Search for other papers by Rikako Nakajima in
Google Scholar
PubMed
Search for other papers by Daisuke Sato in
Google Scholar
PubMed
Search for other papers by Ichirota Togashi in
Google Scholar
PubMed
Search for other papers by Hiroto Idesawa in
Google Scholar
PubMed
Search for other papers by Jun Ito in
Google Scholar
PubMed
Search for other papers by Kei Ito in
Google Scholar
PubMed
Search for other papers by Masanao Fujii in
Google Scholar
PubMed
Search for other papers by Hiroaki Yagyu in
Google Scholar
PubMed
Summary
An 89-year-old woman presented with a 6-year history of occasional episodes of impaired consciousness that were relieved by ingestion of a snack. Three months before presenting to our hospital, she had been hospitalized in a local hospital with subdural hematoma caused by a head contusion, where previously unrecognized hypoglycemia was discovered. Fasting plasma glucose concentration was 37 mg/dL, with a relatively high serum level of insulin (34.9 µU/mL). Computed tomography showed a 14 mm hyperenhancing tumor in the tail of the pancreas and she was referred to our hospital for further investigation. A prolonged fasting test revealed the plasma glucose concentration reduced to 43 mg/dL (2.4 mmol/L) at 8 h after the last meal. Serum insulin, proinsulin, and C-peptide concentrations were 21.1 µU/mL, 16.9 pmol/L, and 2.72 ng/mL, respectively. Subsequent intravenous administration of 1 mg of glucagon increased the plasma glucose concentration to 76 mg/dL (4.2 mmol/L). Moreover, the insulin-to-C-peptide molar ratio was 0.14. These data indicated the presence of insulinoma. Interestingly, serum anti-insulin antibodies were elevated (21.1 U/mL), although she had no history of taking exogenous insulin injection, alpha lipoic acid, or sulfhydryl group-containing agents. Human leukocyte antigen (HLA) typing revealed HLA-DRB1*0407 and HLA-DRB1*1405 alleles. Treatment with diazoxide prevented hypoglycemia, but was discontinued due to weight gain and leg edema. Elevated serum anti-insulin antibodies persisted almost 1 year after the diagnosis of insulinoma. We present a rare case of insulinoma concomitant with serum anti-insulin antibodies.
Learning points
-
Insulinoma presenting with concomitant anti-insulin antibodies appears rare.
-
Insulin/C-peptide molar ratio and serum insulin concentration are useful for differentiating insulinoma and autoimmune syndrome.
-
Flash glucose monitoring systems appear suitable for evaluating treatment outcomes.
Search for other papers by Maria Leonor Guia Lopes in
Google Scholar
PubMed
Nova Medical School, Clinical Medicine, New University of Lisbon, Lisbon, Portugal
Search for other papers by José Pedro Cidade in
Google Scholar
PubMed
Search for other papers by Clara Cunha in
Google Scholar
PubMed
Search for other papers by Clotilde Limbert in
Google Scholar
PubMed
Search for other papers by João Sequeira Duarte in
Google Scholar
PubMed
Summary
Riedel’s thyroiditis is the rarest form of thyroiditis, occasionally resulting in rapid thyroid enlargement and potential tracheal obstruction. Here, we detail the case of an 81-year-old woman with a medical history including Hodgkin lymphoma, Hashimoto’s thyroiditis, and multinodular goiter. She presented to the emergency room with stridor, cervical swelling, and breathing difficulties for over 2 days. CT scans revealed substantial thyroid enlargement causing significant glottal and tracheal compression, to a minimum tracheal diameter of 7 mm. Due to the severity of the compressive symptoms, orotracheal intubation and mechanical ventilation were deemed necessary. Surprisingly, despite the initial suspicion of malignancy given the rapid growth in the elderly, subsequent cytological and histological evaluations indicated a benign form of invasive fibrous thyroiditis – Riedel’s thyroiditis. Although surgical intervention was advised, the patient declined and opted for endobronchial treatment with a prosthetic stent and subsequent treatment with systemic glucocorticoids. Following successful treatment, she was discharged within a week and resumed normal activities without respiratory distress. This case is noteworthy for its rapid benign mass growth, rare emergent presentation, and the patient’s advanced age.
