Diagnosis and Treatment > Signs and Symptoms > Palpitations

You are looking at 31 - 36 of 36 items

I R Wallace Regional Centre for Endocrinology and Diabetes, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

Search for other papers by I R Wallace in
Google Scholar
PubMed
Close
,
E Healy Department of Neuropathology, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

Search for other papers by E Healy in
Google Scholar
PubMed
Close
,
R S Cooke Department of Neurosurgery, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

Search for other papers by R S Cooke in
Google Scholar
PubMed
Close
,
P K Ellis Department of Radiology, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

Search for other papers by P K Ellis in
Google Scholar
PubMed
Close
,
R Harper Department of Endocrinology and Diabetes, Ulster Hospital, Dundonald, BT16 1RH, UK

Search for other papers by R Harper in
Google Scholar
PubMed
Close
, and
S J Hunter Regional Centre for Endocrinology and Diabetes, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, UK

Search for other papers by S J Hunter in
Google Scholar
PubMed
Close

Summary

TSH-secreting pituitary adenomas are rare and the optimal investigation and management is uncertain. We describe a case of a 43 year-old woman with a TSH-secreting pituitary adenoma, highlighting diagnostic testing and our use, pre-operatively of somatostatin analogue therapy, which induced biochemical euthyroidism and a reduction in tumour size.

Learning points

  • The differential diagnosis of the syndrome of inappropriate TSH secretion is non-thyroidal illness, medications, assay interference due to heterophilic antibodies, thyroid hormone resistance and TSH-secreting pituitary adenoma.

  • TRH stimulation test and triiodothyronine suppression test assist in differentiating thyroid hormone resistance and TSH-secreting pituitary adenoma.

  • Somatostatin analogue therapy can induce biochemical euthyroidism and reduce tumour size.

Open access
Philip C Johnston Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic Foundation, 9500 Euclid Avenue Desk F20, Cleveland, Ohio 44195, USA

Search for other papers by Philip C Johnston in
Google Scholar
PubMed
Close
,
Amir H Hamrahian Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic Foundation, 9500 Euclid Avenue Desk F20, Cleveland, Ohio 44195, USA

Search for other papers by Amir H Hamrahian in
Google Scholar
PubMed
Close
,
Richard A Prayson Patholgy and Laboratory Medicine Institute, Rose Ella Burkhardt Brain Tumor and Neuro-Oncology Center, Cleveland Clinic, Cleveland, Ohio 44195, USA

Search for other papers by Richard A Prayson in
Google Scholar
PubMed
Close
,
Laurence Kennedy Department of Endocrinology, Diabetes and Metabolism, Cleveland Clinic Foundation, 9500 Euclid Avenue Desk F20, Cleveland, Ohio 44195, USA

Search for other papers by Laurence Kennedy in
Google Scholar
PubMed
Close
, and
Robert J Weil Department of Neurosurgery and the Neurological Institute, Rose Ella Burkhardt Brain Tumor and Neuro-Oncology Center, Cleveland Clinic, Cleveland, Ohio 44195, USA

Search for other papers by Robert J Weil in
Google Scholar
PubMed
Close

Summary

A 54-year-old woman presented with bi-temporal hemianopia, palpitations, and diaphoresis. An invasive pituitary macroadenoma was discovered. The patient had biochemical evidence of secondary hyperthyroidism and GH excess; however, she did not appear to be acromegalic. Surgical removal of the pituitary mass revealed a plurihormonal TSH/GH co-secreting pituitary adenoma. TSH-secreting adenomas can co-secrete other hormones including GH, prolactin, and gonadotropins; conversely, co-secretion of TSH from a pituitary adenoma in acromegaly is infrequent.

Learning points

  • This case highlights an unusual patient with a rare TSH/GH co-secreting pituitary adenoma with absence of the clinical features of acromegaly.

  • Plurihormonality does not always translate into the clinical features of hormonal excess.

  • There appears to be a clinical and immunohistochemical spectrum present in plurihormonal tumors.

