Introduction: Immunoglobulin G4-related hypophysitis (IgG4-RH) is a rare fibro-inflammatory disorder affecting the pituitary gland. Glucocorticoids remain the first-line therapy, but their use may be complicated in patients with significant metabolic comorbidities. We report a case of suspected IgG4-RH presenting with hyperosmolar hyperglycemic state (HHS), highlighting the challenges of balancing disease control against glucocorticoid metabolic toxicity adverse effects. Case: A 32-year-old female with obesity and newly diagnosed diabetes mellitus was admitted with HHS. Prior to admission, she reported weight fluctuations, episodic headaches, progressive visual disturbance, and secondary amenorrhea. Following resolution of HHS, persistent polyuria of 10–16 L/day prompted further evaluation and led to a diagnosis of arginine vasopressin deficiency. Anterior pituitary hormonal work-up revealed hypogonadotropic hypogonadism. Pituitary magnetic resonance imaging demonstrated infundibular thickening measuring 0.5 cm, with concomitant marked bilateral parotid enlargement. Serum IgG4 was elevated at 2.26 g/L (0.63–2.01), raising strong suspicion for IgG4-RH with systemic involvement. Histopathological confirmation from the parotid gland biopsy was consistent with sialadenosis. She was commenced on sublingual desmopressin and cyclical sex hormone replacement therapy. Given the provisional diagnosis of IgG4-RH, oral prednisolone 40 mg daily was initiated as a reduced induction regimen. However, treatment was poorly tolerated, with rapid weight gain from 93 to 100 kg and worsening glycemic control. Prednisolone was therefore tapered rapidly to 10 mg daily. Repeat imaging demonstrated interval improvement in infundibular thickening, but no functional endocrine recovery was observed. Conclusion This case illustrates the therapeutic challenge of managing IgG4-RH in the setting of pre-existing metabolic syndrome. Although glucocorticoids are effective for induction, their metabolic adverse effects may significantly restrict treatment tolerability. Early consideration of steroidsparing agents, such as rituximab or azathioprine, may be important to achieve remission while minimizing glucocorticoid-related adverse effects.
Autoimmune Hypophysitis

Introduction: Short stature and delayed puberty characterize Turner syndrome (TS). The 2024 international clinical practice guidelines recommend growth hormone (GH) for latediagnosed patients if epiphyses remain open. For patients with remaining growth potential, initiating GH alongside low-dose estrogen effectively balances linear growth with the need for timely pubertal induction. Case: A 15-year-old female, born prematurely at 6 months gestation, presented with delayed puberty, primary amenorrhea, and short stature. Examination revealed a height of 122 cm (<5th percentile), weight of 26 kg, with no syndromic facies, and Tanner stage 1. Investigations confirmed hypergonadotropic hypogonadism. Metabolic screening, including thyroid, renal, and liver profile, was normal. Her baseline insulin-like growth factor 1 (IGF-1) was low at 117.5 ng/mL (127.5–541.5). Karyotyping confirmed mosaic TS (45,X/46,Xr). Her skeletal bone age was delayed at 12 years, indicating a viable window for linear growth prior to complete epiphyseal fusion. Subcutaneous GH was initiated at 0.3 mg up titrated to 1.2 mg (0.45 µg/kg) daily over 4 weeks, then 1.35 mg (50 µg/kg) daily at month 5. Low-dose oral estradiol (0.5 mg three times weekly) was introduced for pubertal induction at month 4. After 9 months of combined GH and estrogen therapy, the patient achieved a height increment of 6 cm, reaching 128 cm without an adverse event. To achieve the clinical target of a 10–15 cm increment in the first year, her GH dose was further increased to 1.50 mg (55 µg/kg) daily. She showed an appropriate biochemical response with IGF-1 increased to 40.2 nmol/L (16.4–67.8) with a total height gain of 6 cm over the first 9 months of GH therapy. Conclusion Concomitant GH and estrogen therapy in late-diagnosed TS successfully induced clinically significant height gain. This dual approach maximized the limited window for linear growth, without delaying pubertal induction and compromising patient’s psychosocial well-being.
Turner Syndrome

Methods: In total, 185 lesions were identified on bone and SPECT-CT scans from 32 patients. Lesions were classified as metastatic (109 sclerotic lesions) and benign (76 lesions) morphologically on low-dose CT. Semiquantitative analysis using SUVmax and mean HU was performed on the lesions and compared. To discriminate benign and metastatic lesions, the correlation between SUVmax and mean HU was determined using the intraclass correlation coefficients. Results: The SUVmax was higher in metastatic lesions (20.66±14.36) but lower in benign lesions (10.18±12.79) (p<0.001). The mean HU was lower in metastatic lesions (166.62±202.02) but higher in benign lesions (517.65±192.8) (p<0.001). A weak negative correlation was found between the SUVmax and the mean HU for benign lesions, and a weak positive correlation was noted between the SUVmax and the mean HU on malignant lesions with no statistical significance (p=0.394 and 0.312, respectively). The cutoff values obtained were 10.8 for SUVmax (82.6% sensitivity and 84.2% specificity) and 240.86 for the mean HU (98.7% sensitivity and 88.1% specificity) in differentiating benign from malignant bone lesions. Conclusions Semiquantitative assessment using SUVmax and HU can complement qualitative analysis. Metastatic lesions had higher SUVmax but lower mean HU than benign lesions, whereas benign lesions demonstrated higher mean HU but lower SUVmax. A weak correlation was found between the SUVmax and the mean HU on malignant and benign lesions. Cutoff values of 10.8 for the SUVmax and 240.86 for the mean HU may differentiate bone metastases from benign lesions.

Methods: A total of 30 randomly selected female breast cancer patients were enrolled in this study. The SUV mean (SUVmean) and SUV maximum (SUVmax) values for 286 normal vertebrae at the thoracic and lumbar levels were calculated based on the patients’ body weight (BW), body surface area (BSA), and lean body mass (LBM). Additionally, 106 degenerative joint disease (DJD) lesions of the spine were also characterized, and both their BW SUVmean and SUVmax values were obtained. A receiver operating characteristic (ROC) curve analysis was then performed to determine the cutoff value of SUV for differentiating DJD from normal vertebrae. Results: The mean±standard deviations for the SUVmean and SUVmax in the normal vertebrae displayed a relatively wide variability: 3.92±0.27 and 6.51±0.72 for BW, 1.05±0.07 and 1.75±0.17 for BSA, and 2.70±0.19 and 4.50±0.44 for LBM, respectively. Generally, the SUVmean had a lower coefficient of variation than the SUVmax. For DJD, the mean±standard deviation for the BW SUVmean and SUVmax was 5.26±3.24 and 7.50±4.34, respectively. Based on the ROC curve, no optimal cutoff value was found to differentiate DJD from normal vertebrae. Conclusions In this study, the SUV of 99mTc-MDP was successfully determined using SPECT/CT. This research provides an approach that could potentially aid in the clinical quantification of radionuclide uptake in normal vertebrae for the management of breast cancer patients.