Diagnosis and Treatment > Investigation > Potassium

You are looking at 31 - 40 of 64 items

Snezana Burmazovic Department of Intensive Care Medicine, Lucerne Cantonal Hospital, Lucerne, Switzerland

Search for other papers by Snezana Burmazovic in
Google Scholar
PubMed
Close
,
Christoph Henzen Department of Internal Medicine and Endocrinology, Lucerne Cantonal Hospital, Lucerne, Switzerland

Search for other papers by Christoph Henzen in
Google Scholar
PubMed
Close
,
Lukas Brander Department of Intensive Care Medicine, Lucerne Cantonal Hospital, Lucerne, Switzerland

Search for other papers by Lukas Brander in
Google Scholar
PubMed
Close
, and
Luca Cioccari Department of Intensive Care Medicine, Lucerne Cantonal Hospital, Lucerne, Switzerland
Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, Prahran, Australia

Search for other papers by Luca Cioccari in
Google Scholar
PubMed
Close

Summary

The combination of hyperosmolar hyperglycaemic state and central diabetes insipidus is unusual and poses unique diagnostic and therapeutic challenges for clinicians. In a patient with diabetes mellitus presenting with polyuria and polydipsia, poor glycaemic control is usually the first aetiology that is considered, and achieving glycaemic control remains the first course of action. However, severe hypernatraemia, hyperglycaemia and discordance between urine-specific gravity and urine osmolality suggest concurrent symptomatic diabetes insipidus. We report a rare case of concurrent manifestation of hyperosmolar hyperglycaemic state and central diabetes insipidus in a patient with a history of craniopharyngioma.

Learning points:

  • In patients with diabetes mellitus presenting with polyuria and polydipsia, poor glycaemic control is usually the first aetiology to be considered.

  • However, a history of craniopharyngioma, severe hypernatraemia, hyperglycaemia and discordance between urine-specific gravity and osmolality provide evidence of concurrent diabetes insipidus.

  • Therefore, if a patient with diabetes mellitus presents with severe hypernatraemia, hyperglycaemia, a low or low normal urinary-specific gravity and worsening polyuria despite correction of hyperglycaemia, concurrent diabetes insipidus should be sought.

Open access
Ali A Zaied Divisions of Pulmonary and Critical Care Medicine, Mayo Clinic, Jacksonville, Florida, USA

Search for other papers by Ali A Zaied in
Google Scholar
PubMed
Close
,
Halis K Akturk Divisions of Endocrinology, Mayo Clinic, Jacksonville, Florida, USA

Search for other papers by Halis K Akturk in
Google Scholar
PubMed
Close
,
Richard W Joseph Divisions of Hematology and Oncology, Mayo Clinic, Jacksonville, Florida, USA

Search for other papers by Richard W Joseph in
Google Scholar
PubMed
Close
, and
Augustine S Lee Divisions of Pulmonary and Critical Care Medicine, Mayo Clinic, Jacksonville, Florida, USA

Search for other papers by Augustine S Lee in
Google Scholar
PubMed
Close

Summary

Nivolumab, a monoclonal antibody against programmed cell death-1 receptor, is increasingly used in advanced cancers. While nivolumab use enhances cancer therapy, it is associated with increased immune-related adverse events. We describe an elderly man who presented in ketoacidosis after receiving nivolumab for metastatic renal cell carcinoma. On presentation, he was hyperpneic and laboratory analyses showed hyperglycemia and anion-gapped metabolic acidosis consistent with diabetic ketoacidosis. No other precipitating factors, besides nivolumab, were identified. Pre-nivolumab blood glucose levels were normal. The patient responded to treatment with intravenous fluids, insulin and electrolyte replacement. He was diagnosed with insulin-dependent autoimmune diabetes mellitus secondary to nivolumab. Although nivolumab was stopped, he continued to require multiple insulin injection therapy till his last follow-up 7 months after presentation. Clinicians need to be alerted to the development of diabetes mellitus and diabetic ketoacidosis in patients receiving nivolumab.

