Introduction: Type 2 diabetes mellitus (T2DM), once perceived as a condition prevalent among affluent elderly urban residents, now affects a more diverse demographic, including populations from less-privileged and rural communities. While providing optimal care, clinicians face challenges, such as the financial constraints of T2DM patients. This underscores the urgent need for affordable interventions to enhance patient outcomes and the necessity for a comprehensive understanding of clinician knowledge, attitudes, and perceptions (KAPs). The aim of this study was to develop a consensus of Indian clinicians to emphasize the need for awareness and access to high-quality, affordable interventional approaches for effectively managing resource-challenged T2DM patients in India. Methods: A mixed method study, including 590 clinicians and 60 subject matter experts, assessed their KAPs regarding managing >18 years of adult resource-challenged (deserving) T2DM patients. A structured questionnaire gathered data on clinicians’ clinical and management practices. Four days in-depth interview with 60 subject matter experts also facilitated the expert opinion development process, ensuring a comprehensive and reliable study. Data were analyzed using SPSS Version 29, with statistical significance at P < 0.05. Results: The findings of this study, based on the responses of 590 clinicians, are significant. About 38.64% of the clinicians encountered 1–5 resource-challenged T2DM patients daily, while 40.33% encountered 6–15 patients, reflecting a significant patient load. Concerning follow-up duration, 59.10% reported 1–3 months, highlighting the challenges in maintaining regular follow-ups. Over 80% agreed that these patients struggle to afford treatment and often miss follow-up appointments, seeking alternative therapies due to financial constraints, which can lead to suboptimal glycemic control ( P < 0.001). In addition, 82.00% agreed that high cost and lack of financial resources as the primary reason for medication non-adherence. The majority of clinicians agreed that “Glipizide + Metformin could be optimally used for these patients” ( P < 0.001). The expert panel identified financial constraints, lifestyle modification difficulties, and psychological challenges as key issues in managing resource-challenged T2DM patients in India. Conclusion: Clinicians and the expert panel agreed on several critical issues, including financial constraints and challenges in adopting lifestyle modifications to manage resource-challenged (deserving) T2DM patients. There is agreement on prescribing low-cost glucose-lowering medications with metformin and glipizide combinations to improve patient adherence and outcomes in resource-constrained settings.

OBJECTIVE:To evaluate whether inflammatory markers and carotid intima-media thickness are increased in patients with Sheehan syndrome. METHODS:This study included 37 patients diagnosed with Sheehan syndrome who met the eligibility criteria, along with 37 healthy controls matched for age, body mass index, and parity. All participants underwent a detailed clinical evaluation, along with measurement of biochemical and hormonal parameters, as well as inflammatory markers, specifically tumor necrosis factor alpha and interleukin-6. Both patients and controls were assessed for carotid intima-media thickness using a high-resolution color Doppler system. RESULTS:Patients with Sheehan syndrome had significantly higher mean levels of triglycerides, total cholesterol, and low-density lipoprotein cholesterol, along with lower levels of high-density lipoprotein cholesterol compared with controls. They also exhibited higher levels of tumor necrosis factor alpha (23.41 ± 10.97 pg/mL versus 20.05 ± 2.76 pg/mL; p = 0.041) and interleukin-6 (37.19 ± 5.38 pg/mL versus 32.08 ± 1.18 pg/mL; p = 0.004), as well as an increased mean carotid intima-media thickness value (0.71 ± 0.07 mm versus 0.59 ± 0.05 mm; p = 0.001). CONCLUSION:Patients with Sheehan syndrome exhibited risk factors that may elevate their likelihood of developing atherosclerosis.

