Diagnosis and Treatment > Medication > Bromocriptine
You are looking at 1 - 9 of 9 items
Search for other papers by Anna Popławska-Kita in
Google Scholar
PubMed
Search for other papers by Marta Wielogórska in
Google Scholar
PubMed
Search for other papers by Łukasz Poplawski in
Google Scholar
PubMed
Search for other papers by Katarzyna Siewko in
Google Scholar
PubMed
Search for other papers by Agnieszka Adamska in
Google Scholar
PubMed
Search for other papers by Piotr Szumowski in
Google Scholar
PubMed
Search for other papers by Piotr Myśliwiec in
Google Scholar
PubMed
Search for other papers by Janusz Myśliwiec in
Google Scholar
PubMed
Search for other papers by Joanna Reszeć in
Google Scholar
PubMed
Search for other papers by Grzegorz Kamiński in
Google Scholar
PubMed
Search for other papers by Janusz Dzięcioł in
Google Scholar
PubMed
Search for other papers by Dorota Tobiaszewska in
Google Scholar
PubMed
Search for other papers by Małgorzata Szelachowska in
Google Scholar
PubMed
Search for other papers by Adam Jacek Krętowski in
Google Scholar
PubMed
Summary
Papillary thyroid gland carcinoma is the most common type of malignancy of the endocrine system. Metastases to the pituitary gland have been described as a complication of papillary thyroid cancer in few reported cases since 1965. We report the case of a 68-year-old female patient with a well-differentiated form of thyroid gland cancer. Despite it being the most common malignant cancer of the endocrine system, with its papillary form being one of the two most frequently diagnosed thyroid cancers, the case we present is extremely rare. Sudden cardiac arrest during ventricular fibrillation occurred during hospitalization. Autopsy of the patient revealed papillary carcinoma of the thyroid, follicular variant, with metastasis to the sella turcica, and concomitant sarcoidosis of heart, lung, and mediastinal and hilar lymph nodes. Not only does atypical metastasis make our patient’s case most remarkable, but also the postmortem diagnosis of sarcoidosis makes her case particularly unusual.
Learning points:
-
The goal of presenting this case is to raise awareness of the clinical heterogeneity of papillary cancer and promote early diagnosis of unexpected metastasis and coexisting diseases to improve clinical outcomes.
-
Clinicians must be skeptical. They should not fall into the trap of diagnostic momentum or accept diagnostic labels at face value. Regardless of the potential mechanisms, clinicians should be aware of the possibility of the coexistence of thyroid cancer and sarcoidosis as a differential diagnosis of lymphadenopathy.
-
This case highlights the importance of the diagnostic and therapeutic planning process and raises awareness of the fact that one uncommon disease could be masked by another extremely rare disorder.
Search for other papers by Sakshi Jhawar in
Google Scholar
PubMed
Search for other papers by Rahul Lakhotia in
Google Scholar
PubMed
Search for other papers by Mari Suzuki in
Google Scholar
PubMed
Search for other papers by James Welch in
Google Scholar
PubMed
Search for other papers by Sunita K Agarwal in
Google Scholar
PubMed
Search for other papers by John Sharretts in
Google Scholar
PubMed
Search for other papers by Maria Merino in
Google Scholar
PubMed
Search for other papers by Mark Ahlman in
Google Scholar
PubMed
Search for other papers by Jenny E Blau in
Google Scholar
PubMed
Search for other papers by William F Simonds in
Google Scholar
PubMed
Search for other papers by Jaydira Del Rivero in
Google Scholar
PubMed
Summary
Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant condition characterized by parathyroid, anterior pituitary and enteropancreatic endocrine cell tumors. Neuroendocrine tumors occur in approximately in 5–15% of MEN1 patients. Very few cases of ovarian NETs have been reported in association with clinical MEN1 and without genetic testing confirmation. Thirty-three-year-old woman with MEN1 was found to have right adnexal mass on computed tomography (CT). Attempt at laparoscopic removal was unsuccessful, and mass was removed via a minilaparotomy in piecemeal fashion. Pathology showed ovarian NET arising from a teratoma. Four years later, patient presented with recurrence involving the pelvis and anterior abdominal wall. She was treated with debulking surgery and somatostatin analogs (SSAs). Targeted DNA sequencing analysis on the primary adnexal mass as well as the recurrent abdominal wall tumor confirmed loss of heterozygosity (LOH) at the MEN1 gene locus. This case represents to our knowledge, the first genetically confirmed case of ovarian NET arising by a MEN1 mechanism in a patient with MEN1. Extreme caution should be exercised during surgery as failure to remove an ovarian NET en masse can result in peritoneal seeding and recurrence. For patients with advanced ovarian NETs, systemic therapy options include SSAs, peptide receptor radioligand therapy (PRRT) and novel agents targeting mammalian target of rapamycin (mTOR) and vascular endothelial growth factor (VEGF).
