Background: Postpartum hypogalactia is a prevalent obstetric complication worldwide, closely associated with excessive oxidative stress and impaired antioxidant defense in mammary tissue. Current hormone-based therapies carry endocrine disruption risks, while natural antioxidant bioactive agents such as extracellular vesicles (EVs) are largely limited by rapid in vivo clearance and poor tissue retention. Methods: We constructed an injectable gelatin methacryloyl (GelMA) hydrogel system to encapsulate chemically induced mammary epithelial cell-derived EVs (CiMECs-EVs) and systematically evaluated their antioxidant and lactogenic activities via multi-omics analysis, cellular functional assays and a bromocriptine-induced murine hypogalactia model. Results: CiMECs-EVs induced a functional mammary epithelial-like phenotype in fibroblasts in a dose-dependent manner with functional cargo enriched in glutathione metabolism and redox-regulatory miRNAs. The GelMA matrix protected EV integrity and enabled sustained release, and the composite system significantly ameliorated mammary duct structure and lactation function in vivo with specific mammary tropism and no systemic toxicity, outperforming free EV treatment. Conclusions: This study presents a safe protein biomacromolecule-based antioxidant delivery platform that effectively restores mammary redox balance and antioxidant defenses, providing a promising non-hormonal therapeutic strategy for postpartum hypogalactia.

Neuroleptic malignant syndrome (NMS) is an uncommon, but potentially life- threatening complication of antipsychotic therapy, primarily resulting from central dopaminergic blockade. NMS is a clinical diagnosis and occurs rarely in patients receiving atypical antipsychotics agents. Gastrointestinal manifestations, including severe hypomotility and paralytic ileus, are recognized adverse effects of antipsychotic medications. However, paralytic ileus preceding the characteristic neuromuscular and autonomic features of NMS is exceptionally rare and underrecognized as an early manifestation of the syndrome. We report the case of a 49-year-old man who presented with progressive abdominal distension secondary to intestinal pseudo-obstruction as an early manifestation of NMS. This atypical and underreported presentation highlights the importance of maintaining a high index of suspicion for NMS in patients receiving antipsychotic therapy who develop unexplained gastrointestinal dysmotility. Prompt recognition, immediate discontinuation of the offending antipsychotic agent, and early initiation of treatment with dantrolene and bromocriptine resulted in a favorable clinical outcome.

Cabergoline is usually not used during breastfeeding because it suppresses lactation. The U.S. Food and Drug Administration considers cabergoline to be not indicated to suppress lactation because the similar drug bromocriptine has caused hypertension, stroke, seizures and psychosis when used for this purpose. However, two systematic reviews found that cabergoline was generally well tolerated for use in suppressing lactation, but dizziness, headache, nausea and vomiting occur occasionally.[1-3] A retrospective study of 225 women who received cabergoline postpartum had a maximum decrease in systolic blood pressure of 10.88 mm Hg at 20 to 24 hours after the dose.[4] Serious reactions are uncommon, but include thromboembolic and neurologic events. Psychiatric symptoms have occurred rarely, but women requesting lactation suppression with cabergoline are more likely to have anxiety and depression.[5] Some experts recommend cabergoline as a safer alternative to bromocriptine for lactation suppression, but others do not.[6-10] The disadvantage of cabergoline is that it has a half-life of about 68 hours, which means that any adverse effects might persist for a prolonged period of time. Women treated with cabergoline for pituitary adenomas who become pregnant can breastfed their infants with no apparent risk of recurrence. A treatment scheme has been reported for mothers with hypergalactia that uses low doses of cabergoline to decrease milk supply.[11] Decreased milk synthesis may occur by 2 days after drug administration.[12]

Bromocriptine is usually not used during breastfeeding because it suppresses lactation. The indication of lactation suppression has been withdrawn in the U.S. and discouraged in other countries because it increases the risk of maternal stroke, seizures, cardiovascular disorders, death and possibly psychosis.[1-4] A low dose of 2.5 mg once daily has been used for 3 days to decrease overproduction of milk.[5] The drug was undetectable in milk with this dosage and infants had no adverse reactions, but the safety of this use is not established. Case reports and series also exist of mothers treated with bromocriptine for amenorrhea-galactorrhea syndrome or prolactinoma during pregnancy and lactation who successfully breastfed their infants. Bromocriptine has been used to treat persistent galactorrhea following breast augmentation surgery.[6]

Peripartum cardiomyopathy (PPCM) is a rare yet potentially life-threatening form of heart failure that occurs during late pregnancy or within the months following delivery. Bromocriptine, which suppresses prolactin secretion, has emerged as a promising adjunctive therapy for PPCM; however, the optimal timing of its initiation remains uncertain. We describe two patients with PPCM who received bromocriptine at different stages of the disease course. The first patient was a 30-year-old woman who presented 33 days after delivery with cardiogenic shock, a left ventricular ejection fraction (LVEF) of 12%, and a left ventricular thrombus. Despite treatment with intra-aortic balloon pumping, venoarterial extracorporeal membrane oxygenation, anticoagulation, and guideline-directed medical therapy, recovery of left ventricular function plateaued. Bromocriptine was initiated on hospital day 44, after which LVEF increased from 38% to 53% within seven days and subsequently recovered to 60%. The second patient was a 35-year-old woman who developed acute heart failure nine days after delivery with an LVEF of 28%. Because left ventricular function remained markedly impaired despite standard heart failure therapy, bromocriptine was initiated on hospital day seven. Her LVEF improved to 39% by hospital day 15 and ultimately recovered to 61%. These cases demonstrate a temporal association between bromocriptine initiation and subsequent improvement in left ventricular systolic function at different stages of the clinical course of PPCM.

