Series of Endocrinology, Diabetes and Metabolism

Current Issue | Volume 7 Issue 3 | JSEDM

Review Article

Metabolic Effects of Prolactin-Lowering Therapy in Prolactinoma: A Systematic Review and Meta-Analysis

McQuade EC, Ruddy M, Lo Piccolo AJ, Lee T-F, Jordan G and Agrawal N*

Metabolic Effects of Prolactin-Lowering Therapy in Prolactinoma: A Systematic Review and Meta-Analysis Read More »

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McQuade EC, Ruddy M, Lo Piccolo AJ, et al. Metabolic effects of prolactin-lowering therapy in prolactinoma: a systematic review and meta-analysis. Series Endo Diab Met. 2025;7(3):1-16.
Context: Hyperprolactinemia has been associated with adverse metabolic effects, and treatment of prolactinoma is directed at lowering prolactin levels; however, little is known about the effects of hypoprolactinemia. Objective: This systematic review and meta-analysis aimed to investigate the metabolic effects of prolactin-lowering therapy in prolactinoma. Methods: PubMed was searched through November 25, 2024. Mixed-effect meta-regression models were employed to assess for an association between prolactin and selected metabolic measures of body mass index (BMI), low-density lipoprotein (LDL) cholesterol, and homeostatic model assessment for insulin resistance (HOMA-IR). Results: A total of 16 studies involving 440 patients (257 women, 183 men) were included. When assessing change with prolactinoma treatment, there was no statistically significant association between change in prolactin levels and change in BMI, LDL, or HOMA-IR. When divided into two groups by post-treatment prolactin levels, the low prolactin group (≤15 mcg/L) trended towards lower BMI (−1.44, 95% CI −4.29–1.41, p = 0.32), lower LDL (−11.02, 95% CI −27.76–5.72, p = 0.20), and lower HOMA-IR (−0.64, 95% CI −2.16–0.87, p = 0.40); however, none of these associations were statistically significant. Conclusion: Our meta-analysis did not demonstrate a statistically significant association between prolactin and the metabolic risk measures selected in our study. These findings suggest that suppressing prolactin levels to below 15 mcg/L may not have as significant a metabolic impact as previously believed; however, there was limited assessment of very suppressed prolactin levels due to data availability. Further investigation of the metabolic effects of hypoprolactinemia is warranted.
Article DOI: 10.54178/jsedmv7i3002
Case Report

Guillain-Barré Syndrome (GBS) Mimicking Diabetic Ketoacidosis (DKA) with Dyselectrolytemia

Madan S*, Puri I and Nagpal N

Guillain-Barré Syndrome (GBS) Mimicking Diabetic Ketoacidosis (DKA) with Dyselectrolytemia Read More »

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Madan S, Puri I, Nagpal N. Guillain-Barré Syndrome (GBS) mimicking diabetic ketoacidosis (DKA) with dyselectrolytemia. Series Endo Diab Met. 2025;7(3):1-3.
Diabetic ketoacidosis (DKA) is a serious complication of diabetes characterized by high blood sugar, acidic pH levels, and increased ketone levels in the body, mostly observed in individuals with type 1 diabetes mellitus (T1DM) but can rarely occur in those with type 2 diabetes mellitus (T2DM). It is commonly triggered by factors like infection, new-onset diabetes, or non-compliance with treatment [1]. The most frequent cause of sudden flaccid paralysis is Guillain-Barré syndrome (GBS). It is due to an autoimmune reaction that destroys peripheral nervous system nerves, resulting in symptoms including tingling, weakness, and numbness that can eventually become paralysis [2]. Case Presentation: We report a case of a 14-year-old female with T1DM admitted with altered sensorium and vomiting. On evaluation, it was found to be DKA. The patient was managed according to the ISPAD guidelines for DKA, with hypotonic fluids, potassium chloride, and phosphorus replacement. After 24 h of treatment, DKA recovered, and the patient regained consciousness, but she still had weakness, was unable to sit without support, and had difficulty swallowing. Clinical examination showed muscle tone was decreased, power at the hip was 2/5, at the knee and ankle was 3/5, and at the shoulder and elbow was also 3/5. The neurologist's opinion was taken, cerebrospinal fluid (CSF) was normal, and the nerve conduction velocity showed axonal and segmental demyelination; GBS was diagnosed. Conclusion: Persistent weakness and dysphagia after DKA recovery and electrolytes are normalized, one should then suspect GBS. In early-onset GBS, CSF can be normal.
Article DOI: 10.54178/jsedmv7i3001
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