CONTEXT:Sheehan's syndrome (SS) is a rare cause of hypopituitarism. Data on skeletal health in patients with this condition is limited and predictors of low bone mineral density (BMD) are not well elucidated. We aimed to explore hormonal profile and BMD in a large multicentric cohort of treated SS patients. DESIGN AND PATIENTS:The study recruited patients with SS on stable hormone replacement (n = 110) and healthy female controls (n = 102). The hormonal profile (cortisol, DHEAS, T4, TSH, prolactin, IGF1) was analyzed. Bone turnover markers (P1NP, β-CTX) were estimated by electrochemiluminescence assay. BMD was evaluated using DXA. Prevalence and predictors of low BMD were assessed. RESULTS:The cohort comprised 110 patients with SS with a mean age of 45.3 ± 10.5 years and a delay of 7.9 ± 6.3 years from disease onset to diagnosis. Patients were on glucocorticoid (94.6%) and levothyroxine (90.5%) replacement, with prior exposure to estrogen-progestin (66.7%). Bone turnover markers were not significantly different between the two groups. Low BMD (osteopenia/osteoporosis) was prevalent in a significantly greater proportion of the cases as compared to controls at the lumbar spine (94% vs 47%) and femoral neck (80% vs 36%). The most important predictor of low BMD at the lumbar spine was the length of delay prior to diagnosis (OR 1.48 (95% CI 1.002-2.206), p = 0.04). CONCLUSION:SS is characterized by a high prevalence of multiple pituitary hormone deficiencies, including hypoprolactinaemia. Low BMD is highly prevalent in SS compared to age, and BMI-matched controls. Despite adequate relevant hormone replacement therapy, a longer delay in diagnosing is the major determinant of low BMD in patients with SS.

OBJECTIVE:Sheehan Syndrome (SS), or postpartum pituitary necrosis, is associated with an elevated risk of atherosclerotic cardiovascular (CV) diseases, driven by factors such as dyslipidemia, chronic inflammation, and growth hormone deficiency. To better understand the prevalence and characteristics of atherosclerotic CV disease in this population, we conducted a noninvasive evaluation of the coronary arteries using computed tomography cardiac angiography. METHODS:This observational cross-sectional study included women diagnosed with SS who were receiving standard replacement therapy including thyroxine and glucocorticoids. All participants underwent computed tomography cardiac angiography to identify the presence of coronary artery plaques. RESULTS:The study included 30 patients with SS, with a mean age of 54.20 ± 8.27 years and a mean duration of pituitary disease of 22.67 ± 6.27 years. Coronary artery calcium (CAC) scoring revealed the following risk stratification for coronary artery disease: minimal risk (CAC 1-10) in 6.7% (n = 2), mild risk (CAC 11-100) in 16.7% (n = 5), and moderate risk (CAC 101-400) in 3.3% (n = 1). Coronary artery plaques were identified in 23.3% (n = 7) of patients. Among these, 4 patients had noncalcified plaques, 2 had calcified plaques, and 1 patient had both calcified and noncalcified plaques. A strong positive correlation was observed between CAC scores and percentage stenosis (r = 0.96, P = .01). CONCLUSION:Approximately one-fourth of patients with SS were found to have atherosclerotic plaques in their coronary arteries, highlighting their increased susceptibility to CV morbidity and mortality.

Objective: Enlargement of the adrenal glands and variable adrenocortical function have been reported in patients with pulmonary tuberculosis and, in a few studies, in patients with extrapulmonary tuberculosis (EPTB). However, none of the studies have evaluated the course of the adrenal morphology in these patients. Subjects and methods: Prospective study including 37 patients with EPTB and 37 healthy age- and sex-matched controls. The adrenal function was evaluated by measurement of cortisol levels at baseline and after stimulation with ACTH (Acton Prolongatum) before and 6 months after antituberculosis treatment. The size of both adrenal glands was evaluated using 64-slice computed tomography (CT) scanning before and 6 months after treatment. The findings were compared with those in a group of healthy matched controls. Results: Clinical and biochemical parameters were comparable between groups. The mean baseline serum cortisol level was significantly lower in the EPTB group (397.1 +/- 184.9 nmol/L) compared with the control group (696.3 +/- 101.8 nmol/L). Compared with controls, patients with EPTB had significantly lower mean cortisol levels at baseline and 1 hour after ACTH, both before (397 +/- 184.9 nmol/L and 750.7 +/- 176.8 nmol/L, respectively) and after (529.7 +/- 100.4 nmol/L and 1017.2 +/- 119.7 nmol/L, respectively) antituberculosis treatment. Both the length and thickness of the right and left adrenal glands were greater in patients with EPTB than in controls but became comparable to those in controls after treatment completion. Conclusions: Patients with EPTB have an enlarged adrenal size and low baseline and stimulated serum cortisol levels. After treatment completion, cortisol levels increased significantly, and the adrenal size normalized in these patients.

