Diagnosis and Treatment > Medication > Diltiazem

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Jai Madhok Department of Anesthesiology, Perioperative and Pain Medicine

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Amy Kloosterboer Department of Anesthesiology, Perioperative and Pain Medicine

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Chitra Venkatasubramanian Department of Neurology & Neurological Sciences, Stanford University Medical Center, Stanford, California, USA

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Frederick G Mihm Department of Anesthesiology, Perioperative and Pain Medicine

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Summary

We report the case of a 76-year-old male with a remote history of papillary thyroid cancer who developed severe paroxysmal headaches in the setting of episodic hypertension. Brain imaging revealed multiple lesions, initially of inconclusive etiology, but suspicious for metastatic foci. A search for the primary malignancy revealed an adrenal tumor, and biochemical testing confirmed the diagnosis of a norepinephrine-secreting pheochromocytoma. Serial imaging demonstrated multiple cerebral infarctions of varying ages, evidence of vessel narrowing and irregularities in the anterior and posterior circulations, and hypoperfusion in watershed areas. An exhaustive work-up for other etiologies of stroke including thromboembolic causes or vasculitis was unremarkable. There was resolution of symptoms, absence of new infarctions, and improvement in vessel caliber after adequate alpha-adrenergic receptor blockade for the management of pheochromocytoma. This clinicoradiologic constellation of findings suggested that the etiology of the multiple infarctions was reversible cerebral vasoconstriction syndrome (RCVS). Pheochromocytoma remains a poorly recognized cause of RCVS. Unexplained multifocal cerebral infarctions in the setting of severe hypertension should prompt the consideration of a vasoactive tumor as the driver of cerebrovascular dysfunction. A missed or delayed diagnosis has the potential for serious neurologic morbidity for an otherwise treatable condition.

Learning points:

  • The constellation of multifocal watershed cerebral infarctions of uncertain etiology in a patient with malignant hypertension should trigger the consideration of undiagnosed catecholamine secreting tumors, such as pheochromocytomas and paragangliomas.

  • Reversible cerebral vasoconstriction syndrome is a serious but reversible cerebrovascular manifestation of pheochromocytomas that may lead to strokes (ischemic and hemorrhagic), seizures, and cerebral edema.

  • Alpha-adrenergic receptor blockade can reverse cerebral vasoconstriction and prevent further cerebral ischemia and infarctions.

  • Early diagnosis of catecholamine secreting tumors has the potential for reducing neurologic morbidity and mortality in patients presenting with cerebrovascular complications.

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Pedro Marques Department of Endocrinology, St. Bartholomew’s Hospital, West Smithfield, London, UK

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Nicola Tufton Department of Endocrinology, St. Bartholomew’s Hospital, West Smithfield, London, UK

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Satya Bhattacharya Hepatobiliary and Pancreatic Surgery Unit, The Royal London Hospital, London, UK

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Mark Caulfield Clinical Pharmacology, William Harvey Research Institute, Queen Mary University of London, London, UK

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Scott A Akker Department of Endocrinology, St. Bartholomew’s Hospital, West Smithfield, London, UK

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Summary

Mineralocorticoid hypertension is most often caused by autonomous overproduction of aldosterone, but excess of other mineralocorticoid precursors can lead to a similar presentation. 11-Deoxycorticosterone (DOC) excess, which can occur in 11-β hydroxylase or 17-α hydroxylase deficiencies, in DOC-producing adrenocortical tumours or in patients taking 11-β hydroxylase inhibitors, may cause mineralocorticoid hypertension. We report a 35-year-old woman who in the third trimester of pregnancy was found to have a large adrenal mass on routine obstetric ultrasound. On referral to our unit, persistent hypertension and long-standing hypokalaemia was noted, despite good compliance with multiple antihypertensives. Ten years earlier, she had hypertension noted in pregnancy which had persisted after delivery. A MRI scan confirmed the presence of a 12 cm adrenal mass and biochemistry revealed high levels of DOC and low/normal renin, aldosterone and dehydroepiandrosterone, with normal catecholamine levels. The patient was treated with antihypertensives until obstetric delivery, following which she underwent an adrenalectomy. Histology confirmed a large adrenal cortical neoplasm of uncertain malignant potential. Postoperatively, blood pressure and serum potassium normalised, and the antihypertensive medication was stopped. Over 10 years of follow-up, she remains asymptomatic with normal DOC measurements. This case should alert clinicians to the possibility of a diagnosis of a DOC-producing adrenal tumours in patients with adrenal nodules and apparent mineralocorticoid hypertension in the presence of low or normal levels of aldosterone. The associated diagnostic and management challenges are discussed.

Learning points:

  • Hypermineralocorticoidism is characterised by hypertension, volume expansion and hypokalaemic alkalosis and is most commonly due to overproduction of aldosterone. However, excess of other mineralocorticoid products, such as DOC, lead to the same syndrome but with normal or low aldosterone levels.

  • The differential diagnosis of resistant hypertension with low renin and low/normal aldosterone includes congenital adrenal hyperplasia, syndrome of apparent mineralocorticoid excess, Cushing’s syndrome, Liddle’s syndrome and 11-deoxycorticosterone-producing tumours.

  • DOC is one intermediate product in the mineralocorticoid synthesis with weaker activity than aldosterone. However, marked DOC excess seen in 11-β hydroxylase or 17-α hydroxylase deficiencies in DOC-producing adrenocortical tumours or in patients taking 11-β hydroxylase inhibitors, may cause mineralocorticoid hypertension.

  • Excessive production of DOC in adrenocortical tumours has been attributed to reduced activity of the enzymes 11-β hydroxylase and 17-α hydroxylase and increased activity of 21-α hydroxylase.

