Diagnosis and Treatment > Investigation > Alanine aminotransferase
You are looking at 1 - 10 of 13 items
Search for other papers by Tomomi Nakao in
Google Scholar
PubMed
Search for other papers by Ken Takeshima in
Google Scholar
PubMed
Search for other papers by Hiroyuki Ariyasu in
Google Scholar
PubMed
Search for other papers by Chiaki Kurimoto in
Google Scholar
PubMed
Search for other papers by Shinsuke Uraki in
Google Scholar
PubMed
Search for other papers by Shuhei Morita in
Google Scholar
PubMed
Search for other papers by Yasushi Furukawa in
Google Scholar
PubMed
Search for other papers by Hiroshi Iwakura in
Google Scholar
PubMed
Search for other papers by Takashi Akamizu in
Google Scholar
PubMed
Summary
Thyroid storm (TS) is a life-threatening condition that may suffer thyrotoxic patients. Therapeutic plasma exchange (TPE) is a rescue approach for TS with acute hepatic failure, but it should be initiated with careful considerations. We present a 55-year-old male patient with untreated Graves’ disease who developed TS. Severe hyperthyroidism and refractory atrial fibrillation with congestive heart failure aggregated to multiple organ failure. The patient was recovered by intensive multimodal therapy, but we had difficulty in introducing TPE treatment considering the risk of exacerbation of congestive heart failure due to plasma volume overload. In addition, serum total bilirubin level was not elevated in the early phase to the level of indication for TPE. The clinical course of this patient instructed delayed elevation of bilirubin until the level of indication for TPE in some patients and also demonstrated the risk of exacerbation of congestive heart failure by TPE.
Learning points:
-
Our patient with thyroid storm could be diagnosed and treated promptly using Japan Thyroid Association guidelines for thyroid storm.
-
Delayed elevation of serum bilirubin levels could make the decision of introducing therapeutic plasma exchange difficult in cases of thyroid storm with acute hepatic failure.
-
The risk of worsening congestive heart failure should be considered carefully when performing therapeutic plasma exchange.
Division of Endocrinology and Metabolism, Dokuz Eylul University, Izmir, Turkey
Search for other papers by Baris Akinci in
Google Scholar
PubMed
Search for other papers by Rasimcan Meral in
Google Scholar
PubMed
Search for other papers by Diana Rus in
Google Scholar
PubMed
Search for other papers by Rita Hench in
Google Scholar
PubMed
Search for other papers by Adam H Neidert in
Google Scholar
PubMed
Search for other papers by Frank DiPaola in
Google Scholar
PubMed
Search for other papers by Maria Westerhoff in
Google Scholar
PubMed
Search for other papers by Simeon I Taylor in
Google Scholar
PubMed
Search for other papers by Elif A Oral in
Google Scholar
PubMed
Summary
A patient with atypical partial lipodystrophy who had a transient initial response to metreleptin experienced acute worsening of her metabolic state when neutralizing antibodies against metreleptin appeared. Because her metabolic status continued to deteriorate, a therapeutic trial with melanocortin-4 receptor agonist setmelanotide, that is believed to function downstream from leptin receptor in the leptin signaling system, was undertaken in an effort to improve her metabolic status for the first time in a patient with lipodystrophy. To achieve this, a compassionate use (investigational new drug application; IND) was initiated (NCT03262610). Glucose control, body fat by dual-energy X-ray absorptiometry and MRI, and liver fat by proton density fat fraction were monitored. Daily hunger scores were assessed by patient filled questionnaires. Although there was a slight decrease in hunger scales and visceral fat, stimulating melanocortin-4 receptor by setmelanotide did not result in any other metabolic benefit such as improvement of hypertriglyceridemia or diabetes control as desired. Targeting melanocortin-4 receptor to regulate energy metabolism in this setting was not sufficient to obtain a significant metabolic benefit. However, complex features of our case make it difficult to generalize these observations to all cases of lipodystrophy. It is still possible that melanocortin-4 receptor agonistic action may offer some therapeutic benefits in leptin-deficient patients.
Learning points:
-
A patient with atypical lipodystrophy with an initial benefit with metreleptin therapy developed neutralizing antibodies to metreleptin (Nab-leptin), which led to substantial worsening in metabolic control. The neutralizing activity in her serum persisted for longer than 3 years.
