Browse
Search for other papers by Mone Murashita in
Google Scholar
PubMed
Search for other papers by Norio Wada in
Google Scholar
PubMed
Search for other papers by Shuhei Baba in
Google Scholar
PubMed
Search for other papers by Hajime Sugawara in
Google Scholar
PubMed
Search for other papers by Arina Miyoshi in
Google Scholar
PubMed
Search for other papers by Shinji Obara in
Google Scholar
PubMed
Summary
We report a 26-year-old Japanese man who visited our outpatient clinic presenting fever immediately after i.m. injection of the second dose of a coronavirus disease 2019 (COVID-19) vaccine (Moderna®). At the first visit, the patient had a fever of 37.7°C and a swollen thyroid gland with mild tenderness. He was diagnosed with subacute thyroiditis (SAT) based on the presence of thyrotoxicosis (free tri-iodothyronine, 32.3 pg/mL; free thyroxine, >7.77 ng/dL; and thyroid-stimulating hormone (TSH) < 0.01 μIU/mL), high C-reactive protein level (7.40 mg/dL), negative TSH receptor antibody, and characteristic ultrasound findings. His HLA types were A*02:01/24:02, B*15:11/35:01, Cw*03:03, DRB1*09:01/12:01, DQB1*03:03, and DPB1*05: 01/41:01. He was initially administered prednisolone 15 mg/day, following which the fever subsided. After 10 days, he developed limb weakness and could not walk. The serum potassium level decreased to 1.8 mEq/L, which confirmed the diagnosis of thyrotoxic periodic paralysis (TPP). Potassium supplementation was initiated. The muscle weakness gradually decreased. Prednisolone therapy was terminated 6 weeks after the first visit. His thyroid function returned to normal 5 months after the first visit, through a hypothyroid state. To our knowledge, this is the first reported case of TPP-associated SAT following COVID-19 vaccination. Persistent fever following vaccination should be suspected of SAT. Additionally, TPP may be associated with SAT in Asian male patients.
Learning points
-
Following coronavirus disease 2019 (COVID-19) vaccination, subacute thyroiditis may develop regardless of the vaccine type.
-
If persistent fever, anterior neck pain, swelling and tenderness of thyroid gland, and symptoms of thyrotoxicosis are observed immediately after the COVID-19 vaccination, examination in consideration of the onset of subacute thyroiditis is recommended.
-
HLA-B35 may be associated with the onset of subacute thyroiditis after the COVID-19 vaccination.
-
Although rare, subacute thyroiditis can be associated with thyrotoxic periodic paralysis, especially in Asian men.
-
Glucocorticoid therapy for subacute thyroiditis may induce thyrotoxic periodic paralysis through hypokalemia.
Search for other papers by Maheswaran Dhanasekaran in
Google Scholar
PubMed
Search for other papers by Siddharth Narayanan in
Google Scholar
PubMed
Search for other papers by Ioannis Mastoris in
Google Scholar
PubMed
Search for other papers by Suchita Mehta in
Google Scholar
PubMed
Summary
Sodium-glucose cotransporter-2 inhibitors (SGLT2i) induce osmotic diuresis by inhibiting the proximal renal tubular reabsorption of the filtered glucose load, which in turn can occasionally lead to severe dehydration and hypotension amidst other adverse effects. We present a case of a 49-year-old man with type 2 diabetes mellitus (T2D) on canagliflozin, a SGLT2i. The patient was brought to the emergency room following a motor vehicle accident. He was confused and had an altered mental status. His blood alcohol and urine toxicology screens were negative. Initial investigations revealed that he had severe hyponatremia with euglycemic ketoacidosis. The adverse condition was reversed with close monitoring and timely management, and the patient was eventually discharged. This is the first report to suggest hyponatremia as a potentially serious adverse effect following SGLT2i therapy. Its impact on the renal tubule handling of sodium and water is not yet well characterized. While further studies are warranted to understand better the pathophysiological mechanisms associated with SGLT2i-induced adverse effects, timely dose reduction or perhaps even its temporary discontinuation may be recommended to prevent complications.
Learning points
-
Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are usually well-tolerated, but some serious adverse effects have been documented.
-
Our case report suggests hyponatremia as a potential, rare side effect of SGLT2i and makes physicians aware of the occurrence of such life-threatening but preventable complications.
-
Timely and close monitoring of the patient, with temporary discontinuation of this drug, may be recommended towards effective management.
-
Studies demonstrating a comprehensive understanding of SGLT2i-related electrolyte derangements are warranted.