Open access
Omayma Elshafie Department of Medicine, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

Search for other papers by Omayma Elshafie in
Google Scholar
PubMed
Close
,
Yahya Al Badaai Department of Surgery, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

Search for other papers by Yahya Al Badaai in
Google Scholar
PubMed
Close
,
Khalifa Alwahaibi Department of Surgery, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

Search for other papers by Khalifa Alwahaibi in
Google Scholar
PubMed
Close
,
Asim Qureshi Department of Pathology, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

Search for other papers by Asim Qureshi in
Google Scholar
PubMed
Close
,
Samir Hussein Department of Radiology, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

Search for other papers by Samir Hussein in
Google Scholar
PubMed
Close
,
Faisal Al Azzri Department of Radiology, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

Search for other papers by Faisal Al Azzri in
Google Scholar
PubMed
Close
,
Ali Almamari Department of Medicine, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

Search for other papers by Ali Almamari in
Google Scholar
PubMed
Close
, and
Nicholas Woodhouse Department of Medicine, Sultan Qaboos University Hospital, Muscat, Sultanate of Oman

Search for other papers by Nicholas Woodhouse in
Google Scholar
PubMed
Close

Summary

A 48-year-old hypertensive and diabetic patient presented with a 10-year history of progressive right facial pain, tinnitus, hearing loss, sweating, and palpitations. Investigations revealed a 5.6 cm vascular tumor at the carotid bifurcation. Her blood pressure (BP) was 170/110, on lisinopril 20 mg od and amlodipine 10 mg od and 100 U of insulin daily. A catecholamine-secreting carotid body paraganglioma (CSCBP) was suspected; the diagnosis was confirmed biochemically by determining plasma norepinephrine (NE) level, 89 000 pmol/l, and chromogranin A (CgA) level, 279 μg/l. Meta-iodobenzylguanidine and octreotide scanning confirmed a single tumor in the neck. A week after giving the patient a trial of octreotide 100 μg 8 h, the NE level dropped progressively from 50 000 to 25 000 pmol/l and CgA from 279 to 25 μg/l. Treatment was therefore continued with labetalol 200 mg twice daily (bid) and long-acting octreotide-LA initially using 40 mg/month and later increasing to 80 mg/month. On this dose and with a reduced labetalol intake of 100 mg bid, BP was maintained at 130/70 and her symptoms resolved completely. CgA levels returned to normal in the first week and these were maintained throughout the 3 month treatment period. During tumor resection, there were minimal BP fluctuations during the 10 h procedure. We conclude that short-term high-dose octreotide-LA might prove valuable in the preoperative management of catecholamine-secreting tumors. To the best of our knowledge, this is the first report on the successful use of octreotide in a CSCBP.

Learning points

  • The value of octreotide scanning in the localization of extra-adrenal pheochromocytoma.

  • Control of catecholamine secretion using high-dose octreotide.

  • This is a report of a rare cause of secondary diabetes and hypertension.

Open access
Maria Pikilidou Hypertension Excellence Center, First Department of Internal Medicine
Second Department of Internal Medicine, Papanikolaou General Hospital, Thessaloniki, Greece

Search for other papers by Maria Pikilidou in
Google Scholar
PubMed
Close
,
Maria Yavropoulou Division of Endocrinology and Metabolism, AHEPA University Hospital, Thessaloniki, Greece

Search for other papers by Maria Yavropoulou in
Google Scholar
PubMed
Close
, and
Marios Katsounaros Second Department of Internal Medicine, Papanikolaou General Hospital, Thessaloniki, Greece

Search for other papers by Marios Katsounaros in
Google Scholar
PubMed
Close

Summary

We report a case of a female with hemihypertrophy, who developed five recurrences of pheochromocytomas until the age of 35. Timely follow-up of the patient's blood pressure assisted in early diagnosis and treatment of recurrent tumors.

Learning points

  • Recurrent benign pheochromocytomas should raise suspicion of a genetic syndrome.

  • A pheochromocytoma at a young age has a high propensity to recur and strict follow-up is mandatory.

Open access
Lauren J Baker Endocrinology Department, Concord Hospital, Sydney, New South Wales, Australia

Search for other papers by Lauren J Baker in
Google Scholar
PubMed
Close
,
Anthony J Gill Pathology Department, Royal North Shore Hospital, Sydney, New South Wales, Australia
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia

Search for other papers by Anthony J Gill in
Google Scholar
PubMed
Close
,
Charles Chan Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
Anatomical Pathology Department, Concord Hospital, Sydney, New South Wales, Australia

Search for other papers by Charles Chan in
Google Scholar
PubMed
Close
,
Betty P C Lin Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia
Anatomical Pathology Department, Concord Hospital, Sydney, New South Wales, Australia

Search for other papers by Betty P C Lin in
Google Scholar
PubMed
Close
, and
Bronwyn A Crawford Endocrinology Department, Concord Hospital, Sydney, New South Wales, Australia
Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia

Search for other papers by Bronwyn A Crawford in
Google Scholar
PubMed
Close

Summary

In 2006, a 58-year-old woman presented with thyrotoxicosis. She had undergone left hemithyroidectomy 14 years before for a benign follicular adenoma. Ultrasound imaging demonstrated bilateral cervical lymphadenopathy with enhanced tracer uptake in the left lateral neck on a Technetium-99m uptake scan. Fine-needle aspiration biopsy of a left lateral neck node was insufficient for a cytological diagnosis; however, thyroglobulin (Tg) washings were strongly positive. The clinical suspicion was of functionally active metastatic thyroid cancer in cervical lymph nodes. A completion thyroidectomy and bilateral cervical lymph node dissection were performed. Histology demonstrated benign multinodularity in the right hemithyroid, with bilateral reactive lymphadenopathy and 24 benign hyperplastic thyroid nodules in the left lateral neck that were classified as parasitic thyroid nodules. As there had been a clinical suspicion of thyroid cancer, and the hyperplastic/parasitic thyroid tissue in the neck was extensive, the patient was given ablative radioactive iodine (3.7 GBq). After 2 years, a diagnostic radioactive iodine scan was clear and the serum Tg was undetectable. The patient has now been followed for 7 years with no evidence of recurrence. Archived tissue from a left lateral neck thyroid nodule has recently been analysed for BRAF V600E mutation, which was negative.

Learning points

  • Thyrotoxicosis due to functional thyroid tissue in the lateral neck is very rare and may be due to metastatic thyroid cancer or benign parasitic thyroid tissue.

  • Parasitic thyroid nodules should be considered as a differential diagnosis of lateral neck thyroid deposits, particularly where there is a history of prior thyroid surgery.

  • Parasitic thyroid nodules may occur as a result of traumatic rupture or implantation from a follicular adenoma at the time of surgery.

  • The use of ablative radioactive iodine may be appropriate, as resection of all parasitic thyroid tissue can prove difficult.

  • BRAF mutational analysis of parasitic thyroid tissue may provide extra reassurance in the exclusion of papillary thyroid carcinoma.

Open access
A Tabasum Diabetes and Endocrinology, Cardiff and Vale NHS Trust, Penlan Road, Penarth, Cardiff CF64 2XX, UK

Search for other papers by A Tabasum in
Google Scholar
PubMed
Close
,
C Shute Diabetes and Endocrinology, Cardiff and Vale NHS Trust, Penlan Road, Penarth, Cardiff CF64 2XX, UK

Search for other papers by C Shute in
Google Scholar
PubMed
Close
,
D Datta Biochemistry, Cardiff and Vale NHS Trust, Penlan Road, Penarth, Cardiff CF64 2XX, UK

Search for other papers by D Datta in
Google Scholar
PubMed
Close
, and
L George Diabetes and Endocrinology, Cardiff and Vale NHS Trust, Penlan Road, Penarth, Cardiff CF64 2XX, UK

Search for other papers by L George in
Google Scholar
PubMed
Close

Summary

Hypokalaemia may present as muscle cramps and Cardiac arrhythmias. This is a condition commonly encountered by endocrinologists and general physicians alike. Herein, we report the case of a 43-year-old gentleman admitted with hypokalaemia, who following subsequent investigations was found to have Gitelman's syndrome (GS). This rare, inherited, autosomal recessive renal tubular disorder is associated with genetic mutations in the thiazide-sensitive sodium chloride co-transporter and magnesium channels in the distal convoluted tubule. Patients with GS typically presents at an older age, and a spectrum of clinical presentations exists, from being asymptomatic to predominant muscular symptoms. Clinical suspicion should be raised in those with hypokalaemic metabolic alkalosis associated with hypomagnesaemia. Treatment of GS consists of long-term potassium and magnesium salt replacement. In general, the long-term prognosis in terms of preserved renal function and life expectancy is excellent. Herein, we discuss the biochemical imbalance in the aetiology of GS, and the case report highlights the need for further investigations in patients with recurrent hypokalaemic episodes.

Learning points

  • Recurrent hypokalaemia with no obvious cause warrants investigation for hereditary renal tubulopathies.

  • GS is the most common inherited renal tubulopathy with a prevalence of 25 per million people.

  • GS typically presents at an older age and clinical suspicion should be raised in those with hypokalaemic metabolic alkalosis associated with hypomagnesaemia.

  • Confirmation of diagnosis is by molecular analysis for mutation in the SLC12A3 gene.

Open access