Learning points:

  • Diabetic ketoacidosis should be considered in the differential of patients presenting with metabolic acidosis following treatment with antibodies to programmed cell death-1 receptor (anti-PD-1).

  • Autoimmune islet cell damage is the presumed mechanism for how insulin requiring diabetes mellitus can develop de novo following administration of anti-PD-1.

  • Because anti-PD-1 works by the activation of T-cells and reduction of ‘self-tolerance’, other autoimmune disorders are likely to be increasingly recognized with increased use of these agents.

Open access
Carine Ghassan Richa Department of Endocrinology, Mount Lebanon Hospital, Beirut, Lebanon
Lebanese University, Hadath, Lebanon

Search for other papers by Carine Ghassan Richa in
Google Scholar
PubMed
Close
,
Khadija Jamal Saad Department of Endocrinology, Mount Lebanon Hospital, Beirut, Lebanon
Lebanese University, Hadath, Lebanon

Search for other papers by Khadija Jamal Saad in
Google Scholar
PubMed
Close
,
Georges Habib Halabi Department of Endocrinology, Mount Lebanon Hospital, Beirut, Lebanon
Mount Lebanon Hospital, Beirut, Lebanon

Search for other papers by Georges Habib Halabi in
Google Scholar
PubMed
Close
,
Elie Mekhael Gharios Department of Endocrinology, Mount Lebanon Hospital, Beirut, Lebanon
Mount Lebanon Hospital, Beirut, Lebanon

Search for other papers by Elie Mekhael Gharios in
Google Scholar
PubMed
Close
,
Fadi Louis Nasr Mount Lebanon Hospital, Beirut, Lebanon

Search for other papers by Fadi Louis Nasr in
Google Scholar
PubMed
Close
, and
Marie Tanios Merheb Department of Endocrinology, Mount Lebanon Hospital, Beirut, Lebanon
Mount Lebanon Hospital, Beirut, Lebanon

Search for other papers by Marie Tanios Merheb in
Google Scholar
PubMed
Close

Summary

The objective of this study is to report three cases of paraneoplastic or ectopic Cushing syndrome, which is a rare phenomenon of the adrenocorticotropic hormone (ACTH)-dependent Cushing syndrome. Three cases are reported in respect of clinical presentation, diagnosis and treatment in addition to relevant literature review. The results showed that ectopic ACTH secretion can be associated with different types of neoplasm most common of which are bronchial carcinoid tumors, which are slow-growing, well-differentiated neoplasms with a favorable prognosis and small-cell lung cancer, which are poorly differentiated tumors with a poor outcome. The latter is present in two out of three cases and in the remaining one, primary tumor could not be localized, representing a small fraction of patients with paraneoplastic Cushing. Diagnosis is established in the setting of high clinical suspicion by documenting an elevated cortisol level, ACTH and doing dexamethasone suppression test. Treatment options include management of the primary tumor by surgery and chemotherapy and treating Cushing syndrome. Prognosis is poor in SCLC. We concluded that in front of a high clinical suspicion, ectopic Cushing syndrome diagnosis should be considered, and identification of the primary tumor is essential.

Learning points:

  • Learning how to suspect ectopic Cushing syndrome and confirm it among all the causes of excess cortisol.

  • Distinguish between occult and severe ectopic Cushing syndrome and etiology.

  • Providing the adequate treatment of the primary tumor as well as for the cortisol excess.

  • Prognosis depends on the differentiation and type of the primary malignancy.

Open access
Charlotte Boughton Endocrinology Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

Search for other papers by Charlotte Boughton in
Google Scholar
PubMed
Close
,
David Taylor Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

Search for other papers by David Taylor in
Google Scholar
PubMed
Close
,
Lea Ghataore Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

Search for other papers by Lea Ghataore in
Google Scholar
PubMed
Close
,
Norman Taylor Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

Search for other papers by Norman Taylor in
Google Scholar
PubMed
Close
, and
Benjamin C Whitelaw Endocrinology Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