Search for other papers by Minna Koivikko in
Google Scholar
PubMed
Search for other papers by Tapani Ebeling in
Google Scholar
PubMed
Search for other papers by Markus Mäkinen in
Google Scholar
PubMed
Search for other papers by Juhani Leppäluoto in
Google Scholar
PubMed
Search for other papers by Antti Raappana in
Google Scholar
PubMed
Search for other papers by Petteri Ahtiainen in
Google Scholar
PubMed
Search for other papers by Pasi Salmela in
Google Scholar
PubMed
Summary
Multiple endocrine neoplasia type 1 NM_001370259.2(MEN1):c.466G>C(p.Gly156Arg) is characterized by tumors of various endocrine organs. We report on a rare, growth hormone-releasing hormone (GHRH)-releasing pancreatic tumor in a MEN1 patient with a long-term follow-up after surgery. A 22-year-old male with MEN1 syndrome, primary hyperparathyroidism and an acromegalic habitus was observed to have a pancreatic tumor on abdominal CT scanning, growth hormone (GH) and insulin-like growth factor 1 (IGF1) were elevated and plasma GHRH was exceptionally high. GHRH and GH were measured before the treatment and were followed during the study. During octreotide treatment, IGF1 normalized and the GH curve was near normal. After surgical treatment of primary hyperparathyroidism, a pancreatic tail tumor was enucleated. The tumor cells were positive for GHRH antibody staining. After the operation, acromegaly was cured as judged by laboratory tests. No reactivation of acromegaly has been seen during a 20-year follow-up. In conclusion, an ectopic GHRH-producing, pancreatic endocrine neoplasia may represent a rare manifestation of MEN1 syndrome.
Learning points
-
Clinical suspicion is in a key position in detecting acromegaly.
-
Remember genetic disorders with young individuals having primary hyperparathyroidism.
-
Consider multiple endocrine neoplasia type 1 syndrome when a person has several endocrine neoplasia.
-
Acromegaly may be of ectopic origin with patients showing no abnormalities in radiological imaging of the pituitary gland.
Department of Endocrinology, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Vietnam
Search for other papers by Nam Quang Tran in
Google Scholar
PubMed
Search for other papers by Chien Cong Phan in
Google Scholar
PubMed
Search for other papers by Thao Thi Phuong Doan in
Google Scholar
PubMed
Department of Endocrinology, University of Medicine and Pharmacy at Ho Chi Minh City, Ho Chi Minh City, Vietnam
Search for other papers by Thang Viet Tran in
Google Scholar
PubMed
Summary
Primary adrenal insufficiency is a rare disease and can masquerade as other conditions; therefore, it is sometimes incorrectly diagnosed. Herein, we reported the case of a 39-year-old Vietnamese male with primary adrenal insufficiency due to bilateral adrenal tuberculosis. The patient presented to the emergency room with acute adrenal crisis and a 3-day history of nausea, vomiting, epigastric pain, and diarrhoea with a background of 6 months of fatigue, weight loss, and anorexia. Abdominal CT revealed bilateral adrenal masses. Biochemically, unequivocal low morning plasma cortisol (<83 nmol/L) and high plasma adrenocorticotropic hormone levels were consistent with primary adrenal insufficiency. There was no evidence of malignancy or lymphoma. As the patient was from a tuberculosis-endemic area, extra-adrenal tuberculosis was excluded during the work up. A retroperitoneal laparoscopic left adrenalectomy was performed, and tuberculous adrenalitis was confirmed by the histopathological results. The patient was started on antituberculous therapy, in addition to glucocorticoid replacement. In conclusion, even without evidence of extra-adrenal tuberculosis, a diagnosis of bilateral adrenal tuberculosis is required. A histopathological examination has a significant role along with clinical judgement and hormonal workup in establishing a definitive diagnosis of adrenal tuberculosis without evidence of active extra-adrenal involvement.
Learning points
-
Primary adrenal insufficiency can be misdiagnosed as other mimicking diseases, such as gastrointestinal illness, leading to diagnostic pitfalls.
-
Adrenal insufficiency can be confirmed with significantly low morning plasma cortisol levels of <83 nmol/L without a dynamic short cosyntropin stimulation test.
-
Tuberculous adrenalitis is an uncommon treatable condition; however, it remains an important cause of primary adrenal insufficiency, especially in developing countries. In the absence of extra-adrenal involvement, adrenal biopsy plays a key role in the diagnostic process. Alternatively, adrenalectomy for histopathological purposes should be considered if CT scan-guided fine needle aspiration is infeasible in cases of small adrenal masses.
