Browse

You are looking at 1 - 10 of 109 items for :

  • Refine by Access: All content x
Clear All
Open access

Darran Mc Donald, Tara Mc Donnell, Rachel Katherine Crowley, and Elizabeth Brosnan

Summary

Hyponatraemia is the most common electrolyte disturbance in hospitalised patients and is associated with numerous adverse outcomes. Patients with schizophrenia are particularly susceptible to hyponatraemia, in part due to the close association between this condition and primary polydipsia. We report the case of a 57-year-old woman with schizophrenia and primary polydipsia who was receiving inpatient psychiatric care. She became increasingly confused, had multiple episodes of vomiting, and collapsed 1 week after being commenced on quetiapine 300 mg. On examination, she was hypertensive and her Glasgow coma scale was nine. She had a fixed gaze palsy and a rigid, flexed posture. Investigations revealed extreme hyponatraemia with a serum sodium of 97 mmol/L. A CT brain demonstrated diffused cerebral oedema with sulcal and ventricular effacement. A urine sodium and serum osmolality were consistent with SIAD, which was stimulated by the introduction of quetiapine. The antidiuretic effect of vasopressin limited the kidney’s ability to excrete free water in response to the patients' excessive water intake, resulting in extreme, dilutional hyponatraemia. The patient was treated with two 100 mL boluses of hypertonic 3% saline but deteriorated further and required intubation. She had a complicated ICU course but went on to make a full neurological recovery. This is one of the lowest sodium levels attributed to primary polydipsia or second-generation antipsychotics reported in the literature.

Learning points

  • The combination of primary polydipsia and SIAD can lead to a life-threatening, extreme hyponatraemia.

  • SIAD is an uncommon side effect of second-generation anti-psychotics.

  • Serum sodium should be monitored in patients with primary polydipsia when commencing or adjusting psychotropic medications.

  • Symptomatic hyponatraemia is a medical emergency that requires treatment with boluses of hypertonic 3% saline.

  • A serum sodium of less than 105 mmol/L is associated with an increased risk of osmotic demyelination syndrome, therefore the correction should not exceed 8 mmol/L over 24 h.

Open access

Punith Kempegowda, Wentin Chen, Eka Melson, Annabelle Leong, Prashant Amrelia, and Ateeq Syed

Summary

A 37-year-old female of South Asian origin was referred to our diabetes clinic for evaluation of an unusual finding during her retinal screening. Her retinal blood vessels appeared white in contrast to the normal pink-red colour. She had type I hyperlipidaemia, confirmed by genotype, and was recently diagnosed with diabetes, secondary to pancreatic insufficiency, for which she had suboptimal control and multiple hospitalisations with recurrent pancreatitis. On examination, she had multiple naevi on her skin; the rest of the examination was unremarkable. The patient did not report any visual disturbances and had intact visual acuity. Investigations showed raised total cholesterol (12.5 mmol/L) and triglycerides (57.7 mmol/L). Following evaluation, the patient was diagnosed with lipaemia retinalis, secondary to type I hyperlipidaemia. The patient was managed conservatively to reduce the cholesterol and triglyceride burdens. However, therapies with orlistat, statin, fibrates and cholestyramine failed. Only a prudent diet, omega-3 fish oil, medium-chain triglycerides oil and glycaemic control optimised with insulin showed some improvements in her lipid profile. Unfortunately, this led her to becoming fat-soluble vitamin deficient; hence, she was treated with appropriate supplementation. She was also recently started on treatment with volanesorsen. Following this, her lipid parameters improved and lipaemia retinalis resolved.

Learning points

  • Lipaemia retinalis is an uncommon incidental finding of type I hyperlipidaemia that may not affect vision.

  • Management of associated dyslipidaemia is challenging with minimal response to conventional treatment.

  • Increased awareness of lipaemia retinalis and specialist management is needed as part of regular patient monitoring and personalised management.