Learning points
-
The rapid enlargement of the thyroid gland in elderly patients poses a diagnostic challenge, stemming from the higher occurrence of aggressive thyroid carcinomas.
-
Despite the clinical presentation, a comprehensive diagnostic workup, including fine-needle aspiration and core-needle biopsy, is crucial for accurately distinguishing between benign and malignant causes of thyroid nodule enlargement.
-
This case report illustrates diverse treatment options for Riedel’s thyroiditis, and the importance of individualized treatment plans based on the degree of airway obstruction, patient preferences, and response to initial interventions.
-
Clinicians should contemplate the inclusion of glucocorticoids in the therapeutic regimen for Riedel’s thyroiditis, particularly in cases where surgical intervention is not feasible or declined by the patient.
Search for other papers by Daniel S Brenner in
Google Scholar
PubMed
Search for other papers by Keith Kleinman in
Google Scholar
PubMed
Search for other papers by Amy Manzo in
Google Scholar
PubMed
Search for other papers by Melania M Bembea in
Google Scholar
PubMed
Search for other papers by David W Cooke in
Google Scholar
PubMed
Summary
Anaphylaxis is a rapidly progressive potentially lethal condition, and epinephrine is the most crucial medication in its treatment. In this study, we present a case of diabetic ketoacidosis in a young woman that was precipitated by the administration of epinephrine to treat anaphylaxis. This patient had diabetes mellitus and poor glycemic control and developed ketoacidosis despite having evidence of ongoing endogenous insulin production and having been treated with exogenous long-acting insulin less than 24 h prior to the event. This is a rare, serious, adverse side effect of life-saving medication. This report demonstrates that the risk of diabetic ketoacidosis should be considered when administering epinephrine to patients with diabetes, even in the absence of complete insulin deficiency.
Learning points
-
Epinephrine directly suppresses insulin secretion, stimulates lipolysis, and causes ketone body generation.
-
High-dose catecholamine administration can cause unexpected diabetic ketoacidosis in patients with risk factors.
-
Early administration of insulin may not protect patients from developing ketoacidosis in the setting of high-dose catecholamine administration.
Search for other papers by Ana Dugic in
Google Scholar
PubMed
Search for other papers by Michael Kryk in
Google Scholar
PubMed
Search for other papers by Claudia Mellenthin in
Google Scholar
PubMed
Search for other papers by Christoph Braig in
Google Scholar
PubMed
Search for other papers by Lorenzo Catanese in
Google Scholar
PubMed
Search for other papers by Sandy Petermann in
Google Scholar
PubMed
Search for other papers by Jürgen Kothmann in
Google Scholar
PubMed
Search for other papers by Steffen Mühldorfer in
Google Scholar
PubMed
Summary
Drinking fruit juice is an increasingly popular health trend, as it is widely perceived as a source of vitamins and nutrients. However, high fructose load in fruit beverages can have harmful metabolic effects. When consumed in high amounts, fructose is linked with hypertriglyceridemia, fatty liver and insulin resistance. We present an unusual case of a patient with severe asymptomatic hypertriglyceridemia (triglycerides of 9182 mg/dL) and newly diagnosed type 2 diabetes mellitus, who reported a daily intake of 15 L of fruit juice over several weeks before presentation. The patient was referred to our emergency department with blood glucose of 527 mg/dL and glycated hemoglobin (HbA1c) of 17.3%. Interestingly, features of diabetic ketoacidosis or hyperosmolar hyperglycemic state were absent. The patient was overweight with an otherwise unremarkable physical exam. Lipase levels, liver function tests and inflammatory markers were closely monitored and remained unremarkable. The initial therapeutic approach included i.v. volume resuscitation, insulin and heparin. Additionally, plasmapheresis was performed to prevent potentially fatal complications of hypertriglyceridemia. The patient was counseled on balanced nutrition and detrimental effects of fruit beverages. He was discharged home 6 days after admission. At a 2-week follow-up visit, his triglyceride level was 419 mg/dL, total cholesterol was 221 mg/dL and HbA1c was 12.7%. The present case highlights the role of fructose overconsumption as a contributory factor for severe hypertriglyceridemia in a patient with newly diagnosed diabetes. We discuss metabolic effects of uncontrolled fructose ingestion, as well as the interplay of primary and secondary factors, in the pathogenesis of hypertriglyceridemia accompanied by diabetes.