-
Whether the worsening in her metabolic state was truly caused by the development of Nab-leptin cannot be fully ascertained, but there was a temporal relationship. The experience noted in our patient at least raises the possibility for concern for substantial metabolic worsening upon emergence and persistence of Nab-leptin. Further studies of cases where Nab-leptin is detected and better assay systems to detect and characterize Nab-leptin are needed.
-
The use of setmelanotide, a selective MC4R agonist targeting specific neurons downstream from the leptin receptor activation, was not effective in restoring metabolic control in this complex patient with presumed diminished leptin action due to Nab-leptin.
-
Although stimulating the MC4R pathway was not sufficient to obtain a significant metabolic benefit in lowering triglycerides and helping with her insulin resistance as was noted with metreleptin earlier, there was a mild reduction in reported food intake and appetite.
-
Complex features of our case make it difficult to generalize our observation to all leptin-deficient patients. It is possible that some leptin-deficient patients (especially those who need primarily control of food intake) may still theoretically benefit from MC4R agonistic action, and further studies in carefully selected patients may help to tease out the differential pathways of metabolic regulation by the complex network of leptin signaling system.
Search for other papers by Yuri Tanaka in
Google Scholar
PubMed
Search for other papers by Taisuke Uchida in
Google Scholar
PubMed
Search for other papers by Hideki Yamaguchi in
Google Scholar
PubMed
Search for other papers by Yohei Kudo in
Google Scholar
PubMed
Search for other papers by Tadato Yonekawa in
Google Scholar
PubMed
Search for other papers by Masamitsu Nakazato in
Google Scholar
PubMed
Summary
We report the case of a 48-year-old man with thyroid storm associated with fulminant hepatitis and elevated levels of soluble interleukin-2 receptor (sIL-2R). Fatigue, low-grade fever, shortness of breath, and weight loss developed over several months. The patient was admitted to the hospital because of tachycardia-induced heart failure and liver dysfunction. Graves’ disease with heart failure was diagnosed. He was treated with methimazole, inorganic iodide, and a β-blocker. On the day after admission, he became unconscious with a high fever and was transferred to the intensive care unit. Cardiogenic shock with atrial flutter was treated with intra-aortic balloon pumping and cardioversion. Hyperthyroidism decreased over 10 days, but hepatic failure developed. He was diagnosed with thyroid storm accompanied by fulminant hepatitis. Laboratory investigations revealed elevated levels of sIL-2R (9770 U/mL). The fulminant hepatitis was refractory to plasma exchange and plasma filtration with dialysis, and no donors for liver transplantation were available. He died of hemoperitoneum and gastrointestinal hemorrhage due to fulminant hepatitis 62 days after admission. Elevated circulating levels of sIL-2R might be a marker of poor prognosis in thyroid storm with fulminant hepatitis.
Learning points:
-
The prognosis of thyroid storm when fulminant hepatitis occurs is poor.
-
Liver transplantation is the preferred treatment for fulminant hepatitis induced by thyroid storm refractory to plasma exchange.
-
Elevated levels of soluble interleukin-2 receptor might be a marker of poor prognosis in patients with thyroid storm.