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Glucocorticoid (GC) therapy can ameliorate debilitating and life-threatening symptoms in several inflammatory/immunological disorders. However, it can also cause significant side effects, especially with higher doses and longer duration of use. Therefore, GCs should be used at the lowest effective dose for the shortest possible time to minimise adverse effects. GC therapy may cause suppression of the endogenous hypothalamic-pituitary-adrenal (HPA) axis and abrupt discontinuation predisposes patients to features of GC-induced adrenal insufficiency. The practice of tapering GC therapy allows for recovery of the HPA axis while minimising the risk of a disease flare-up or symptoms of AI. Moderate-to-high dose GC therapy may be tapered rapidly to near-physiological doses while watching for features of disease reactivation. Once close to the physiological dose, tapering is slower and at longer intervals to allow for recovery of the HPA axis. It is important to use short- or intermediate-acting GC preparations such as hydrocortisone or prednisolone in physiological doses, administered in the morning to mimic the endogenous cortisol rhythm. A general principle to follow is that HPA axis recovery takes longer if the period of suppression has been long. In such cases, tapering should be slower over a few months to even a year. In select cases at high risk of AI or if symptoms appear during tapering, the decision to further taper and discontinue steroids may be based on testing of HPA axis function using basal and/or stimulated serum cortisol. All patients on exogenous steroids should be advised about the need for an appropriate increase in GC doses during acute medical or surgical illness and should carry a steroid alert card to avoid adrenal crisis.

Introduction:Sheehan syndrome (SS) typically involves the loss of anterior pituitary cells and rarely affects the posterior pituitary. The water deprivation test (WDT) is the gold standard for diagnosing central diabetes insipidus (CDI), but it is cumbersome. Serum copeptin measurements are an alternative for CDI diagnosis. In this study, we measured hypoglycaemia-stimulated serum copeptin in SS patients to assess posterior pituitary function alongside anterior pituitary hormone levels. Methods:This study recruited 43 patients with SS on stable hormonal replacement except for growth hormone (GH), 18 patients with CDI, and 19 body mass index (BMI) and parity-matched controls. All patients with SS and four patients with CDI underwent an insulin tolerance test (ITT), and hypoglycaemia-stimulated copeptin levels were measured at 0, 30, 45, and 90 minutes after insulin injection. Results:The mean serum copeptin level among patients with SS (26.01 ± 12.41 pmol/L) was significantly lower than that in healthy controls (31.92 ± 7.85 pmol/L) and higher than that in patients with CDI (1.81 ± 0.14 pmol/L). Using pre-defined cut-offs for CDI, basal serum copeptin <2.69 pmol/L and stimulated levels <4.92 pmol/L for complete central DI, and basal copeptin levels >2.69 pmol/L and stimulated copeptin <4.92 pmol/L for partial central DI, 9.2% (n = 4) of patients with SS had CDI, of which half had complete CDI and half had partial CDI. Conclusion:A significant number of patients with SS who are on hormone replacement therapy show involvement of the posterior pituitary, despite not displaying symptoms.

Sheehan’s syndrome (SS) is a rare but well-characterized cause of hypopituitarism. Data on skeletal health is limited and on microarchitecture is lacking in SS patients. We aimed to explore skeletal health in SS with bone mineral density (BMD), turnover, and microarchitecture. Thirty-five patients with SS on stable replacement therapy for respective hormone deficiencies and 35 age- and BMI-matched controls were recruited. Hormonal profile and bone turnover markers (BTMs) were measured using electrochemiluminescence assay. Areal BMD and trabecular bone score were evaluated using DXA. Bone microarchitecture was assessed using a second-generation high-resolution peripheral quantitative computed tomography. The mean age of the patients was 45.5 ± 9.3 years with a lag of 8.3 ± 7.2 years prior to diagnosis. Patients were on glucocorticoid (94