  • The diagnosis of DOC-producing adrenal tumours is challenging because of its rarity and poor availability of DOC laboratory assays.

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Gautam Das Department of Diabetes and Endocrinology, Prince Charles Hospital, Cwm Taf University Health Board, Merthyr Tydfil, Mid Glamorgan, CF47 9DT, UK

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Peter N Taylor Department of Diabetes and Endocrinology, Prince Charles Hospital, Cwm Taf University Health Board, Merthyr Tydfil, Mid Glamorgan, CF47 9DT, UK

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Arshiya Tabasum Department of Diabetes and Endocrinology, Prince Charles Hospital, Cwm Taf University Health Board, Merthyr Tydfil, Mid Glamorgan, CF47 9DT, UK

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L N Rao Bondugulapati Department of Diabetes and Endocrinology, Maelor Hospital, Betsi Cadwaldr University Health Board, Wrexham, LL13 7TD, UK

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Danny Parker Department of Histopathology, University Hospital of Wales, Cardiff and Vale University Health Board, Cardiff, CF14 4XW, UK

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Piero Baglioni Department of Diabetes and Endocrinology, Prince Charles Hospital, Cwm Taf University Health Board, Merthyr Tydfil, Mid Glamorgan, CF47 9DT, UK

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Onyebuchi E Okosieme Department of Diabetes and Endocrinology, Prince Charles Hospital, Cwm Taf University Health Board, Merthyr Tydfil, Mid Glamorgan, CF47 9DT, UK

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David Scott Coombes Department of Endocrine Surgery, University Hospital of Wales, Cardiff and Vale University Health Board, Cardiff, CF14 4XW, UK

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Summary

Resistant hypertension is often difficult to treat and may be associated with underlying primary aldosteronism (PA). We describe the case of an elderly gentleman who presented with severe and resistant hypertension and was found to have a left adrenal incidentaloma during evaluation but had aldosterone excess secondary to unilateral adrenal hyperplasia (UAH) of the contralateral gland, which needed surgical intervention. A 65-year-old gentleman was evaluated for uncontrolled high blood pressure (BP) in spite of taking four antihypertensive medications. The high BP was confirmed on a 24-h ambulatory reading, and further biochemical evaluation showed an elevated serum aldosterone renin ratio (ARR) (1577 pmol/l per ng per ml per h). Radiological evaluation showed an adrenal nodule (15 mm) in the left adrenal gland but an adrenal vein sampling demonstrated a lateralization towards the opposite site favouring the right adrenal to be the source of excess aldosterone. A laparoscopic right adrenalectomy was performed and the histology of the gland confirmed nodular hyperplasia. Following surgery, the patient's BP improved remarkably although he remained on antihypertensives and under regular endocrine follow-up. PA remains the most common form of secondary and difficult-to-treat hypertension. Investigations may reveal incidental adrenal lesions, which may not be the actual source of excess aldosterone, but UAH may be a contributor and may coexist and amenable to surgical treatment. An adrenal vein sampling should be undertaken for correct lateralization of the source, otherwise a correctable diagnosis may be missed and the incorrect adrenal gland may be removed.

Learning points

  • Severe and resistant hypertension can often be associated with underlying PA.

  • ARR is an excellent screening tool in patients with suspected PA.

  • Lateralization with adrenal venous sampling is essential to isolate the source and differentiate between unilateral and bilateral causes of hyperaldosteronism.

  • Adrenal incidentalomas and UAH may coexist and the latter may often be the sole cause of excess aldosterone secretion.

  • Decisions about adrenalectomy should be made only after integrating and interpreting radiological and biochemical test findings properly.

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Stephanie Teasdale
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Elham Reda Endocrinology, Gold Coast University Hospital, Southport, Queensland, Australia

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Summary

We present two cases of adrenal phaeochromocytoma in patients with a previous diagnosis of neurofibromatosis type 1 (NF1). One had an adrenergic phenotype. The other had a more noradrenergic phenotype. Both had large primary tumours, which increases the likelihood of malignancy. Both also had elevated plasma-free methoxytyramine, which has been linked with malignancy even in non-SDHB phaeochromocytomas.

Learning points

  • Phaeochromocytoma can have varied clinical presentations.

  • Methoxytyramine can be useful in the biochemical work-up of both SDHB-positive and SDHB-negative phaeochromocytoma.

  • The utility of methoxytyramine as a marker of malignancy in NF1-related phaeochromocytoma is unclear, and cases with elevated titres warrant longer follow-up.

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Jiman Kim
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Eulsun Moon Seoul 365 Medical Clinic, Seoul, Korea

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Seungwon Kwon Department of Cardiovascular and Neurologic Diseases, College of Korean Medicine, KyungHee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul 130-702, Korea

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Summary

Diabetic nephropathy, a microvascular complication of diabetes, is a progressive kidney disease caused by angiopathy of the capillaries in the kidney glomeruli. Herein, we report a case of a 62-year-old patient with a 30 year history of diabetes, who showed a substantial improvement in diabetic nephropathy on administration of 30 g of Astragalus membranaceus extract per day. After 1 month, estimated glomerular filtration rate increased from 47 to 72 ml/min per 1.73 m2 and was subsequently maintained at the 1-month follow-up. Urinary protein levels also decreased following treatment. Herein, we present and discuss the evidence and mechanism of A. membranaceus on diabetic nephropathy in this patient.

Learning points

  • Diabetic nephropathy is a progressive kidney disease.

  • Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are currently used to prevent and delay the progression of diabetic nephropathy. However, their effects are not sufficient to prevent a decline in kidney function.

  • Furthermore, combination therapy with an ACE inhibitor and an ARB can produce adverse effects without additional benefits.

  • In the early phase of diabetic nephropathy, administration of Astragalus membranaceus can be a therapeutic option.

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