Search for other papers by Chad Bisambar in
Google Scholar
PubMed
Search for other papers by Andrew Collier in
Google Scholar
PubMed
Search for other papers by Fraser Duthie in
Google Scholar
PubMed
Search for other papers by Carron Meney in
Google Scholar
PubMed
Summary
A 40-year-old Caucasian female presented with hyperglycaemia, polyuria, polydipsia and weight loss of 6 kg over a 1-month period. There was no personal or family history of malignancy or diabetes mellitus. On examination, she was jaundiced with pale mucous membranes and capillary glucose was 23.1 mmol/L. Initial investigations showed iron deficiency anaemia and obstructive pattern of liver function tests. HbA1c was diagnostic of diabetes mellitus at 79 mmol/mol. Malignancy was suspected and CT chest, abdomen and pelvis showed significant dilatation of intra- and extra-hepatic biliary tree including pancreatic duct, with periampullary 30 mm mass lesion projecting into lumen of duodenum. Enlarged nodes were seen around the superior mesenteric artery. This was confirmed on MRI liver. Fasting gut hormones were normal except for a mildly elevated somatostatin level. Chromogranin A was elevated at 78 pmol/L with normal chromogranin B. Duodenoscopy and biopsy showed possible tubovillous adenoma with low-grade dysplasia, but subsequent endoscopic ultrasound and biopsy revealed a grade 1, well differentiated neuroendocrine tumour. The patient was started on insulin, transfused to Hb >8 g/dL and Whipple’s pancreatico-duodenectomy was undertaken. This showed a well-differentiated neuroendocrine carcinoma arising in duodenum (Grade G1 with Ki67: 0.5%), with areas of chronic pancreatitis and preservation of pancreatic islet cells. There was complete resolution of diabetes post Whipple’s procedure and patient was able to come of insulin treatment. Her last HBA1C was 31 mmol/mol, 4 months post tumour resection.
Learning points:
-
Diabetes mellitus and malignancy can be related.
-
A high index of suspicion is needed when diabetes mellitus presents atypically.
-
Non-functional neuroendocrine tumours can present with diabetes mellitus.
Search for other papers by Clarissa Ern Hui Fang in
Google Scholar
PubMed
HRB Clinical Research Facility, National University of Ireland Galway, Galway, Ireland
Search for other papers by Mohammed Faraz Rafey in
Google Scholar
PubMed
Search for other papers by Aine Cunningham in
Google Scholar
PubMed
HRB Clinical Research Facility, National University of Ireland Galway, Galway, Ireland
Search for other papers by Sean F Dinneen in
Google Scholar
PubMed
HRB Clinical Research Facility, National University of Ireland Galway, Galway, Ireland
Search for other papers by Francis M Finucane in
Google Scholar
PubMed
Summary
A 28-year-old male presented with 2 days of vomiting and abdominal pain, preceded by 2 weeks of thirst, polyuria and polydipsia. He had recently started risperidone for obsessive-compulsive disorder. He reported a high dietary sugar intake and had a strong family history of type 2 diabetes mellitus (T2DM). On admission, he was tachycardic, tachypnoeic and drowsy with a Glasgow Coma Scale (GCS) of 10/15. We noted axillary acanthosis nigricans and obesity (BMI 33.2 kg/m2). Dipstick urinalysis showed ketonuria and glycosuria. Blood results were consistent with diabetic ketoacidosis (DKA), with hyperosmolar state. We initiated our DKA protocol, with intravenous insulin, fluids and potassium, and we discontinued risperidone. His obesity, family history of T2DM, acanthosis nigricans and hyperosmolar state prompted consideration of T2DM presenting with ‘ketosis-prone diabetes’ (KPD) rather than T1DM. Antibody markers of beta-cell autoimmunity were subsequently negative. Four weeks later, he had modified his diet and lost weight, and his metabolic parameters had normalised. We reduced his total daily insulin dose from 35 to 18 units and introduced metformin. We stopped insulin completely by week 7. At 6 months, his glucometer readings and glycated haemoglobin (HbA1c) level had normalised.
Learning points:
-
Risperidone-induced diabetic ketoacidosis (DKA) is not synonymous with type 1 diabetes, even in young white patients and may be a manifestation of ‘ketosis-prone’ type 2 diabetes (KPD).
-
KPD is often only confirmed after the initial presentation, when islet autoimmunity and cautious phasing out of insulin therapy have been assessed, and emergency DKA management remains the same.
-
As in other cases of KPD, a family history of T2DM and presence of cutaneous markers of insulin resistance were important clinical features suggestive of an alternative aetiology for DKA.
