ng/dL (n 250-1100 ng/dL), IGF-1 38 ng/ml (n 52-328 ng/mL), ACTH 5.6 pg/mL (n 7.2-63 pg/mL), AM cortisol 4.9 ug/mL (n 4-10 ug/dL). Prolactin was normal (14.7 ng/mL, n <15 ng/mL). TSH was elevated to 4.88 uU/mL (n 0.3-4.2 uU/mL) with a low FT4 of 0.5 ng/dL (n 0.6-1.5 ng/dL) on levothyroxine 75mcg daily. He was started on stress doses of hydrocortisone and underwent trans-sphenoidal pituitary resection. Intraoperative findings were significant for 3-5 mL of purulent debris in the sella suggestive of a pituitary abscess. He was started on Ceftriaxone, Metronidazole, and Vancomycin, with improvement in headache. Pituitary abscess cultures grew Staphylococcus epidermidis and Corynebacterium propinquum. Blood cultures were negative for any bacterial growth. Post-operative course was complicated by transient DI. The patient was discharged on Linezolid to complete six weeks of antibiotics, a physiological dose of hydrocortisone (20mg daily), and levothyroxine 88mcg daily. At outpatient Endocrine follow-up a month later, he was found to have a recurrence of DI and started on maintenance desmopressin with improvement in polyuria and polydipsia. Conclusion Pituitary abscesses are rare, life-threatening pituitary lesions. 70% of cases are primary pituitary abscesses, which develop in a previously healthy gland. Secondary pituitary abscesses arise within a pre-existing pituitary lesion and are less common. Clinical manifestations include headache, visual disturbance, and hypopituitarism. The diagnosis is challenging since classical signs of infection, such as fever and leukocytosis, are uncommon, and pre-operative radiological findings can be non-specific. The majority of cases are confirmed intra-operatively. Commonly isolated organisms are Gram-positive cocci (Staphylococcus and Streptococcus) and Gram-negative bacteria (Neisseria, Escherichia coli and Corynebacterium). This case highlights the importance of considering pituitary abscesses in the differential diagnosis of patients presenting with a sellar mass. Prompt recognition of a pituitary abscess will allow for rapid treatment with trans-sphenoidal evacuation, antibiotic therapy, and pituitary hormonal replacement when indicated. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

Activation of hypothalamic KATP channels reduces endogenous glucose production (EGP) in nondiabetic rodents and humans, but this response is lost in T2D. Lowering FFA with nicotinic acid (NA) restored central regulation of EGP in T2D subjects (Diabetes 2019; 1799P). High FFA levels, typical of T2D, may increase endoplasmic reticulum (ER) stress and thereby impair hypothalamic control of EGP. To explore how increased FFA might impact central regulation of EGP, we harvested hypothalamic wedges from n=10 Zucker Diabetic Fatty (ZDF) rats (glucose ~ 370 mg/dL) following infusion of NA or saline (Alzet minipump) for 18 h. Nondiabetic rats (n=5) were studied as controls. Gene expression of KATP channel subunit Kir6.2 was decreased in ZDF rats. Upon lowering FFA with NA, hypothalamic expression of this major subunit was restored (Fig 1a). Conversely, increased expression of genes regulating ER stress was reversed by NA (Fig 1b). Directly treating ZDF rat brain slices with NA did not alter the expression of these genes, suggesting that NA's effects were mediated by lowering FFA (Fig 1c). In conclusion, hypothalamic effects of elevated FFA include reduced KATPchannel expression and increased expression of ER stress genes, both of which may contribute reversibly to the loss of central regulation of EGP in T2D. These findings are consistent with our observations in humans noted above, suggesting that FFA could be a therapeutic target in T2D. Disclosure M. Nogueira Cordeiro: None. V.H. Routh: None. A. Manavalan: None. P.M. Mathias: None. C.E. Boyle: None. A.C. Rios Chen: None. N. Jiang: None. N. Friedman: None. Y. Demirhan: None. M. Hawkins: None. K. Zhang: None. Funding American Diabetes Association (7-08-CR-28 to M.H.); National Institutes of Health (R01DK069861); Diabetes Action Research and Education Foundation

HAAF, which has been defined as >20% reduction in average epinephrine (Epi) levels following recurrent hypoglycemia (PMID: 28911152), complicates insulin therapy in T1D. We previously showed that activation of opioid receptors induces HAAF, while intravenous (IV) administration of the opioid receptor antagonist naloxone prevents HAAF. Because of its wide clinical use and possible direct CNS effects, we examined the effects of intranasal naloxone (IN) on hypoglycemia and HAAF. Seventeen (15M, age 43.8±8.7) healthy adults were enrolled in a randomized, placebo-controlled, cross-over, double-blinded study in which they underwent three hyperinsulinemic hypoglycemic clamp studies (duration 2h, glucose nadir 54 mg/dL), with administration of IN (4mg) or placebo during the first two clamps. Two subjects were excluded for lack of Epi response to hypoglycemia. Nine of the remaining 15 subjects developed HAAF, confirming inter-individual variability in susceptibility to HAAF (PMID: 32915987, 35475026). Among the 15 subjects included in the analysis, Epi levels trended downward between the 1st and 3rd clamps in placebo studies (mean ± SEM: 677 ± 114 vs. 512 ± 78 pg/mL, p=0.054), whereas Epi levels remained stable in IN studies (1st vs. 3rd: 519 ± 70 vs. 487 ± 77 pg/mL, p= 0.69). Among the 9 subjects who developed HAAF, Epi levels during the 1st clamp were significantly lower with IN vs. placebo (493 ± 102 vs. 858 ± 161 pg/mL, p=0.03), but there was no further reduction in Epi with IN (1st vs. 3rd: 493±102 vs. 539±101 pg/ml, p=0.67). In summary, these studies suggest differential effects of intranasal naloxone on initial vs. repeated hypoglycemic episodes. Specifically, IN may be effective in preventing Epi blunting during repeated exposure to hypoglycemia. In subjects susceptible to HAAF, IN may paradoxically blunt the Epi response to initial hypoglycemic exposure. Future studies should investigate the clinical significance of initial vs. ongoing epinephrine responses to hypoglycemia. Disclosure C.E.Boyle: None. M.Hawkins: None. E.Lontchi yimagou: Employee; Sanofi. S.Aleksic: None. P.M.Mathias: None. M.Nogueira cordeiro: None. A.Manavalan: None. M.Carey: None. N.Jiang: None. O.Sandu: None. I.Gabriely: None. K.Zhang: None. Funding National Institutes of Health (R01DK079974)