Learning points
-
Excessive dietary fructose intake can exacerbate hypertriglyceridemia in patients with underlying type 2 diabetes mellitus (T2DM) and absence of diabetic ketoacidosis or hyperosmolar hyperglycemic state.
-
When consumed in large amounts, fructose is considered a highly lipogenic nutrient linked with postprandial hypertriglyceridemia and de novo hepatic lipogenesis (DNL).
-
Severe lipemia (triglyceride plasma level > 9000 mg/dL) could be asymptomatic and not necessarily complicated by acute pancreatitis, although lipase levels should be closely monitored.
-
Plasmapheresis is an effective adjunct treatment option for rapid lowering of high serum lipids, which is paramount to prevent acute complications of severe hypertriglyceridemia.
Search for other papers by Alejandra Perez-Montes de Oca in
Google Scholar
PubMed
Search for other papers by Silvia Pellitero in
Google Scholar
PubMed
Search for other papers by Manel Puig-Domingo in
Google Scholar
PubMed
Summary
Hypoglycemia is an uncommon clinical problem in non-diabetic patients or patients not being treated for diabetes mellitus. It is a rare, but well-established complication of bariatric surgery and, in some cases, it can be the only symptom of another medical problem. A 50-year-old woman with a history of partially recovered hypopituitarism after transsphenoidal surgery for a non-functioning pituitary macroadenoma complained about symptomatic hypoglycemia after sleeve gastrectomy surgery. Our initial studies failed to determine the cause for these episodes and treatment with acarbose (suspecting a dumping syndrome) was not helpful. Finally, laboratory findings revealed growth hormone (GH) deficiency. The patient received treatment with GH, with the resolution of symptoms after 3 months of treatment. Our case suggests that all causes of hypoglycemia should be considered and studied after bariatric surgery. An improvement in insulin-resistance following bariatric surgery can trigger clinical manifestations of GH deficiency.
Learning points:
-
Postprandial hypoglycemia after bariatric surgery is usually due to dumping syndrome.
-
Even after bariatric surgery, all causes of hypoglycemia should be considered and studied.
-
After significant weight loss, insulin sensitivity is usually restored and can trigger clinical manifestations of GH deficiency.
-
Hypoglycemia is a rare symptom of GH deficiency.
Ricardo Cruzado Rivarola Hospital, Nasca, Perú
Search for other papers by Anthony Ramos-Yataco in
Google Scholar
PubMed
Search for other papers by Kelly Meza in
Google Scholar
PubMed
Search for other papers by Reyna Cecilia Farfán-García in
Google Scholar
PubMed
Search for other papers by Solange Ortega-Rojas in
Google Scholar
PubMed
Search for other papers by Isaac Salinas-Mamani in
Google Scholar
PubMed
Search for other papers by Ivonne Silva-Arrieta Ontaneda in
Google Scholar
PubMed
Search for other papers by Ricardo Correa in
Google Scholar
PubMed
Summary
The first case of the novel coronavirus infection (COVID-19) in Peru was reported on March 6, 2020. As of September 7, 2020, about 700 000 cases of COVID-19 resulting in 29,976 deaths have been confirmed by the Ministry of Health. Among COVID-19 patients with co-morbidities, type 2 diabetes mellitus (T2DM) has been recognized as a risk factor for severe disease. Patients with T2DM may experience diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic (HHS) if infected with the coronavirus 2 (SARS-CoV-2). Regular blood analysis including arterial blood gas is essential in monitoring the care of patients with T2DM infected with COVID-19. We report five cases of DKA in patients with underlying T2DM that presented with severe COVID-19 infection.
Learning points:
-
COVID-19 may cause acute metabolic dysregulations in patients with T2DM.
-
It is important to monitor basic metabolic panel (BMP) and arterial blood gases (ABGs) in patients with COVID-19 since metabolic complications can develop unexpectedly.