Background & objectives Neuronal hypoxia associated with conditions like traumatic brain injury and cardiac tachyarrhythmia has been implicated in causing hypopituitarism. Individuals with complete heart block (CHB) may be predisposed to develop anterior pituitary hormone dysfunction in the long term. The objective of this study was to investigate anterior pituitary hormone functions in individuals after CHB. Methods This prospective cohort study included 30 individuals (21 men and 9 women) with CHB requiring pacemaker implantation, who were evaluated at admission and then at a mean follow up of 12.4 ± 2.2 months to look for development of any degree of hypopituitarism. In addition to the measurement of hormones like follicle-stimulating hormone (FSH), luteinising hormone (LH), thyroid stimulating hormone (TSH), total tetra iodothyronines (TT4), free tetraiodothyronines (FT4), cortisol, insulin-like growth factor-1 (IGF-1), testosterone and estradiol, a fixed-dose glucagon stimulation test (GST) was performed to assess growth hormone (GH) and adrenocorticotrophic hormone (ACTH) axis. Results The mean age of the participants was 64.9 ± 11.3 yr. At follow up evaluation, 17 (56.7%) had low serum IGF-1, and among them, seven (23%) had growth hormone deficiency (GHD) (peak GH <1.0 ng/ml after GST). Six participants (20%) had ACTH deficiency (peak cortisol <9 ug/dl after GST) and one had TSH deficiency. None had prolactin (PRL) or gonadotropin deficiency. Overall, hormone deficiencies were observed in nine patients (30%). Interpretation & conclusions This pilot study detected loss of anterior pituitary hormones in a significant number of individuals of CHB at 12 months follow up. Unrecognised hypopituitarism may have resulted in significant morbidity and mortality in these individuals.

Introduction:Sheehan syndrome is a common cause of hypopituitarism in developing countries. Among risk factors, in addition to post-partum haemorrhage, a smaller sellar volume is also believed to predispose to pituitary necrosis. Some earlier studies have reported smaller sellar volume in these patients but involved a small number of patients and lacked matched controls. The main of the present study was to study the sellar volume in a large cohort of patients with Sheehan syndrome and compare it with age- and parity-matched controls. Methods:Fifty women with Sheehan syndrome and an equal number of age- and parity-matched controls were studied. Baseline investigations, relevant hormonal assay, and MRI of pituitary were studied in all. Results:Sellar volume was significantly lower in patients with Sheehan syndrome (334.50 ± 129.08 mm3 in patients as against 456.64 ± 169.25 mm3 in controls, P = 0.000). Far more women with Sheehan syndrome than controls had decreased sellar volume (40% vs. 12%). Conclusions:Patients with Sheehan syndrome have a smaller sellar volume that may be a non-modifiable risk factor for the development of post-partum pituitary necrosis.

Background and objective Individuals with prolactinoma exhibit elevated rates of obesity, metabolic syndrome (MS), and dyslipidemia compared to their healthy counterparts. However, there is a lack of data regarding metabolic variance between male and female prolactinoma patients. Consequently, this study aimed to investigate and compare sex-specific discrepancies in metabolic abnormalities among individuals diagnosed with prolactinoma. Methods In this prospective study, 80 treatment-naïve patients with prolactinoma (12 males and 68 females) underwent clinical assessments and laboratory investigations. The measured parameters included blood glucose, total cholesterol (TC), triglycerides (TG), LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), urea, creatinine, uric acid, and blood glucose levels. The patients were treated with cabergoline, a dopamine agonist, and reevaluated after 12 weeks. Results Forty-eight patients had microprolactinomas (all females), and 32 had macroprolactinomas (20 females, 12 males). The mean age was 28.30±7.49 years for females and 28.91±7.12 years for males (p=0.71). The median symptom duration was 12 months (range 1-72 months, IQR 4-16 months), with no significant difference between males (median 12 months, IQR 5-54 months) and females (median 12 months, IQR 10-24 months, p=0.620). The median serum prolactin (PRL) was 988 ng/mL (IQR 471-1,439) in males and 165 ng/mL (IQR 90-425) in females (p<0.05). Males showed higher HbA1c, BGF, TC, TG, LDL-C, and higher rates of obesity, MS, and diabetes mellitus. Treatment with cabergoline resulted in significant improvements in the HbA1c, BGF, TC, TG, and LDL-C levels. Conclusion Males with prolactinomas had larger tumor sizes and higher serum PRL levels than females. Additionally, males exhibited worse metabolic parameters than females. However, there was no significant difference in the duration of symptoms or age at diagnosis between the two groups.