Search for other papers by Benjamin C Whitelaw in
Google Scholar
PubMed
Close

Summary

We describe severe hypokalaemia and hypertension due to a mineralocorticoid effect in a patient with myelodysplastic syndrome taking posaconazole as antifungal prophylaxis. Two distinct mechanisms due to posaconazole are identified: inhibition of 11β hydroxylase leading to the accumulation of the mineralocorticoid hormone 11-deoxycorticosterone (DOC) and secondly, inhibition of 11β hydroxysteroid dehydrogenase type 2 (11βHSD2), as demonstrated by an elevated serum cortisol-to-cortisone ratio. The effects were ameliorated by spironolactone. We also suggest that posaconazole may cause cortisol insufficiency. Patients taking posaconazole should therefore be monitored for hypokalaemia, hypertension and symptoms of hypocortisolaemia, at the onset of treatment and on a monthly basis. Treatment with mineralocorticoid antagonists (spironolactone or eplerenone), supplementation of glucocorticoids (e.g. hydrocortisone) or dose reduction or cessation of posaconazole should all be considered as management strategies.

Learning points:

  • Combined hypertension and hypokalaemia are suggestive of mineralocorticoid excess; further investigation is appropriate.

  • If serum aldosterone is suppressed, then further investigation to assess for an alternative mineralocorticoid is appropriate, potentially using urine steroid profiling and/or serum steroid panelling.

  • Posaconazole can cause both hypokalaemia and hypertension, and we propose that this is due to two mechanisms – both 11β hydroxylase inhibition and 11β HSD2 inhibition.

  • Posaconazole treatment may lead to cortisol insufficiency, which may require treatment; however, in this clinical case, the effect was mild.

  • First-line treatment of this presentation would likely be use of a mineralocorticoid antagonist.

  • Patients taking posaconazole should be monitored for hypertension and hypokalaemia on initiation and monthly thereafter.

Open access
Ken Takeshima First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

Search for other papers by Ken Takeshima in
Google Scholar
PubMed
Close
,
Hiroyuki Ariyasu First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

Search for other papers by Hiroyuki Ariyasu in
Google Scholar
PubMed
Close
,
Tatsuya Ishibashi First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

Search for other papers by Tatsuya Ishibashi in
Google Scholar
PubMed
Close
,
Shintaro Kawai First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

Search for other papers by Shintaro Kawai in
Google Scholar
PubMed
Close
,
Shinsuke Uraki First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

Search for other papers by Shinsuke Uraki in
Google Scholar
PubMed
Close
,
Jinsoo Koh Department of Neurology, Wakayama Medical University, Wakayama,, Japan

Search for other papers by Jinsoo Koh in
Google Scholar
PubMed
Close
,
Hidefumi Ito Department of Neurology, Wakayama Medical University, Wakayama,, Japan

Search for other papers by Hidefumi Ito in
Google Scholar
PubMed
Close
, and
Takashi Akamizu First Department of Internal Medicine, Wakayama Medical University, Wakayama,, Japan

Search for other papers by Takashi Akamizu in
Google Scholar
PubMed
Close

Summary

Myotonic dystrophy type 1 (DM1) is an autosomal dominant multisystem disease affecting muscles, the eyes and the endocrine organs. Diabetes mellitus and primary hypogonadism are endocrine manifestations typically seen in patients with DM1. Abnormalities of hypothalamic–pituitary–adrenal (HPA) axis have also been reported in some DM1 patients. We present a case of DM1 with a rare combination of multiple endocrinopathies; diabetes mellitus, a combined form of primary and secondary hypogonadism, and dysfunction of the HPA axis. In the present case, diabetes mellitus was characterized by severe insulin resistance with hyperinsulinemia. Glycemic control improved after modification of insulin sensitizers, such as metformin and pioglitazone. Hypogonadism was treated with testosterone replacement therapy. Notably, body composition analysis revealed increase in muscle mass and decrease in fat mass in our patient. This implies that manifestations of hypogonadism could be hidden by symptoms of myotonic dystrophy. Our patient had no symptoms associated with adrenal deficiency, so adrenal dysfunction was carefully followed up without hydrocortisone replacement therapy. In this report, we highlight the necessity for evaluation and treatment of multiple endocrinopathies in patients with DM1.

Learning points:

  • DM1 patients could be affected by a variety of multiple endocrinopathies.