Search for other papers by Clare E Bonnar in
Google Scholar
PubMed
Search for other papers by John F Brazil in
Google Scholar
PubMed
Search for other papers by Julie O Okiro in
Google Scholar
PubMed
Search for other papers by Louise Giblin in
Google Scholar
PubMed
Search for other papers by Yvonne Smyth in
Google Scholar
PubMed
Search for other papers by Paula M O’Shea in
Google Scholar
PubMed
Search for other papers by Francis M Finucane in
Google Scholar
PubMed
Summary
A 32-year-old Caucasian male presented to the emergency department with a one-day history of acute severe bilateral lower limb weakness, three days after competing in a bodybuilding competition. He consumed large quantities of carbohydrate-rich foods following the competition. His past medical history was significant for anxiety, and family history was non-contributory. Examination was normal except for reduced power and hyporeflexia in both legs, despite his muscular physique. He was noted to have severe hypokalaemia (K+= 1.9 mmol/L). His thyroid function tests were consistent with thyrotoxicosis. He reported taking thyroxine and several other agents to facilitate muscle mass generation before the bodybuilding competition. His presentation was reminiscent of thyrotoxic periodic paralysis, albeit uncommon with Caucasian ethnicity. He also had transient hyperglycaemia at presentation with concomitant hyperinsulinaemia, which could be attributed to the carbohydrate load and may have exacerbated his hypokalaemia through a transcellular shift. Urine toxicology screen subsequently ruled out the use of diuretics but confirmed the presence of a long-acting beta agonist (clenbuterol) which, along with other substances, may have aggravated the hypokalaemia further. After 12 h of i.v. replacement, the potassium level normalised and leg weakness resolved. The patient agreed to stop taking thyroxine and beta agonists and was well during the clinic visit at one month follow-up. This case highlights the potential for thyrotoxicosis factitia to exacerbate hypokalaemia and muscle weakness from other causes in bodybuilders presenting with acute severe weakness, irrespective of ethnicity.
Learning points
-
In patients presenting with muscle weakness and hypokalaemia, early consideration of thyrotoxicosis is essential, even in the absence of a past history of thyroid disease or specific symptoms of thyrotoxicosis, in order to allow prompt initiation of appropriate treatment and to prevent recurrence.
-
Bodybuilders may constitute a uniquely ‘at-risk’ group for thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia, especially where there is concomitant use of beta-adrenergic agonists, even in the absence of diuretic use.
-
Although rare and usually described in patients of Asian or Polynesian ethnicity, this case highlights that thyrotoxic periodic paralysis secondary to thyrotoxicosis factitia can also occur in patients with Caucasian ethnicity.
-
We speculate that consuming large quantities of carbohydrates may induce hyperinsulinaemia, which could theoretically contribute to worse hypokalaemia, though mechanistic studies would be needed to explore this further.
Search for other papers by Ayesha Ghayur in
Google Scholar
PubMed
Search for other papers by Qurrat Elahi in
Google Scholar
PubMed
Search for other papers by Chinmay Patel in
Google Scholar
PubMed
Search for other papers by Rishi Raj in
Google Scholar
PubMed
Summary
Hypothyroidism is a common medical condition and is often easily managed with excellent outcomes, when treated adequately. Compliance with levothyroxine (LT4) therapy is often compromised because of the need for a daily and lasting schedule. Overt rhabdomyolysis due to under-treatment or non-compliance is a rare occurrence. We report a case of rhabdomyolysis leading to acute kidney injury (AKI) on chronic kidney disease (CKD) requiring hemodialysis (HD) in a 68-year-old Caucasian male due to non-compliance with levothyroxine (LT4) therapy. Our patient 'ran out of levothyroxine' for approximately 4 weeks and developed gradually progressive muscle pain. The diagnosis of severe AKI due to rhabdomyolysis was made based on oliguria, elevated creatinine kinase (CK), and renal failure. Resuming the home dose of LT4 failed to correct CK levels, and there was a progressive decline in renal function. Although increasing doses of LT4 and three cycles of HD improved CK levels, they remained above baseline at the time of discharge. The patient recovered gradually and required HD for 4 weeks. CK levels normalized at 6 weeks. Through this case report, we highlight that non-compliance with LT4 therapy can lead to life-threatening complications such as renal failure and hence the need to educate patients on the significance of compliance with LT4 therapy should be addressed.
Learning points
-
Non-compliance to levothyroxine therapy is common and can lead to serious complications, including rhabdomyolysis.
-
Rhabdomyolysis is an uncommon presentation of hypothyroidism and severe rhabdomyolysis can result in renal failure requiring hemodialysis.
-
Rhabdomyolysis associated with hypothyroidism can be further exacerbated by concomitant use of statins.
Search for other papers by Ziadoon Faisal in
Google Scholar
PubMed
Search for other papers by Miguel Debono in
Google Scholar
PubMed
Summary
In this case report, we describe the management of a patient who was admitted with an ectopic ACTH syndrome during the COVID pandemic with new-onset type 2 diabetes, neutrophilia and unexplained hypokalaemia. These three findings when combined should alert physicians to the potential presence of Cushing’s syndrome (CS). On admission, a quick diagnosis of CS was made based on clinical and biochemical features and the patient was treated urgently using high dose oral metyrapone thus allowing delays in surgery and rapidly improving the patient’s clinical condition. This resulted in the treatment of hyperglycaemia, hypokalaemia and hypertension reducing cardiovascular risk and likely risk for infection. Observing COVID-19 pandemic international guidelines to treat patients with CS has shown to be effective and offers endocrinologists an option to manage these patients adequately in difficult times.