Abstract Disclosure: L. Das: None. B. Laway: None. J. Sahoo: None. S.K. Bhadada: None. P. Dutta: None. Introduction: Sheehan’s syndrome (SS) is a rare cause of hypopituitarism. Evidence on skeletal health in patients with this condition is limited, and data on bone geometry, structure and volumetric bone mineral density (BMD) are lacking. We aimed to comprehensively explore skeletal fragility in a multicentric cohort of treated SS. Patients and Methods: Patients with SS were recruited for analysis of demographic, clinico-biochemical and hormonal profile including bone turnover markers. Areal BMD, T- and Z-scores and trabecular bone score (TBS) were evaluated using DXA. In a subset of patients (n=29) as well as age-and BMI-matched controls (n=34), high-resolution peripheral quantitative computed tomography (HRpQCT, XtremeCT II, Scanco Medical AG, Switzerland) was performed to assess bone geometry and microarchitecture. Results: There were a total of 105 patients with SS with a mean age 45.2 ± 10.5 years and a lag of 7.4 ± 5.5 years from disease onset to diagnosis. Regular levothyroxine replacement was ongoing in 91.2% and glucocorticoid replacement in 86.1% of the cohort. Past HRT replacement was done in 66.7% patients. Bone turnover markers (P1NP, CTX) were not significantly different between cases and controls. The T- score [-2.3 (-3.0 to -1.6) vs -1.5 (-3.0 to -0.7)] and Z-score [-1.4 (-2.1 to -1.2) vs -0.6 (-2.1 to -0.1)] at the lumbar spine (LS) and the T- score [-1.8 (-2.3 to -1.3) vs -0.8 (-2.1 to -0.1)] and Z-score [-1.1 (-1.7 to -0.4) vs -0.4 (-1.0 to 0.2)] at the femoral neck (FN) were lower in cases as compared to controls (trend towards significance). Osteopenia or osteoporosis was prevalent in significantly greater proportion of the cases as compared to controls, at LS (96.3% vs 64.7%), FN (91.7% vs 47%) and ultradistal radius (65.2% vs 11.8%). Bone microarchitectural assessment showed no significant differences between TBS, or bone geometry. However, trabecular volumetric bone mineral density was higher at both tibia (p<0.05) and radius (p>0.05) in cases as opposed to age-and BMI-matched controls. There was a weak negative correlation between glucocorticoid and levothyroxine replacement duration and BMD at both LS and FN (p<0.05), but not with replacement dose. Conclusion: Osteopenia-osteoporosis is highly prevalent in SS. BMD at both LS and FN is negatively correlated with duration of glucocorticoid and levothyroxine exposure. There are no significant differences in bone microarchitecture or geometry but tibial trabecular volumetric BMD is greater in treated SS. Presentation: Friday, June 16, 2023

