High sodium loads were administered intravenously to a group of subjects whose blood pressures covered a wide range. Despite large individual variations, the water and sodium excretion of the group were found to be significantly and directly correlated with blood pressure. (and, presumably, sodium) was lower in the hypertensive group. Differences in dietary salt intake prior to the studies were assumed to be inconspicuous, but were not measured.The present experiments were designed to study over a wide pressure range the relationship of the blood pressure level to sodium clearance and excretion rates in response to a fixed sodium load. METHODS AND MATERIALSThe subjects for these studies consisted of 45 patients from the wards and outpatient department of the Evanston Hospital. The majority were suffering from some form of cardiovascular disease (table 1). The group included 14 patients with a history of chronic congestive failure, who were well controlled at the time of study.No dietary restrictions were imposed except that the subject was instructed to take nothing by mouth from the prior midnight until completion of the test. Upon reporting to the laboratory at 7:30 a.m., height and weight were measured and the surface area was calculated. The patient was placed at bed rest and catheterized. The bladder was drained, washed with two 10 cc. portions of sterile distilled water and blown out with two 20 cc. portions of air. The specimen and washings from this collection were discarded. The catheter was clamped and left in place.At the end of a 30 minute control period the urine was collected by the procedure outlined above, the volume measured and the specimen saved for analysis. During this period, control blood samples were taken.Following the control period, 100 cc. per square meter of body surface area of a 5 per cent sodium chloride solution were infused into an arm vein over a 25-minute interval. Urine collections were made at 30, 60, 90, 120 and 180 minutes, respectively from the time of the start of the infusion. Blood samples were taken at the end of the first period and at the midpoint of all succeeding periods.

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BackgroundCombination drug therapy is the standard of care for HIV treatment. PI monotherapy is considered experimental in the United States. However, some patients end up receiving PI monotherapy secondary to resistance and/or drug intolerance to other antiretroviral (cART) classes. This study will discuss real-life clinical results in patients on PI monotherapy and examine the potential for the development of primary PI mutations.MethodsAn observational retrospective study conducted in an inner-city HIV clinic identified 10 patients on PI monotherapy who each had two GenoSure Archive® (Labcorp) resistance profiles performed. Gender, race, prior cART, and baseline VL and CD4+ count were captured. VL and CD4+ count were trended in the time period between resistance tests. These profiles were then compared checking for the emergence of new primary PI mutations.ResultsSeven out of 10 patients were African American, two were Hispanic, one was Caucasian, and half were male. The mean time interval between archived resistance tests was 6.87 months. During the time between resistance profiles, nine were on darunavir and one switched from lopinavir to darunavir for less pill burden. Eight had an undetectable VL (defined by <50 copies/mL) at the first resistance test, seven had undetectable VL at the second resistance test, and six remained undetectable over the entire period between profiles. There were three that demonstrated blips in VL and one that experienced virological failure between the two sets of resistance tests. One patient had an initial resistance profile showing primary resistance to lopinavir. No patients gained any primary PI mutations to darunavir.ConclusionThe results of this study suggest that mainly darunavir-based PI monotherapy has good genetic barrier, even in the setting of virological failure. Larger studies examining similar data over longer durations are needed to confirm this finding.Disclosures All authors: No reported disclosures.

Introduction While androgens are associated with decreased risk for type 2 diabetes in males, the opposite is seen in females. Despite this, a "chicken or the egg" argument exists regarding hyperandrogenism and insulin resistance in women. Ovarian hyperthecosis, a condition that mostly affects post-menopausal women, causes androgen excess due to hyperplasia of the theca interna of the ovaries. Akin to polycystic ovarian syndrome, it is associated with obesity and insulin resistance. We describe a case of ovarian hyperthecosis in a woman with type 2 diabetes with improved glycemic control following oophorectomy. Case A 63-year-old post-menopausal female with a history of autoimmune hepatitis, primary biliary cirrhosis, and chronic pancreatitis presented for recently diagnosed type 2 diabetes, discovered on routine point-of-care Hemoglobin A1c (HbA1c) testing in December 2020 (HbA1c 7.1%, weight: 86 kg). In January, she started repaglinide which was titrated to 2 mg with meals, also that month started prednisone for autoimmune hepatitis. Despite tapering doses of prednisone, her hyperglycemia paradoxically worsened and persisted following completion in June. In May, HbA1c was 7.8%. In August, she endorsed hirsutism, present for 2 years but worsening over the past few months. Labs showed elevated total testosterone (508 ng/dL), free testosterone (32.7 pg/mL), and androstenedione (305 ng/dL), with normal sex hormone binding globulin. DHEA-S was low (28.9 ug/dL, range: 29.4-220.5), midnight salivary cortisol was elevated (0.12 mcg/dL; range: &lt;0. 09), and morning serum ACTH and cortisol were within normal range, with appropriate suppression to dexamethasone. Estradiol was above post-menopausal range (68.1 pg/mL; range: &lt;6. 0-54.7). FSH and LH were within the post-menopausal range, with an approximate 1: 1 ratio. A pelvic ultrasound revealed two intramural myomas and a simple cyst of the right ovary, but otherwise unremarkable. She underwent bilateral salpingo-oophorectomy in October 2021. Post-surgical total testosterone was 27 ng/dL. Surgical pathology revealed unremarkable fallopian tubes and bilateral stromal hyperplasia and hyperthecosis of the ovaries. At one month follow-up, HbA1c was 6.5%, weight decreased from 89 kg pre-surgery to 86, and she endorsed improved hirsutism but frequent hypoglycemia on repaglinide 2 mg with meals. Repaglinide was decreased to 0.5 mg with meals. Three months later, HbA1c was 6.3% with unchanged weight. Conclusion Improved glycemic control, corresponding with timing of oophorectomy but not discontinuation of steroids, suggests insulin resistance in this case may be due to hyperandrogenism. Though some studies and case reports suggest hyperandrogenism causes insulin resistance, others suggest the contrary. The relationship between androgens and insulin sensitivity is likely complex, and further research is necessary. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.