Pituitary apoplexy after COVID-19 vaccination: A case report.

Background: Pituitary apoplexy is a rare endocrine emergency, which commonly presents with headache and is occasionally associated with visual disturbances. Prompt diagnosis and treatment can be both life and vision saving. In the emergence of novel coronavirus and global pandemic, rapid development of new vaccines have shown to reduce morbidity and mortality associated with Covid-19. Recognition of rare potential adverse effects of these vaccines including pituitary apoplexy are yet to be reported. A causal link between pituitary apoplexy and COVID-19 vaccination has not been established. Case presentation: We report a case of a 24-year-old woman who presented with progressively worsening headache soon after completing her COVID-19 vaccination. Imaging showed pituitary apoplexy with an underlying pituitary mass. In view of the age and the typical presentation of severe headache, pituitary hypophysitis was considered, despite the absence of the almost pathognomonic feature of a thickened pituitary stalk in the initial imaging. In the context that the headache had started shortly after the administration of the second dose of COVID-19 vaccine, this potentially could have been the trigger for the occurrence of pituitary apoplexy. Conclusion: Although the pathophysiology is not entirely clear and no direct link could be ascertained, our patient may have developed an exaggerated immunological response after the vaccine, with a possible pituitary hypophysitis leading to a pituitary apoplexy.

Primary hyperparathyroidism presenting with sudden onset paraplegia.

A 48-year-old female with long-standing type 2 diabetes mellitus presented with acute onset of bilateral lower limb weakness. She had been previously well and denied any constitutional symptoms. Physical examinations revealed generalized lower limb weakness with bilateral lower limb hypotonia, power of 0 over 5, reduced deep tendon reflexes, and loss of peripheral sensations up to the level of T10. Upper limb functions were normal. Rectal examination showed a lax anal tone and reduced anal grip. Blood investigations showed elevated serum alkaline phosphatase, corrected serum calcium, and parathyroid hormone. Magnetic resonance imaging of the spine revealed an expansile mass at the posterior element of the ninth thoracic vertebrae, causing spinal compression with possible impingement of the right T9 exiting spinal nerve. An urgent surgical decompression and tissue biopsy were performed for stabilization of the spine. Intraoperative findings included spinal cord compression secondary to an epidural tumour mass extending from T9 to T10 disc levels. Histopathological analysis showed a giant cell tumour of the spine. A 99mTc Sestamibi-SPECT parathyroid scintigraphy showed an ectopic parathyroid adenoma at the left suprasternal region. A diagnosis of Brown tumour secondary to ectopic parathyroid adenoma was made. She underwent an exploratory parathyroidectomy procedure with removal of the ectopic parathyroid gland, which resulted in a normalization of the serum calcium and parathyroid hormone. Unfortunately, her lower limb functions did not return to normal, and she remained paraplegic at 6 months postoperatively.

A rare case of macroprolactinoma in a patient with Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome.

SUMMARY: A 17-year-old lady presented with primary amenorrhoea, headache, nausea and lethargy. She had delayed pubertal development that also includes under-developed breast (Tanner Stage 2). Hormonal investigations showed a high serum prolactin level of 1 680 000 mIU/L (normal value: 45-375 mIU/L), with low oestradiol, progesterone, follicular-stimulating hormone and luteinizing hormone. Early morning cortisol level was 206 nmol/L (normal value: >450 nmol/L), thyroxine was 7.5 pmol/L (normal value: 9.0-24.0 pmol/L) with TSH 5.091 mIU/L (normal value: 0.4-4.5 mlU/L). A pituitary MRI showed a 2.7 (AP) × 3.7 (W) × 4.6 cm (CC) macroadenoma, with invasion into the left cavernous sinus and encasement of cavernous portion of the left internal carotid artery. MRI pelvis showed absent uterus, cervix and 2/3 upper vagina confirming Mullerian hypoplasia. Cytogenetics showed 46XX. These findings were suggestive of Mayer-Rokitansky-Kauser-Hauser (MRKH) syndrome with the presence of a pituitary macroprolactinoma and panhypopituitarism. She was treated with hydrocortisone, levothyroxine and cabergoline. Repeated MRI showed a reduction in tumour size by approximately 50%. This case illustrated a rare coexistence of these two conditions, being only the third reported case in the world. In addition, this would be the first case of a functioning pituitary adenoma in a patient with MRKH syndrome. LEARNING POINTS: Comprehensive hormonal and radiological investigations are important in the management of a young patient with primary amenorrhoea. Coexistence pathology of two separate pathologies should be considered in patient presenting with primary amenorrhoea. Early diagnosis of MRKH or any disorders of sex development should be treated early, providing pharmacological, surgical, psychological and emotional support to the patient and reducing risk of associated complications. Abnormal pituitary hormones, particularly panhypopituitarism, would impose greater impact not only psychologically but also metabolically leading to cardiovascular, morbidity and mortality risks in this patient if not treated early. A multidisciplinary approach is necessary for patients presenting with MRKH to ensure appropriate treatments and follow-up across the lifespan of the patient.

Safety and efficacy of very low carbohydrate diet in patients with diabetic kidney disease-A randomized controlled trial.