Background: Hyperprolactinemia is associated with obesity, dyslipidemia, insulin resistance, and low-grade inflammation which may promote endothelial dysfunction (EnD). Limited work has been done on EnD in prolactinomas and we, therefore, studied serum markers of inflammation and EnD in patients with prolactinomas before and after treatment with dopamine agonists. Methodology: Fifty-six treatment naïve patients with prolactinomas and fifty-three (apparently healthy age and sex-matched) controls were enrolled in the study and subjected to clinical assessment and laboratory investigations including blood glucose, total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, urea, creatinine, uric acid, erythrocyte sedimentation rate (ESR), highly sensitive C-reactive protein (hsCRP) and markers of EnD i.e., intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Patients were treated with a dopamine agonist (cabergoline) and parameters (like ESR, hsCRP, ICAM-1, and VCAM-1) were measured at 12 weeks. Results: The majority of the patients (84%) were female, more than half (52%) had metabolic syndrome and over a third (36%) were obese. Blood glucose fasting, HbA1c, lipid fractions, ESR, hsCRP, ICAM-1, and VCAM-1 were significantly higher in patients than in controls. Median ICAM-1 was 1331.95 ng/ml (IQR 803.43-1825.99) in patients vs 753.04 ng/ml (IQR 402.04-871.55) in controls, P < 0.001 and median VCAM-1in patients was 971.35 ng/ml (IQR 695.03-1285.23) as against 634.56 ng/ml (IQR 177.49-946.50) in controls, p 0.001. Serum ICAM-1 and VCAM-1 correlated positively with hsCRP. On multivariate regression analysis, serum hsCRP was the only significant predictor of change in ICAM-1 and VCAM-1. Normalization of serum PRL with CAB resulted in a significant decrease in metabolic parameters, ESR, hsCRP, ICAM-1, and VCAM-1. Conclusion: Hyperprolactinemia because of prolactinoma is associated with EnD secondary to systemic inflammation and metabolic abnormalities which improve after treatment with DA.

Sheehan syndrome (SS) caused by postpartum hemorrhage leads to partial or complete pituitary hormone deficiency. In addition to lipid and glucose abnormalities, patients with SS have increased body fat, insulin resistance (IR), coagulation abnormalities, increased leptin concentration, low-grade inflammation, and endothelial dysfunction that predispose them to cardiovascular diseases. Untreated growth hormone (GH) deficiency, hypogonadism, and excess glucocorticoid use are considered risk factors for these abnormalities. Compared to other hypopituitary subjects, patients with SS are younger and have a longer duration of disease and severe GH deficiency. Replacement with GH in addition to standard hormone replacement improves their cardiometabolic profile.

The use of high-resolution ultrasound (HRUS) thyroid imaging has resulted in a significant revolution in the treatment of thyroid nodules. The enigma of thyroid nodules has been a blind spot for radiologists for a long period. Reporting a thyroid nodule as benign or malignant is quite difficult and many times not accurate. The American Collage of Radiology-Thyroid Imaging Reporting and Data System (ACR-TIRADS) 2017 classification has solved this problem to a large extent. However, the classification needed pathological confirmation for it to be highly accurate. We compared our HRUS-based TIRADS labeling of thyroid nodules with thyroid cytopathology using revised Bethesda classification system. Patients detected with thyroid nodules by HRUS were categorized using ACR-TIRADS and further were taken for fine needle aspiration cytology (FNAC) in our department. The pathological results were compared with the initial TIRADS category of the nodule and the effectiveness of the TIRADS classification in categorizing nodules into benign and malignant was assessed using various statistical variables. The initial USG and the FNAC were performed by a single radiologist with over 10 years of experience. A total of 201 patients underwent HRUS followed by FNAC after obtaining written consent in our department. The thyroid nodules labeled as true benign on ACR-TIRADS (TIRADS 2) were all true benign on Bethesda cytopathology (less than Bethesda III), confirming the high accuracy of HRUS. The diagnostic accuracy of HRUS in cases of ACR-TIRADS 3 nodules was approximately 90.6% with an error rate of 9.4%. Nodules labeled as ACR-TIRADS 4 and 5 had error rates of 47% and 10% in labeling nodules as malignant. The ultrasound-based ACR-TIRADS system can accurately predict the likelihood of specific nodules being benign. There is a strong concordance between Bethesda cytology and ACR-TIRADS classification, particularly for benign nodules. In resource-constrained system like ours, patients with TIRADS 2 and 3 nodules can be safely followed obviating the need for an invasive procedure like FNAC.