  • Our patients with DM1 presented rare combinations of multiple endocrinopathies; diabetes mellitus, combined form of primary and secondary hypogonadism and dysfunction of HPA axis.

  • Testosterone treatment of hypogonadism in patients with DM1 could improve body composition.

  • The patients with DM1 should be assessed endocrine functions and treated depending on the degree of each endocrine dysfunction.

Open access
Joseph Cerasuolo Department of Neurology and Department of Internal Medicine, St. Vincent Hospital, Worcester, Massachusetts, USA

Search for other papers by Joseph Cerasuolo in
Google Scholar
PubMed
Close
and
Anthony Izzo Department of Neurology and Department of Internal Medicine, St. Vincent Hospital, Worcester, Massachusetts, USA

Search for other papers by Anthony Izzo in
Google Scholar
PubMed
Close

Summary

Acute hyperglycemia has been shown to cause cognitive impairments in animal models. There is growing appreciation of the numerous effects of hyperglycemia on neuronal function as well as blood–brain barrier function. In humans, hypoglycemia is well known to cause cognitive deficits acutely, but hyperglycemia has been less well studied. We present a case of selective neurocognitive deficits in the setting of acute hyperglycemia. A 60-year-old man was admitted to the hospital for an episode of acute hyperglycemia in the setting of newly diagnosed diabetes mellitus precipitated by steroid use. He was managed with insulin therapy and discharged home, and later, presented with complaints of memory impairment. Deficits included impairment in his declarative and working memory, to the point of significant impairment in his overall functioning. The patient had no structural lesions on MRI imaging of the brain or other systemic illnesses to explain his specific deficits. We suggest that his acute hyperglycemia may have caused neurological injury, and may be responsible for our patient’s memory complaints.

Learning points:

  • Acute hyperglycemia has been associated with poor outcomes in several different central nervous system injuries including cerebrovascular accident and hypoxic injury.

  • Hyperglycemia is responsible for accumulation of reactive oxygen species in the brain, resulting in advanced glycosylated end products and a proinflammatory response that may lead to cellular injury.

  • Further research is needed to define the impact of both acute and chronic hyperglycemia on cognitive impairment and memory.

Open access
Carlos Tavares Bello Endocrinology Department, Hospital de Egas Moniz, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal

Search for other papers by Carlos Tavares Bello in
Google Scholar
PubMed
Close
,
Emma van der Poest Clement Faculty of Medicine, Erasmus University, Rotterdam, The Netherlands

Search for other papers by Emma van der Poest Clement in
Google Scholar
PubMed
Close
, and
Richard Feelders Endocrinology Department, Erasmus MC, Rotterdam, The Netherlands

Search for other papers by Richard Feelders in
Google Scholar
PubMed
Close

Summary

Cushing’s syndrome is a rare disease that results from prolonged exposure to supraphysiological levels of glucocorticoids. Severe and rapidly progressive cases are often, but not exclusively, attributable to ectopic ACTH secretion. Extreme hypercortisolism usually has florid metabolic consequences and is associated with an increased infectious and thrombotic risk. The authors report on a case of a 51-year-old male that presented with severe Cushing’s syndrome secondary to an ACTH-secreting pituitary macroadenoma, whose diagnostic workup was affected by concurrent subclinical multifocal pulmonary infectious nodules. The case is noteworthy for the atypically severe presentation of Cushing’s disease, and it should remind the clinician of the possible infectious and thrombotic complications associated with Cushing’s syndrome.

Learning points:

  • Severe Cushing’s syndrome is not always caused by ectopic ACTH secretion.

  • Hypercortisolism is a state of immunosuppression, being associated with an increased risk for opportunistic infections.

  • Infectious pulmonary infiltrates may lead to imaging diagnostic dilemmas when investigating a suspected ectopic ACTH secretion.

  • Cushing’s syndrome carries an increased thromboembolic risk that may even persist after successful surgical management.

  • Antibiotic and venous thromboembolism prophylaxis should be considered in every patient with severe Cushing’s syndrome.