Open access

Gabriele Costanzo, Salvatore Curatolo, Barbara Busà, Antonino Belfiore, and Damiano Gullo

Summary

Semaglutide is a glucagon-like peptide 1 (GLP-1) receptor agonist, approved for the treatment of type 2 diabetes mellitus (T2DM). GLP-1 analogs exert several biological activities connected not only with an insulinotropic effect but also with immunoregulation and reduction of inflammation. A 73-year-old male patient with class III obesity was referred to us for T2DM, which was not controlled with metformin therapy. He had suffered from plaque psoriasis for some years and was treated with topical therapy and adalimumab, without success. The psoriasis area and severity index (PASI) was 33.2 (indicating severe psoriasis), and the dermatology life quality index (DLQI) was 26.0 (indicating an extremely negative effect on the patient's life). Semaglutide (starting with 0.25 mg/week for 4 weeks, increased to 0.50 mg/week for 12 weeks, and then to 1 mg/week) was added to metformin. After 4 months, glycemic parameters had improved, and his body weight decreased. Unexpectedly, skin lesions of plaque psoriasis improved. PASI decreased by 19% compared with baseline and quality of life, assessed with the DLQI, markedly ameliorated. After 10 months, glycemic and obesity parameters, as well as psoriasis, improved further. HbA1c, BMI, and PASI were reduced by 32, 16.3, and 92%, respectively, compared with the baseline. DLQI declined to 0, meaning there was no effect of plaque psoriasis on the patient’s life.

Learning points

  • Psoriasis in patients with type 2 diabetes is often resistant to therapy.

  • We observed an obese patient with type 2 diabetes mellitus who achieved glycemic control and weight loss with the addition of semaglutide to metformin and had a relevant and long-lasting improvement of plaque psoriasis, which was previously resistant to biologic therapy.

  • Therapy with semaglutide may be attempted in eligible patients with difficult to treat plaque psoriasis.

Open access

Milad Darrat, Brian Gilmartin, Carmel Kennedy, and Diarmuid Smith

Summary

Acute respiratory distress syndrome (ARDS) is a rare but life-threatening complication of diabetic ketoacidosis (DKA). We present the case of a young female, with no previous diagnosis of diabetes, presenting in DKA complicated by ARDS requiring extra corporeal membrane oxygenation (ECMO) ventilator support. This case report highlights the importance of early recognition of respiratory complications of severe DKA and their appropriate management.

Learning points

  • ARDS is a very rare but life-threatening complication in DKA.

  • The incidence of ARDS remains unknown but less frequent than cerebral oedema in DKA.

  • The mechanism of ARDS in DKA has multifactorial aetiology, including genetic predisposition.

  • Early recognition and consideration of rare pulmonary complication of DKA can increase survival rate and provide very satisfactory outcomes.

  • DKA patients who present with refractory ARDS can be successfully rescued by ECMO support.

Open access

Ulla Kampmann, Per Glud Ovesen, Niels Møller, and Jens Fuglsang

Summary

During pregnancy, maternal tissues become increasingly insensitive to insulin in order to liberate nutritional supply to the growing fetus, but occasionally insulin resistance in pregnancy becomes severe and the treatment challenging. We report a rare and clinically difficult case of extreme insulin resistance with daily insulin requirements of 1420 IU/day during pregnancy in an obese 36-year-old woman with type 2 diabetes (T2D) and polycystic ovary syndrome (PCOS). The woman was referred to the outpatient clinic at gestational week 12 + 2 with a hemoglobin A1c (HbA1c) at 59 mmol/mol. Insulin treatment was initiated immediately using Novomix 30, and the doses were progressively increased, peaking at 1420 units/day at week 34 + 4. At week 35 + 0, there was an abrupt fall in insulin requirements, but with no signs of placental insufficiency. At week 36 + 1 a, healthy baby with no hypoglycemia was delivered by cesarean section. Blood samples were taken late in pregnancy to search for causes of extreme insulin resistance and showed high levels of C-peptide, proinsulin, insulin-like growth factor (IGF-1), mannan-binding-lectin (MBL) and leptin. CRP was mildly elevated, but otherwise, levels of inflammatory markers were normal. Insulin antibodies were undetectable, and no mutations in the insulin receptor (INSR) gene were found. The explanation for the severe insulin resistance, in this case, can be ascribed to PCOS, obesity, profound weight gain, hyperleptinemia and inactivity. This is the first case of extreme insulin resistance during pregnancy, with insulin requirements close to 1500 IU/day with a successful outcome, illustrating the importance of a close interdisciplinary collaboration between patient, obstetricians and endocrinologists.