Sheehan’s syndrome (SS) is characterised by chronic pituitary insufficiency following a vascular insult to the pituitary in the peripartum period. There is a lack of substantial evidence on the long-term hepatic and cardiac consequences in these patients, following hormone replacement. Patients with a diagnosis of SS were recruited for the study. Detailed clinico-biochemical and radiological evaluation were performed in all patients (n = 60). Hepatic and cardiac complications were assessed using fibroscan and echocardiography (2D speckle-tracking) respectively, in a subset of patients (n = 29) as well as age-and BMI-matched controls (n = 26). Controlled attenuation parameter (for steatosis) and liver stiffness measurement (for fibrosis) were used to define non-alcoholic fatty liver disease (NAFLD). Diastolic cardiac function was evaluated using standard criteria and systolic function by ejection fraction and global longitudinal strain (GLS). The mean age of the cohort was 42.7 ± 11.6 years. Multiple (≥ 2) hormone deficiencies were present in 68.8

Background: This study was aimed at determining the frequency of thyroid autoimmunity and subclinical hypothyroidism in patients with hyperprolactinemia due to prolactinoma compared to well-matched healthy controls. Methods: This was a cross-sectional study wherein 78 treatment naïve prolactinoma patients and ninety-two healthy control subjects were recruited. Serum prolactin (PRL), thyroid-stimulating hormone (TSH), total thyroxine (T4), circulating anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin (anti-Tg) antibody levels were measured in all study subjects. Progression of the antibody-positive population to subclinical hypothyroidism was determined. Results: The median PRL level among patients was 166 ng/ml (IQR 85-467) compared to 11.4 ng/ml (IQR 8.5-15.9) in controls (P < 0.001). There was no significant difference in levels of T4 (P = 0.83) and TSH (P = 0.82) between the cases and controls. Overall, 25% of patients had the presence of anti-thyroid antibodies as compared to 20% of controls (P = 0.56). SCH was more common in antibody-positive hyperprolactinemia subjects compared with antibody-positive controls. Conclusion: We did not find an increased prevalence of thyroid autoimmunity among untreated prolactinoma patients compared to healthy controls. At the same time, subclinical hypothyroidism was more common in thyroid antibody-positive patients with hyperprolactinemia than positive controls.