Learning points:
-
Ovarian NET can arise from a MEN1 mechanism, and any adnexal mass in a MEN1 patient can be considered as a possible malignant NET.
-
Given the rarity of this disease, limited data are available on prognostication and treatment. Management strategies are extrapolated from evidence available in NETs from primaries of other origins.
-
Care should be exercised to remove ovarian NETs en bloc as failure to do so may result in peritoneal seeding and recurrence.
-
Treatment options for advanced disease include debulking surgery, SSAs, TKIs, mTOR inhibitors, PRRT and chemotherapy.
Centre for Endocrinology, Diabetes & Metabolism, Birmingham Health Partners, Birmingham, UK
Institute for Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Search for other papers by Anne de Bray in
Google Scholar
PubMed
Centre for Endocrinology, Diabetes & Metabolism, Birmingham Health Partners, Birmingham, UK
Search for other papers by Zaki K Hassan-Smith in
Google Scholar
PubMed
Centre for Endocrinology, Diabetes & Metabolism, Birmingham Health Partners, Birmingham, UK
Search for other papers by Jamal Dirie in
Google Scholar
PubMed
Search for other papers by Edward Littleton in
Google Scholar
PubMed
Search for other papers by Swarupsinh Chavda in
Google Scholar
PubMed
Centre for Endocrinology, Diabetes & Metabolism, Birmingham Health Partners, Birmingham, UK
Search for other papers by John Ayuk in
Google Scholar
PubMed
Search for other papers by Paul Sanghera in
Google Scholar
PubMed
Centre for Endocrinology, Diabetes & Metabolism, Birmingham Health Partners, Birmingham, UK
Institute for Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Search for other papers by Niki Karavitaki in
Google Scholar
PubMed
Summary
A 48-year-old man was diagnosed with a large macroprolactinoma in 1982 treated with surgery, adjuvant radiotherapy and bromocriptine. Normal prolactin was achieved in 2005 but in 2009 it started rising. Pituitary MRIs in 2009, 2012, 2014 and 2015 were reported as showing empty pituitary fossa. Prolactin continued to increase (despite increasing bromocriptine dose). Trialling cabergoline had no effect (prolactin 191,380 mU/L). In January 2016, he presented with right facial weakness and CT head was reported as showing no acute intracranial abnormality. In late 2016, he was referred to ENT with hoarse voice; left hypoglossal and recurrent laryngeal nerve palsies were found. At this point, prolactin was 534,176 mU/L. Just before further endocrine review, he had a fall and CT head showed a basal skull mass invading the left petrous temporal bone. Pituitary MRI revealed a large enhancing mass within the sella infiltrating the clivus, extending into the left petrous apex and occipital condyle with involvement of the left Meckel’s cave, internal acoustic meatus, jugular foramen and hypoglossal canal. At that time, left abducens nerve palsy was also present. CT thorax/abdomen/pelvis excluded malignancy. Review of previous images suggested that this lesion had started becoming evident below the fossa in pituitary MRI of 2015. Temozolomide was initiated. After eight cycles, there is significant tumour reduction with prolactin 1565 mU/L and cranial nerve deficits have remained stable. Prolactinomas can manifest aggressive behaviour even decades after initial treatment highlighting the unpredictable clinical course they can demonstrate and the need for careful imaging review.
Learning points:
-
Aggressive behaviour of prolactinomas can manifest even decades after first treatment highlighting the unpredictable clinical course these tumours can demonstrate.
-
Escape from control of hyperprolactinaemia in the absence of sellar adenomatous tissue requires careful and systematic search for the anatomical localisation of the lesion responsible for the prolactin excess.
-
Temozolomide is a valuable agent in the therapeutic armamentarium for aggressive/invasive prolactinomas, particularly if they are not amenable to other treatment modalities.