Open access
Swapna Talluri Internal Medicine

Search for other papers by Swapna Talluri in
Google Scholar
PubMed
Close
,
Raghu Charumathi Internal Medicine

Search for other papers by Raghu Charumathi in
Google Scholar
PubMed
Close
,
Muhammad Khan Internal Medicine

Search for other papers by Muhammad Khan in
Google Scholar
PubMed
Close
, and
Kerri Kissell Endocrinology, Guthrie Robert Packer Hospital, Sayre, Pennsylvania, USA

Search for other papers by Kerri Kissell in
Google Scholar
PubMed
Close

Summary

Central pontine myelinolysis (CPM) usually occurs with rapid correction of severe chronic hyponatremia. Despite the pronounced fluctuations in serum osmolality, CPM is rarely seen in diabetics. This is a case report of CPM associated with hyperglycemia. A 45-year-old non-smoking and non-alcoholic African American male with past medical history of type 2 diabetes, hypertension, stage V chronic kidney disease and hypothyroidism presented with a two-week history of intermittent episodes of gait imbalance, slurred speech and inappropriate laughter. Physical examination including complete neurological assessment and fundoscopic examination were unremarkable. Laboratory evaluation was significant for serum sodium: 140 mmol/L, potassium: 3.9 mmol/L, serum glucose: 178 mg/dL and serum osmolality: 317 mosmol/kg. His ambulatory blood sugars fluctuated between 100 and 600 mg/dL in the six weeks prior to presentation, without any significant or rapid changes in his corrected serum sodium or other electrolyte levels. MRI brain demonstrated a symmetric lesion in the central pons with increased signal intensity on T2- and diffusion-weighted images. After neurological consultation and MRI confirmation, the patient was diagnosed with CPM secondary to hyperosmolar hyperglycemia. Eight-week follow-up with neurology was notable for near-complete resolution of symptoms. This case report highlights the importance of adequate blood glucose control in diabetics. Physicians should be aware of complications like CPM, which can present atypically in diabetics and is only diagnosed in the presence of a high index of clinical suspicion.

Learning points:

  • Despite the pronounced fluctuations in serum osmolality, central pontine myelinolysis (CPM) is rarely seen in diabetics. This case report of CPM associated with hyperglycemia highlights the importance of adequate blood glucose control in diabetics.

  • Physicians should be aware of complications like CPM in diabetics.

  • CPM can present atypically in diabetics and is only diagnosed in the presence of a high index of clinical suspicion.

Open access
Hodaka Yamada Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan

Search for other papers by Hodaka Yamada in
Google Scholar
PubMed
Close
,
Shunsuke Funazaki Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan

Search for other papers by Shunsuke Funazaki in
Google Scholar
PubMed
Close
,
Masafumi Kakei Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan

Search for other papers by Masafumi Kakei in
Google Scholar
PubMed
Close
,
Kazuo Hara Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan

Search for other papers by Kazuo Hara in
Google Scholar
PubMed
Close
, and
San-e Ishikawa Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara, Japan

Search for other papers by San-e Ishikawa in
Google Scholar
PubMed
Close

Summary

Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure.

Learning points:

  • Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment.

  • Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria.

  • Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium.

  • Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis.

Open access
Prashanth Rawla Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA

Search for other papers by Prashanth Rawla in
Google Scholar
PubMed
Close
,
Anantha R Vellipuram Texas Tech University Health Sciences Center, El Paso, Texas, USA

Search for other papers by Anantha R Vellipuram in
Google Scholar
PubMed
Close
,
Sathyajit S Bandaru Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA

Search for other papers by Sathyajit S Bandaru in
Google Scholar
PubMed
Close
, and
Jeffrey Pradeep Raj Department of Pharmacology, St John’s Medical College, Bangalore, India

Search for other papers by Jeffrey Pradeep Raj in
Google Scholar
PubMed
Close

Summary

Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA.

Learning points:

  • Euglycemic diabetic ketoacidosis is rare.

  • Consider ketosis in patients with DKA even if their serum glucose levels are normal.

  • High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma.

  • Blood pH and blood or urine ketones should be checked in ill patients with diabetes regardless of blood glucose levels.

Open access