-
Patients with T2DM develop an inflammatory syndrome characterized by severe insulin resistance and B cell dysfunction that can lead to DKA.
Search for other papers by Shunsuke Shimazaki in
Google Scholar
PubMed
Search for other papers by Itsuro Kazukawa in
Google Scholar
PubMed
Search for other papers by Kyoko Mori in
Google Scholar
PubMed
Search for other papers by Makiko Kihara in
Google Scholar
PubMed
Search for other papers by Masanori Minagawa in
Google Scholar
PubMed
Summary
Ammonium acid urate (AAU) crystals are rare in industrialized countries. Furthermore, the number of children with diabetic ketoacidosis (DKA) who develop severe acute kidney injury (AKI) after hospitalization is small. We encountered two patients with AKI caused by AAU crystals during the recovery phase of DKA upon admission. They were diagnosed with severe DKA and hyperuricemia. Their urine volume decreased and AKI developed several days after hospitalization; however, acidosis improved in both patients. Urine sediment analysis revealed AAU crystals. They were treated with urine alkalization and diuretics. Excretion of ammonia in the urine and urine pH levels increased after treatment of DKA, which resulted in the formation of AAU crystals. In patients with severe DKA, the urine and urine sediment should be carefully examined as AAU can form in the recovery phase of DKA.
Learning points:
-
Ammonium acid urate crystals could be formed in the recovery phase of diabetic ketoacidosis.
-
Diabetic ketoacidosis patients may develop acute kidney injury caused by ammonium acid urate crystals.
-
Urine and urine sediment should be carefully checked in patients with severe DKA who present with hyperuricemia and volume depletion.
Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK
Search for other papers by A Chinoy in
Google Scholar
PubMed
Search for other papers by N B Wright in
Google Scholar
PubMed
Search for other papers by M Bone in
Google Scholar
PubMed
Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK
Search for other papers by R Padidela in
Google Scholar
PubMed
Summary
Hypokalaemia at presentation of diabetic ketoacidosis is uncommon as insulin deficiency and metabolic acidosis shifts potassium extracellularly. However, hypokalaemia is a recognised complication of the management of diabetic ketoacidosis as insulin administration and correction of metabolic acidosis shifts potassium intracellularly. We describe the case of a 9-year-old girl with newly diagnosed type 1 diabetes mellitus presenting in diabetic ketoacidosis, with severe hypokalaemia at presentation due to severe and prolonged emesis. After commencing management for her diabetic ketoacidosis, her serum sodium and osmolality increased rapidly. However, despite maximal potassium concentrations running through peripheral access, and multiple intravenous potassium ‘corrections’, her hypokalaemia persisted. Seventy two hours after presentation, she became drowsy and confused, with imaging demonstrating central pontine myelinolysis – a rare entity seldom seen in diabetic ketoacidosis management in children despite rapid shifts in serum sodium and osmolality. We review the literature associating central pontine myelinolysis with hypokalaemia and hypothesise as to how the hypokalaemia may have contributed to the development of central pontine myelinolysis. We also recommend an approach to the management of a child in diabetic ketoacidosis with hypokalaemia at presentation.
Learning points:
-
Hypokalaemia is a recognised complication of treatment of paediatric diabetic ketoacidosis that should be aggressively managed to prevent acute complications.
-
Central pontine myelinolysis is rare in children, and usually observed in the presence of rapid correction of hyponatraemia. However, there is observational evidence of an association between hypokalaemia and central pontine myelinolysis, potentially by priming the endothelial cell membrane to injury by lesser fluctuations in osmotic pressure.
-
Consider central pontine myelinolysis as a complication of the management of paediatric diabetic ketoacidosis in the presence of relevant symptoms with profound hypokalaemia and/or fluctuations in serum sodium levels.
-
We have suggested an approach to the management strategies of hypokalaemia in paediatric diabetic ketoacidosis which includes oral potassium supplements if tolerated, minimising the duration and the rate of insulin infusion and increasing the concentration of potassium intravenously (via central line if necessary).