Fundacion de Endocrinologia
Search for other papers by Oscar D Bruno in
Google Scholar
PubMed
Search for other papers by Ricardo Fernández Pisani in
Google Scholar
PubMed
Search for other papers by Gabriel Isaac in
Google Scholar
PubMed
Search for other papers by Armando Basso in
Google Scholar
PubMed
Summary
The role of mechanical forces influencing the growth of a pituitary adenoma is poorly understood. In this paper we report the case of a young man with hyperprolactinaemia and an empty sella secondary to hydrocephalia, who developed a macroprolactinoma following the relief of high intraventricular pressure.
Learning points:
-
The volume of a pituitary tumour may be influenced not only by molecular but also by local mechanical factors.
-
Intratumoural pressure, resistance of the sellar diaphragm and intracranial liquid pressure may play a role in the final size of a pituitary adenoma.
-
The presence of hydrocephalus may hide a pituitary macroadenoma.
Search for other papers by Nikolaos Kyriakakis in
Google Scholar
PubMed
Search for other papers by Jacqueline Trouillas in
Google Scholar
PubMed
Search for other papers by Mary N Dang in
Google Scholar
PubMed
Search for other papers by Julie Lynch in
Google Scholar
PubMed
Search for other papers by Paul Belchetz in
Google Scholar
PubMed
Search for other papers by Márta Korbonits in
Google Scholar
PubMed
Search for other papers by Robert D Murray in
Google Scholar
PubMed
Summary
A male patient presented at the age of 30 with classic clinical features of acromegaly and was found to have elevated growth hormone levels, not suppressing during an oral glucose tolerance test. His acromegaly was originally considered to be of pituitary origin, based on a CT scan, which was interpreted as showing a pituitary macroadenoma. Despite two trans-sphenoidal surgeries, cranial radiotherapy and periods of treatment with bromocriptine and octreotide, his acromegaly remained active clinically and biochemically. A lung mass was discovered incidentally on a chest X-ray performed as part of a routine pre-assessment for spinal surgery 5 years following the initial presentation. This was confirmed to be a bronchial carcinoid tumour, which was strongly positive for growth hormone-releasing hormone (GHRH) and somatostatin receptor type 2 by immunohistochemistry. The re-examination of the pituitary specimens asserted the diagnosis of pituitary GH hyperplasia. Complete resolution of the patient’s acromegaly was achieved following right lower and middle lobectomy. Seventeen years following the successful resection of the bronchial carcinoid tumour the patient remains under annual endocrine follow-up for monitoring of the hypopituitarism he developed after the original interventions to his pituitary gland, while there has been no evidence of active acromegaly or recurrence of the carcinoid tumour. Ectopic acromegaly is extremely rare, accounting for <1% of all cases of acromegaly. Our case highlights the diagnostic challenges differentiating between ectopic acromegaly and acromegaly of pituitary origin and emphasises the importance of avoiding unnecessary pituitary surgery and radiotherapy. The role of laboratory investigations, imaging and histology as diagnostic tools is discussed.
Learning points:
-
Ectopic acromegaly is rare, accounting for less than 1% of all cases of acromegaly.
-
Ectopic acromegaly is almost always due to extra-pituitary GHRH secretion, mainly from neuroendocrine tumours of pancreatic or bronchial origin.
-
Differentiating between acromegaly of pituitary origin and ectopic acromegaly can cause diagnostic challenges due to similarities in clinical presentation and biochemistry.
-
Serum GHRH can be a useful diagnostic tool to diagnose ectopic acromegaly.
-
Pituitary imaging is crucial to differentiate between a pituitary adenoma and pituitary hyperplasia, which is a common finding in ectopic acromegaly.
-
Diagnosing ectopic acromegaly is pivotal to avoid unnecessary interventions to the pituitary and preserve normal pituitary function.
Search for other papers by Ekaterina Manuylova in
Google Scholar
PubMed
Search for other papers by Laura M Calvi in
Google Scholar
PubMed
Search for other papers by Catherine Hastings in
Google Scholar
PubMed
Search for other papers by G Edward Vates in
Google Scholar
PubMed
Search for other papers by Mahlon D Johnson in
Google Scholar
PubMed
Search for other papers by William T Cave Jr in
Google Scholar
PubMed
Search for other papers by Ismat Shafiq in
Google Scholar
PubMed
Summary
Co-secretion of growth hormone (GH) and prolactin (PRL) from a single pituitary adenoma is common. In fact, up to 25% of patients with acromegaly may have PRL co-secretion. The prevalence of acromegaly among patients with a newly diagnosed prolactinoma is unknown. Given the possibility of mixed GH and PRL co-secretion, the current recommendation is to obtain an insulin-like growth factor-1 (IGF-1) in patients with prolactinoma at the initial diagnosis. Long-term follow-up of IGF-1 is not routinely done. Here, we report two cases of well-controlled prolactinoma on dopamine agonists with the development of acromegaly 10–20 years after the initial diagnoses. In both patients, a mixed PRL/GH-cosecreting adenoma was confirmed on the pathology examination after transsphenoidal surgery (TSS). Therefore, periodic routine measurements of IGF-1 should be considered regardless of the duration and biochemical control of prolactinoma.