Search for other papers by Natasha Shrikrishnapalasuriyar in
Google Scholar
PubMed
Search for other papers by Mirena Noyvirt in
Google Scholar
PubMed
Search for other papers by Philip Evans in
Google Scholar
PubMed
Search for other papers by Bethan Gibson in
Google Scholar
PubMed
Search for other papers by Elin Foden in
Google Scholar
PubMed
Search for other papers by Atul Kalhan in
Google Scholar
PubMed
A 54-year-old woman was admitted to hospital with a presumed allergic reaction to a single dose of amoxicillin given for a suspected upper respiratory tract infection. She complained of chest tightness although there was no wheeze or stridor. On examination, she was pyrexial, tachycardic, hypertensive and had a diffuse mottled rash on her lower limbs. Her initial investigations showed raised inflammatory markers. She was treated in the intensive care for a presumed anaphylactic reaction with an underlying sepsis. Further investigations including CT head and CSF examination were unremarkable; however, a CT abdomen showed a 10 cm heterogeneous right adrenal mass. Based on review by the endocrine team, a diagnosis of pheochromocytoma crisis was made, which was subsequently confirmed on 24-h urinary metanephrine measurement. An emergency adrenalectomy was considered although she was deemed unfit for surgery. Despite intensive medical management, her conditioned deteriorated and she died secondary to multi-organ failure induced by pheochromocytoma crisis.
Learning points:
-
Pheochromocytoma have relatively higher prevalence in autopsy series (0.05–1%) suggestive of a diagnosis, which is often missed.
-
Pheochromocytoma crisis is an endocrine emergency characterized by hemodynamic instability induced by surge of catecholamines often precipitated by trauma and medications (β blockers, general anesthetic agents, ephedrine and steroids).
-
Pheochromocytoma crisis can mimic acute coronary syndrome, cardiogenic or septic shock.
-
Livedo reticularis can be a rare although significant cutaneous marker of underlying pheochromocytoma crisis.
Search for other papers by Snezana Burmazovic in
Google Scholar
PubMed
Search for other papers by Christoph Henzen in
Google Scholar
PubMed
Search for other papers by Lukas Brander in
Google Scholar
PubMed
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
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.
Department of Medicine, Endocrinology Division, Lebanese University, Hadath, Lebanon
Endocrinology Department, Rafic Hariri University Hospital, Beirut, Lebanon
Search for other papers by Carine Ghassan Richa in
Google Scholar
PubMed
Department of Medicine, Endocrinology Division, Lebanese University, Hadath, Lebanon
Endocrinology Department, Mount Lebanon Hospital, Beirut, Lebanon
Search for other papers by Khadija Jamal Saad in
Google Scholar
PubMed
Department of Radiology, Beirut Governmental University Hospital, Beirut, Lebanon
Diagnostic Radiology, Radiology Department
Search for other papers by Ali Khaled Chaaban in
Google Scholar
PubMed
Department of Medicine, Endocrinology Division, Lebanese University, Hadath, Lebanon
Clinical Endocrinology, Endocrinology Department, Rafic Hariri University Hospital, Beirut, Lebanon
Search for other papers by Mohamad Souheil El Rawas in
Google Scholar
PubMed
Summary
The objective of the study is to report a case of acute pancreatitis secondary to hypercalcemia induced by primary hyperparathyroidism in a pregnant woman at the end of the first trimester. The case included a 32-year-old woman who was diagnosed with acute pancreatitis and severe hypercalcemia refractory to many regimens of medical therapy in the first trimester of pregnancy. She was successfully treated with parathyroidectomy in the early second trimester with complete resolution of hypercalcemia and pancreatitis. Neonatal course was unremarkable. To our best knowledge, this is a rare case when primary hyperparathyroidism and its complications are diagnosed in the first trimester of pregnancy. In conclusion, primary hyperparathyroidism is a rare life-threatening condition to the fetus and mother especially when associated with complications such as pancreatitis. Early therapeutic intervention is important to reduce the morbidity and mortality. Parathyroidectomy performed in the second trimester can be the only solution.
Learning points:
-
Learning how to make diagnosis of primary hyperparathyroidism in a woman during the first trimester of pregnancy.
-
Understanding the complications of hypercalcemia and be aware of the high mortality and sequelae in both fetus and mother.
-
Providing the adequate treatment in such complicated cases with coordinated care between endocrinologists and obstetricians to ensure optimal outcomes.