Learning points
-
This case report highlights the importance of having a low threshold for suspicion and investigation for Cushing’s syndrome in a patient with neutrophilia and hypokalaemia, recently diagnosed with type 2 diabetes especially in someone with catabolic features of the disease irrespective of losing weight.
-
It also supports the use of alternative methods of approaching the diagnosis and treatment of Cushing’s syndrome during a pandemic as indicated by international protocols designed specifically for managing this condition during Covid-19.
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 Edmond Puca in
Google Scholar
PubMed
Search for other papers by Entela Puca in
Google Scholar
PubMed
Search for other papers by Pellumb Pipero in
Google Scholar
PubMed
Search for other papers by Holta Kraja in
Google Scholar
PubMed
Search for other papers by Najada Como in
Google Scholar
PubMed
Summary
Comorbidities are a risk factor for patients with COVID-19 and the mechanisms of disease remain unclear. The aim of this paper is to present a case report of an COVID-19 patient with severe hypocalcaemia. This is a report of an 81-year-old female, suffered from myalgia and fatigue for more than 3–4 weeks. Fever and cough appear 2 days before she presented to the emergency room. On physical examination, she was febrile with a temperature of 38.8°C, accompanied by cough, sore throat, headache, fatigue, and muscle ache. Her past medical history was remarkable with no chronic disease. She had lymphopenia. Laboratory test revealed moderate liver dysfunction, hypoalbuminemia, and severe hypocalcaemia (serum corrected calcium level: 5.7 mg/dL). Parathyroid hormone (PTH) was 107.9 pg/mL (range: 15–65) and 25(OH)2D levels was 4.5 ng/mL (range: 25–80). Chest CT scan detected peripheral ground-glass opacity. Throat swab for coronavirus by RT-PCR assay tested positive for the virus. She was treated with lopinavir/ritonavir, third generation cephalosporin, anticoagulant, daily high-dose calcium acetate, vitamin D3, fresh frozen plasma and oxygen therapy. She was discharged after two negative throat swab tests for coronavirus by conventional RT-PCR.
Learning points:
-
Comorbidities are a risk factor for patients with COVID-19.
-
Laboratory findings are unspecific in COVID-19 patients; laboratory abnormalities include lymphopenia, elevated of LDH, CPK and the inflammatory markers, such as C reactive protein, ferritinemia and the erythrocyte sedimentation rate.
-
In addition to inflammatory markers, in COVID-19 patients it is crucial to check the level of vitamin D and calcium.
-
There may be a correlation between vitamin D deficiency and the severity of COVID-19 disease.
Search for other papers by Omayma Elshafie in
Google Scholar
PubMed
Search for other papers by Nicholas Woodhouse in
Google Scholar
PubMed
Summary
A 79-year-old male presented with a 10-year history of intermittent headache, sweating, persistent hand numbness and uncontrolled hypertension. He was receiving Nifedipine and Hydrochorothizide. On examination (O/E), his BP was 180/100 he was acromegalic. His growth hormone (GH) was 10 mIU/L (0.0–0.1) and his insulin-like growth factor (IGF-1): 952 µg/L (76–160). An MRI of the pituitary revealed a 3 × 2 cm pituitary macroadenoma. Surgery was refused and the family agreed for a therapeutic trial of octreotide. His GH levels fell immediately. Two weeks later he was switched to long-acting monthly octreotide in September 2003. During his 16-year follow-up, he has remained well and asymptomatic off medications for hypertension. His BP and IGF-1 levels were also normal until octreotide Long acting (LA) octrotide was stopped for 3 months at age 96. During this period the IGF-1 level returned to pretreatment levels 500 ng/L (50–141), GH 24 mIU/L (0.0–0.1), and a small residual tumour 0.5–0.8 cm was seen on the MRI. Octreotide LA was restarted and the IGF-1 and GH levels returned to normal. He continues the same treatment to date age 97 without side effects. We conclude that the successful control of IGF-1, GH levels, hypertension, tumour size and clinical symptoms for more than 16 years occurred using octreotide LA in an elderly advanced acromegalic patient. To the best of our knowledge, this is the first report of the successful use of octreotide LA for more than 16 years.
Learning points:
-
The value of a therapeutic trial of octreotide to identify responders.
-
Control of GH and IGF-1 secretion using octreotide LA.
-
The report of the successful use of octreotide for more than 16 years irrespective of age.