Learning points:
-
Acromegaly can develop in patients with well-controlled prolactinoma on dopamine agonists.
-
The interval between prolactinoma and acromegaly diagnoses can be several decades.
-
Periodic screening of patients with prolactinoma for growth hormone excess should be considered and can lead to an early diagnosis of acromegaly before the development of complications.
Search for other papers by Ilse C A Bakker in
Google Scholar
PubMed
Search for other papers by Chris D Schubart in
Google Scholar
PubMed
Search for other papers by Pierre M J Zelissen in
Google Scholar
PubMed
Summary
In this report, we describe a female patient with both prolactinoma and psychotic disorder who was successfully treated with aripiprazole, a partial dopamine 2 receptor agonist. During the follow-up of more than 10 years, her psychotic symptoms improved considerably, prolactin levels normalised and the size of the prolactinoma decreased. This observation may be of clinical relevance in similar patients who often are difficult to treat with the regular dopaminergic drugs.
Learning points
-
Prolactinoma coinciding with psychosis can represent a therapeutic challenge.
-
In contrast to many other antipsychotic drugs, aripiprazole is associated with a decrease in prolactin levels.
-
Aripiprazole can be a valuable pharmaceutical tool to treat both prolactinoma and psychosis.
Search for other papers by Satoru Sakihara in
Google Scholar
PubMed
Search for other papers by Kazunori Kageyama in
Google Scholar
PubMed
Search for other papers by Satoshi Yamagata in
Google Scholar
PubMed
Search for other papers by Ken Terui in
Google Scholar
PubMed
Search for other papers by Makoto Daimon in
Google Scholar
PubMed
Search for other papers by Toshihiro Suda in
Google Scholar
PubMed
Summary
ACTH-dependent Cushing's syndrome includes Cushing's disease and ectopic ACTH syndrome (EAS). The differential diagnosis of Cushing's disease from EAS in cases of ACTH-dependent Cushing's syndrome is a challenging problem. We report here a case of EAS with an unknown source of ACTH secretion. Extensive imaging procedures, involving computed tomography (neck to pelvis), pituitary magnetic resonance imaging, and whole-body 18F-fluorodeoxyglucose-positron emission tomography, failed to reveal the source of ACTH secretion. Intermittent administration of bromocriptine, a short-acting and nonselective dopamine agonist, has afforded adequate suppression of plasma ACTH and cortisol levels over the long term.
Learning points
-
Tumor excision is the primary treatment for EAS. However, when surgery is impossible, medical therapy is needed to treat hypercortisolism.
-
In cases where the source of ACTH secretion is unknown, inhibitors of steroidogenesis, such as metyrapone, mitotane, ketoconazole, and etomidate, are mostly used to suppress cortisol secretion.
-
Medications that suppress ACTH secretion are less effective, therefore less popular, as standard treatments.
-
In the present case, short-term treatment with dopamine agonists was effective for the long-term suppression of both ACTH and cortisol levels.
Search for other papers by Sowmya Gururaj in
Google Scholar
PubMed
Search for other papers by K Nisal in
Google Scholar
PubMed
Search for other papers by Q Davies in
Google Scholar
PubMed
Search for other papers by S Deen in
Google Scholar
PubMed
Search for other papers by P G McNally in
Google Scholar
PubMed
Summary
Ectopic hormone secretion is a well-recognised phenomenon; however, ectopic prolactin secretion is exceptionally rare. Hoffman and colleagues reported the first ever well-documented case of ectopic prolactin secretion secondary to a gonadoblastoma. We report a lady who presented with galactorrhoea and a large ovarian tumour that was found to secrete high levels of prolactin.
Learning points
-
Aim of this case report is to highlight the occurrence of this condition.
-
Lack of awareness can often lead to a diagnostic conundrum.