INTRODUCTION: There is limited data on the effects of low carbohydrate diets on renal outcomes particularly in patients with underlying diabetic kidney disease. Therefore, this study determined the safety and effects of very low carbohydrate (VLCBD) in addition to low protein diet (LPD) on renal outcomes, anthropometric, metabolic and inflammatory parameters in patients with T2DM and underlying mild to moderate kidney disease (DKD). MATERIALS AND METHODS: This was an investigator-initiated, single-center, randomized, controlled, clinical trial in patients with T2DM and DKD, comparing 12-weeks of low carbohydrate diet (<20g daily intake) versus standard low protein (0.8g/kg/day) and low salt diet. Patients in the VLCBD group underwent 2-weekly monitoring including their 3-day food diaries. In addition, Dual-energy x-ray absorptiometry (DEXA) was performed to estimate body fat percentages. RESULTS: The study population (n = 30) had a median age of 57 years old and a BMI of 30.68kg/m2. Both groups showed similar total calorie intake, i.e. 739.33 (IQR288.48) vs 789.92 (IQR522.4) kcal, by the end of the study. The VLCBD group showed significantly lower daily carbohydrate intake 27 (IQR25) g vs 89.33 (IQR77.4) g, p<0.001, significantly higher protein intake per day 44.08 (IQR21.98) g vs 29.63 (IQR16.35) g, p<0.05 and no difference in in daily fat intake. Both groups showed no worsening of serum creatinine at study end, with consistent declines in HbA1c (1.3(1.1) vs 0.7(1.25) %) and fasting blood glucose (1.5(3.37) vs 1.3(5.7) mmol/L). The VLCBD group showed significant reductions in total daily insulin dose (39(22) vs 0 IU, p<0.001), increased LDL-C and HDL-C, decline in IL-6 levels; with contrasting results in the control group. This was associated with significant weight reduction (-4.0(3.9) vs 0.2(4.2) kg, p = <0.001) and improvements in body fat percentages. WC was significantly reduced in the VLCBD group, even after adjustments to age, HbA1c, weight and creatinine changes. Both dietary interventions were well received with no reported adverse events. CONCLUSION: This study demonstrated that dietary intervention of very low carbohydrate diet in patients with underlying diabetic kidney disease was safe and associated with significant improvements in glycemic control, anthropometric measurements including weight, abdominal adiposity and IL-6. Renal outcomes remained unchanged. These findings would strengthen the importance of this dietary intervention as part of the management of patients with diabetic kidney disease.

A case report on a protracted course of a hidden insulinoma.

INTRODUCTION: Insulinoma is a functioning pancreatic neuroendocrine tumor primarily leading due to hypoglycemia due to hypersecretion of insulin. This case illustrates the real challenges faced in the detection of an occult insulinoma, which resulted in a protracted course of the disease. CASE PRESENTATION: A 33-year-old female presented with recurrent hypoglycemia. Endogenous hyperinsulinemia was confirmed by a prolonged fast, however serial imaging was negative. Incidental finding of an ovarian mass gave rise to the suspicion of an insulin-producing ovarian tumor. Subsequent multimodality pancreatic imaging remained negative, requiring more invasive investigations. The tumor was localized by specialized arteriography using calcium stimulation to support the diagnosis of an insulinoma. However, repeated negative imaging led to further delays in definitive management, with worsening hypoglycemia. The surgery was finally performed three years after the initial presentation with successful removal of the tumor using intra-operative ultrasound. CLINICAL DISCUSSION: It is important to emphasize that preoperative radiological imaging is useful to localize pancreatic lesions. However, most insulinomas could only be detected intraoperatively. The absence of suggestive radiological evidence should not deter surgeons from proceeding with definitive surgical intervention. CONCLUSION: The case highlights the importance of a multidisciplinary approach in the management of a complicated case.

Effects of Dapagliflozin on Endothelial Dysfunction in Type 2 Diabetes With Established Ischemic Heart Disease (EDIFIED).

OBJECTIVES: To evaluate the effect of the sodium-glucose cotransporter 2 inhibitor (SGLT2-I) dapagliflozin on endothelial function in patients with high-risk type 2 diabetes mellitus (T2DM). METHODS: This was a prospective, double-blind, randomized, placebo-controlled, clinical trial of patients with T2DM with underlying ischemic heart disease who were receiving metformin and insulin therapy (n = 81). After 12-weeks of additional therapy with either dapagliflozin (n = 40) or placebo (n = 41), systemic endothelial function was evaluated by change in flow-mediated dilation (ΔFMD), change in nitroglycerin-mediated dilation (ΔNMD) and surrogate markers including intercellular adhesion molecule 1 (ICAM-1), endothelial nitric oxide synthase (eNOS), high-sensitivity C-reactive protein (hs-CRP), and lipoprotein(a) (Lp[a]). Glycemic and lipid profiles were also measured. RESULTS: The dapagliflozin group demonstrated significant reductions of hemoglobin A1c (HbA1c) and fasting blood glucose (FBG) compared to the placebo group (ΔHbA1c -0.83 ± 1.47% vs -0.16 ± 1.25%, P = 0.042 and ΔFBG vs -0.73 ± 4.55 mmol/L vs -1.90 ± 4.40 mmol/L, P = 0.015, respectively). The placebo group showed worsening of ΔFMD while the dapagliflozin group maintained similar measurements pre- and posttherapy (P = not significant). There was a reduction in ICAM-1 levels in the dapagliflozin group (-83.9 ± 205.9 ng/mL, P < 0.02), which remained unchanged in the placebo group (-11.0 ± 169.1 ng/mL, P = 0.699). Univariate correlation analysis revealed a significant negative correlation between HbA1c and ΔFMD within the active group. CONCLUSION: A 12-week therapy with dapagliflozin, in addition to insulin and metformin therapies, in high-risk patients resulted in significant reductions in HbA1c, FBG, and surrogate markers of the endothelial function. Although the dapagliflozin group demonstrated a significant association between reduction in HbA1c and improvement in FMD, there was no significant difference in FMD between the 2 groups.