Gestational gigantomastia is a very rare disorder characterised by massive, bilateral breast enlargement during pregnancy. Clinically, it is characterised by rapid breast enlargement associated with severe mastodynia, back and shoulder pain, and erythema of the skin. In its most severe forms, it can lead to ulceration, necrosis, haemorrhage, or septicaemia. The underlying pathophysiology is not completely understood, but is thought to be multifactorial, involving hormonal hypersensitivity and autoimmune mechanisms. Histopathological confirmation is necessary for definitive diagnosis because its clinical presentation can closely mimic that of inflammatory breast carcinoma or other malignant neoplasms. We report a case of a 28-year-old primigravida who presented at 24 weeks of gestation with progressive bilateral breast enlargement that reached its maximal extent at 36 weeks and caused significant functional impairment. On clinical examination, there was symmetrical breast hypertrophy with diffuse erythema and a marked peau d'orange appearance. Breast ultrasound revealed glandular hypertrophy with ductal ectasia and marked oedema. No suspicious focal lesions were seen. Hormonal and immunological workup was normal, and skin and glandular biopsy showed benign hyperplasia without atypia. Throughout the pregnancy, conservative management with analgesics and postural support was continued until an uncomplicated vaginal delivery at 39 weeks of gestation. Cabergoline was then administered to suppress lactation. Given the absence of spontaneous regression of the breasts, a multidisciplinary decision was taken to perform a bilateral reduction mammoplasty at 12 months postpartum. This case demonstrates the phenotypic variability of gestational gigantomastia that may present without any preceding breast pathology. In severe cases, surgical treatment (reduction mammoplasty or bilateral mastectomy with delayed reconstruction) is the mainstay of treatment, and bromocriptine is the best-established medical alternative, but with variable success. Coordinated multidisciplinary care is essential to optimise patient outcomes and minimise life-threatening complications.

Neuroleptic malignant syndrome (NMS) is a rare but potentially life-threatening neurological emergency, most commonly associated with antipsychotic drugs and other dopamine receptor-blocking agents. Although its incidence has declined over recent decades, NMS remains a diagnostic challenge due to its heterogeneous clinical presentation and overlap with other drug-induced syndromes. The classic clinical picture is defined by a tetrad of hyperthermia, generalized muscle rigidity, altered mental status, and autonomic dysfunction, frequently accompanied by marked creatine kinase elevation secondary to rhabdomyolysis. Diagnosis is primarily clinical and supported by complementary studies aimed at assessing severity, excluding differential diagnoses, and monitoring systemic complications. The underlying pathophysiology involves dopamine D2 receptor blockade within the central nervous system, particularly in the hypothalamus and basal ganglia, leading to impaired thermoregulation and motor control. Management relies on immediate discontinuation of the offending agent, intensive supportive care, and, in moderate to severe cases, pharmacological treatment with benzodiazepines, dopaminergic agents such as bromocriptine or amantadine, and muscle relaxants such as dantrolene. Early recognition and timely treatment are crucial to ensure favorable outcomes and reduce morbidity and mortality.

Traumatic brain injury (TBI) is a leading cause of long-term neurological disability worldwide and is frequently associated with persistent impairments in consciousness, cognition, mood, and functional independence. Despite advances in acute neurocritical care, effective therapies that enhance neurological recovery remain limited. Neuromodulation has emerged as a promising strategy to augment neuroplasticity and improve recovery through both pharmacologic and non-pharmacologic approaches. This narrative review summarizes current evidence supporting pharmacologic neuromodulatory therapies, including central nervous system stimulants (methylphenidate and modafinil), dopaminergic agents (amantadine and bromocriptine), acetylcholinesterase inhibitors (donepezil and rivastigmine), and selective serotonin reuptake inhibitors (sertraline and fluoxetine). Mechanisms of action, clinical efficacy, adverse effects, and practical considerations across the acute, subacute, and chronic phases of TBI recovery are discussed. Emerging non-pharmacologic neuromodulation techniques, including repetitive transcranial magnetic stimulation, transcranial direct current stimulation, electroconvulsive therapy, vagus nerve stimulation, and deep brain stimulation, are also reviewed. Although amantadine remains the only neuromodulator supported by moderate-quality guideline recommendations for accelerating recovery in disorders of consciousness, accumulating evidence suggests that several additional pharmacologic and non-pharmacologic neuromodulation interventions may improve attention, executive function, fatigue, mood, and rehabilitation participation in carefully selected patients. However, current evidence is limited by heterogeneous study populations, small sample sizes, inconsistent outcome measures, and a paucity of long-term randomized controlled trials. Future research should prioritize adequately powered comparative studies, standardized outcome measures, biomarker-guided patient selection, and multimodal treatment strategies to optimize neurological recovery following TBI.