Sir, Graves' hyperthyroidism in addition to diffuse thyroid enlargement is characterized by extrathyroidal manifestations in the form of orbitopathy (GO), thyroid acropachy, and dermopathy (also known as pretibial myxedema).[1] Among these, pretibial myxedema (PTM) is an uncommon manifestation with an estimated incidence of 0.5%–4.3%.[2] Most commonly, it presents as nonpitting edema or formation of plaques or nodules and rarely as elephantiasic form.[1] Severe forms of PTM may cause functional impairment in the form of difficulty in wearing shoes or sometimes entrapment neuropathy. We present a case of severe Graves' dermopathy successfully treated with intralesional steroid, triamcinolone acetonide (TAC). A 52-year-old female has had Graves' disease (GD) since 2019, currently was on carbimazole 5 mg once a day and was clinically and biochemically euthyroid. Two years ago, she presented with elephantiatic myxedema on the right lower limb with a similar lesion but of a lesser extent on the lower left limb. The patient also had bilateral inactive thyroid-associated orbitopathy (TAO). On clinical examination, there was nondepressible edema associated with nonpitting indurated yellowish-brown plaques coalescing with each other forming elephantiasic pattern on the dorsum of the right foot. The left foot also had nonpitting edema, relatively smooth, without diffuse nodules/plaques [Figure 1a]. The patient was concerned about the unsightly appearance of the lesions and difficulty in wearing shoes/socks.Figure 1: (a) Before treatment: Pretibial myxedema, right foot>left foot. (b) After treatment: Marked regression after intralesional steroidConsidering background clinical condition and the patient's desire to improve her appearance, a therapeutic program was decided with the use of intralesional TAC 20 mg (Tricort 10 mg/mL), applied without dilution, under aseptic conditions, over multiple points – 0.1 mL per point via 1 mL syringe with a 26 G × 0.5-inch needle into the dermis. The injected sites per session were mapped out, and the frequency of the procedure was followed as monthly. After three sessions, a very satisfactory clinical response was achieved. A clear decrease of edema and nodules was observed, allowing the patient to wear shoes that were previously almost difficult [Figure 1b]. She received the last injection 2 years back, and there is no recurrence. The treatment of disfiguring PTM is challenging. Traditionally topical and intralesional steroids, with or without occlusion, have been tried with some moderate response, especially in big lesions. Other treatment options have been tried such as systemic glucocorticoids, pentoxifylline, gamma globulin, plasmapheresis, and surgical excision.[3] The potential limitation of such therapy is the continued development of nodules in some patients; thus, a long-term benefit cannot be anticipated. However, earlier reports suggest that most of these recurrences involve the development of only one or two nodules that are easily and similarly retreated, without any serious side effects.[4] A retrospective study at a tertiary care center in northern India reported the use of intralesional TAC in combination with topical clobetasol under occlusion, resulting in complete clearance in lesions by 3.4 years and 4 years post-treatment, none had a reactivation in older lesions or development of newer lesions.[5] Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Sir, Patients with Sheehan syndrome (SS) have low bone mineral density mainly because of gonadotroph and somatotroph deficiency together with long-term thyroxine and glucocorticoid treatment.[12] Bisphosphonates along with calcium and vitamin D supplementation are commonly used for the treatment of osteoporosis. Zoledronic acid (ZA) prescribed as yearly infusion is safe and well tolerated except transient and self-limiting flu-like symptoms. Here, we report a patient of SS who developed mild transient hepatitis after ZA infusion. A 55-year-old woman was diagnosed with SS 6 years back based on post-partum haemorrhage, lactotroph, gonadotroph, thyrotroph and corticotroph failure and empty sella on MR imaging. She was prescribed thyroxine (75 micrograms daily) and prednisolone (5 milligrams daily) along with elemental calcium of 500 mgs and 1000 units of cholecalciferol daily. DXA scan revealed osteoporosis (T-score L1-L4 spine = -3.9). She is a non-smoker, does not consume alcohol and did not take any other drug causing liver disease. Her baseline liver function test (LFT) was within normal limits [Table 1]. The patient received injection ZA, 5 mgs in 100 ml of ready-to-infuse solution (Stoplos One 5 mgs/100 ml; Akums Drugs and Pharmaceuticals Ltd., Haridwar, India) over a period of 30 minutes. Few hours after the infusion, she experienced flu-like symptoms; these symptoms continued on the second day. On the second day, clinical examination revealed an icteric tinge. LFT revealed hyperbilirubinemia with elevated liver enzymes, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma-glutamyl transpeptidase (GGT) [Table 1]. Ultrasound revealed evidence of grade 1 fatty liver without any focal lesion of liver parenchyma and biliary tract. A diagnosis of acute hepatitis was considered, and she was further investigated for the aetiology of hepatitis. Serological tests for hepatitis A, B, E and C were negative, ruling out the possibility of viral hepatitis. Meanwhile, C-reactive protein (CRP), antinuclear antibody–indirect fluorescent antibody (ANA-IFA), anti-mitochondrial antibody (AMA) and anti-smooth muscle antibody were negative, ruling out the possibility of autoimmune hepatitis [Table 1]. In view of a normal LFT before ZA infusion, clinical jaundice, abnormal liver enzymes, negative viral and autoimmune screen, possibility of drug-induced liver injury secondary to ZA was entertained. The patient was managed conservatively and was kept in hospital for observation. The patient had a normal appetite and did not need parental fluids. LFTs were repeated at days 3, 5 and 6, which revealed a downward trend and finally normalization of liver enzymes on day 6.Table 1: Serial liver function tests in the patient with zoledronic acid-induced hepatitisAs many as one-third of ZA-naïve patients experience an acute phase reaction manifesting as fever, myalgia, headache or other flu-like symptoms. The other rare potential side effects of ZA are atrial fibrillation, uveitis, osteonecrosis of the jaw (ONJ) and atypical femoral fracture.[3] Few cases of drug-induced liver injury because of ZA are reported. The liver injury may be mild and transient or severe and recurrent requiring glucocorticoids.[456] Our patient had a mild and transient liver injury, which resolved within a week. Idiosyncratic sensitivity to ZA may be the cause of liver injury in the present patient. The clinical significance of mild and transient liver injury may be mild, but clinicians should be aware of this adverse effect, and it may be advisable to get a routine LFT performed before administering a dose of ZA. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.