Search for other papers by Takatoshi Anno in
Google Scholar
PubMed
Search for other papers by Hideaki Kaneto in
Google Scholar
PubMed
Search for other papers by Ryo Shigemoto in
Google Scholar
PubMed
Search for other papers by Fumiko Kawasaki in
Google Scholar
PubMed
Search for other papers by Yasuhiro Kawai in
Google Scholar
PubMed
Search for other papers by Noriyo Urata in
Google Scholar
PubMed
Search for other papers by Hirofumi Kawamoto in
Google Scholar
PubMed
Search for other papers by Kohei Kaku in
Google Scholar
PubMed
Search for other papers by Niro Okimoto in
Google Scholar
PubMed
Summary
Hypoglycemia is induced by many causes, especially over-dose of insulin or oral hypoglycemic agents in diabetic subjects. In such a case, hyperinsulinemic hypoglycemia is usually observed. On the other hand, it is important to classify secondary hypoglycemia and hypoinsulinemic hypoglycemia. Liver injury-induced hypoglycemia is one of the causes of hypoinsulinemic hypoglycemia but rarely observed in clinical practice. Herein, we experienced similar 2 cases of non-diabetic hypoinsulinemic hypoglycemia. Both of them were elderly subjects with low body weight. Furthermore, it is likely that hypoinsulinemic hypoglycemia in both subjects was triggered by severe liver injury, at least in part, due to possible limited liver glycogen store. In elderly subjects with low body weight and/or malnutrition, metabolism in the liver is reduced and glycogen accumulation is decreased. Such alteration brings out acute and marked liver injury, which finally leads to the onset of severe hypoglycemia. It is known that not only liver injury but also multiple organ failure could be induced due to extreme emaciation in subjects. It is likely that in elderly subjects with low body weight and/or malnutrition, multiple organ failure including liver failure could be induced due to the similar reason. Therefore, we should be very careful of such subjects in order to avoid the development of multiple organ failure which leads to life-threatening situations. In conclusion, we should keep in mind the possibility of hypoinsulinemic hypoglycemia when we examine severe liver injury, especially in elderly or starving subjects with low body weight and limited liver glycogen stores.
Learning points:
-
It is important to classify secondary hypoglycemia and hypoinsulinemic hypoglycemia.
-
Liver injury-induced hypoglycemia is one of the causes of hypoinsulinemic hypoglycemia but rarely observed in everyday clinical practice.
-
Herein, we reported similar 2 cases of hypoinsulinemic hypoglycemia without diabetes presumably triggered by severe liver injury.
-
In both cases, hypoglycemia was improved by glucose infusion, although their liver injury was not improved.
-
We should keep in mind the possibility of hypoinsulinemic hypoglycemia when we examine severe liver injury, especially in elderly subjects with low body weight.
Search for other papers by Charlotte S Schömig in
Google Scholar
PubMed
Search for other papers by Marie-Ève Robinson in
Google Scholar
PubMed
Search for other papers by Julia E von Oettingen in
Google Scholar
PubMed
Summary
Congenital hypothyroidism requires prompt treatment to prevent adverse health outcomes. Poor intestinal levothyroxine absorption can complicate management. We present a case of a term female newborn with necrotizing enterocolitis (NEC) requiring subtotal ileum resection. Congenital hypothyroidism was diagnosed by newborn screening. Treatment was complicated by intestinal malabsorption of levothyroxine. Intravenous levothyroxine substitution restored euthyroidism and supraphysiologic PO doses subsequently maintained a euthyroid state. After several months, the required levothyroxine dose was weaned down to typical recommended dosing. In conclusion, small bowel resection secondary to NEC may lead to malabsorption of oral levothyroxine. An intravenous levothyroxine dose of approximately 50% typical PO dosing is effective in providing rapid normalization of free T4 and TSH. High PO doses may be required to maintain euthyroidism. Close thyroid function monitoring and immediate therapy adjustment are essential as the individual absorption may vary widely. Normal absorption levels may be regained due to adaption of the neonatal intestines.
Learning points:
-
In neonates with malabsorption after ileum resection intravenous levothyroxine replacement should be used to provide normalization of free T4 and TSH.
-
Very high doses of up to 500% usual oral levothyroxine may be required to maintain euthyroidism. The estimated degree of malabsorption can be used to determine the initial dose.
-
Close thyroid function monitoring and immediate therapy adjustment are essential as the absorption and intestinal adaption may vary widely.