Search for other papers by Ilan Rahmani Tzvi-Ran in
Google Scholar
PubMed
Search for other papers by Judith Olchowski in
Google Scholar
PubMed
Search for other papers by Merav Fraenkel in
Google Scholar
PubMed
Search for other papers by Asher Bashiri in
Google Scholar
PubMed
Search for other papers by Leonid Barski in
Google Scholar
PubMed
Summary
A previously healthy 24-year-old female underwent an emergent caesarean section without a major bleeding described. During the first post-operative days (POD) she complained of fatigue, headache and a failure to lactate with no specific and conclusive findings on head CT. On the following days, fever rose with a suspicion of an obstetric surgery-related infection, again with no evidence to support the diagnosis. On POD5 a new-onset hyponatremia was documented. The urine analysis suggested SIADH, and following a treatment failure, further investigation was performed and demonstrated both central hypothyroidism and adrenal insufficiency. The patient was immediately treated with hydrocortisone followed by levothyroxine with a rapid resolution of symptoms and hyponatremia. Further laboratory investigation demonstrated anterior hypopituitarism. The main differential diagnosis was Sheehan’s syndrome vs lymphocytic hypophysitis. Brain MRI was performed as soon as it was available and findings consistent with Sheehan’s syndrome confirmed the diagnosis. Lifelong hormonal replacement therapy was initiated. Further complaints on polyuria and polydipsia have led to a water deprivation testing and the diagnosis of partial central insipidus and appropriate treatment with DDAVP.
Learning points:
-
Sheehan’s syndrome can occur, though rarely, without an obvious major post-partum hemorrhage.
-
The syndrome may resemble lymphocytic hypophysitis clinically and imaging studies may be crucial in order to differentiate both conditions.
-
Hypopituitarism presentation may be variable and depends on the specific hormone deficit.
-
Euvolemic hyponatremia workup must include thyroid function test and 08:00 AM cortisol levels.
Department of Pediatrics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
Search for other papers by Suguru Watanabe in
Google Scholar
PubMed
Search for other papers by Jun Kido in
Google Scholar
PubMed
Search for other papers by Mika Ogata in
Google Scholar
PubMed
Search for other papers by Kimitoshi Nakamura in
Google Scholar
PubMed
Search for other papers by Tomoyuki Mizukami in
Google Scholar
PubMed
Summary
Hyperglycemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are the most severe acute complications of diabetes mellitus (DM). HHS is characterized by severe hyperglycemia and hyperosmolality without significant ketosis and acidosis. A 14-year-old Japanese boy presented at the emergency room with lethargy, polyuria and polydipsia. He belonged to a baseball club team and habitually drank sugar-rich beverages daily. Three weeks earlier, he suffered from lassitude and developed polyuria and polydipsia 1 week later. He had been drinking more sugar-rich isotonic sports drinks (approximately 1000–1500 mL/day) than usual (approximately 500 mL/day). He presented with HHS (hyperglycemia (1010 mg/dL, HbA1c 12.3%) and mild hyperosmolality (313 mOsm/kg)) without acidosis (pH 7.360), severe ketosis (589 μmol/L) and ketonuria. He presented HHS in type 1 diabetes mellitus (T1DM) with elevated glutamate decarboxylase antibody and islet antigen 2 antibody. Consuming beverages with high sugar concentrations caused hyperglycemia and further exacerbates thirst, resulting in further beverage consumption. Although he recovered from HHS following intensive transfusion and insulin treatment, he was significantly sensitive to insulin therapy. Even the appropriate amount of insulin may result in dramatically decreasing blood sugar levels in patients with T1DM. We should therefore suspect T1DM in patients with HHS but not those with obesity. Moreover, age, clinical history and body type are helpful for identifying T1DM and HHS. Specifically, drinking an excess of beverages rich in sugars represents a risk of HHS in juvenile/adolescent T1DM patients.
Learning points:
-
Hyperglycemic hyperosmolar state (HHS) is characterized by severe hyperglycemia and hyperosmolality without significant ketosis and acidosis.
-
The discrimination between HHS of type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) in initial presentation is difficult.
-
Pediatrician should suspect T1DM in patients with HHS but not obesity.
-
Age, clinical history and body type are helpful for identifying T1DM and HHS.
-
Children with T1DM are very sensitive to insulin treatment, and even appropriate amount of insulin may result in dramatically decreasing blood sugar levels.