Learning points

  • This is the first case of extreme insulin resistance during pregnancy, with insulin requirements of up to 1420 IU/day with a successful outcome without significant fetal macrosomia and hypoglycemia.

  • Obesity, PCOS, T2D and high levels of leptin and IGF-1 are predictors of severe insulin resistance in pregnancy.

  • A close collaboration between patient, obstetricians and endocrinologists is crucial for tailoring the best possible treatment for pregnant women with diabetes, beneficial for both the mother and her child.

Open access

Wann Jia Loh, Lily Mae Dacay, Clara Si Hua Tan, Su Fen Ang, Fabian Yap, Su Chi Lim, and Joan Khoo

Summary

Activating mutation of glucokinase gene (GCK) causes resetting of insulin inhibition at a lower glucose threshold causing hyperinsulinaemic hypoglycaemia (GCK-HH). This is the first reported case who tolerated years of regular fasting during Ramadhan, presenting only with seizure and syncope now. We describe a case with GCK gene variant p.T65I diagnosed in a 51-year-old woman with hypoglycaemia unawareness even at glucose level of 1.6 mmol/L. Insulin and C-peptide levels during hypoglycaemia were suggestive of hyperinsulinism, but at a day after intravenous glucagon, hypoglycaemia occurred with low insulin and C-peptide levels, pointing against insulinoma as the underlying aetiology. Imaging studies of the pancreas and calcium arterial stimulation venous sampling were unremarkable. A review of old medical records revealed asymptomatic hypoglycaemia years ago. Genetic testing confirmed activating mutation of GCK. Hypoglycaemia was successfully controlled with a somatostatin analogue. This case highlights the importance of consideration of genetic causes of hypoglycaemia in adulthood, especially when imaging is uninformative.

Learning points

  • Consider genetic causes of endogenous hyperinsulinism hypoglycaemia in adulthood, especially when imaging is uninformative.

  • Late presentation of activating mutation of GCK can occur because of hypoglycaemia unawareness.

  • Long-acting somatostatin analogue may be useful for the treatment of activating mutation of GCK causing hypoglycaemia.

  • Depending on the glucose level when the blood was taken, and the threshold of glucose-stimulated insulin release (GSIR), the serum insulin and C-peptide levels may be raised (hyperinsulinaemic) or low (hypoinsulinaemic) in patients with activating mutation of GCK.

  • Glucagon may be useful to hasten the process of unmasking the low insulin level during hypoglycaemia below the GSIR level of which insulin released is suppressed.

Open access

Rajiv Singh and Cynthia Mohandas

Summary

A phaeochromocytoma is a rare neuroendocrine tumour derived from the chromaffin cells of the adrenal medulla. Tumours can produce excessive amounts of catecholamines. The presenting symptoms can vary but often include the classic triad of episodic headaches, sweating and palpitations. Due to catecholamine excess, patients can develop cardiomyopathy. Bradycardia and collapse could be the result of sinus node dysfunction or transient dysregulation of the autonomic nervous system. Patients with co-existing diabetes can have improvement or resolution of their diabetes after successful adrenalectomy. We report a case of an 87-year-old lady who initially presented with sweating, palpitations and collapse, resulting in a permanent pacemaker insertion. She was later found to have a large adrenal incidentaloma with subsequent markedly elevated plasma metanephrine levels. She later presented with chest pain and in acute pulmonary oedema with normal coronary arteries visualised on coronary angiogram. After surgical excision of her phaeochromocytoma, her diabetes resolved with her HbA1c improving from 68 to 46 mmol/mol, with no further requirement for diabetic medications. Her pulmonary oedema improved with no ongoing need for diuretic therapy. This case highlights that phaeochromocytomas can affect multiple systems and there should be a very high index of suspicion in patients presenting with sweating, palpitations, hypertension and a history of diabetes and even in those with collapse.

Learning points

  • There should be a high index of suspicion for phaeochromocytomas in patients with palpitations, diaphoresis, anxiety, hypertension and diabetes.

  • Rarely phaeochromocytomas can present as bradycardia and collapse due to sinus node dysfunction or transient autonomic dysregulation and that should be considered in older patients.

  • Catecholamine cardiomyopathy can occur in phaeochromocytoma with potential resolution after successful surgical excision.

  • Diabetes can resolve after successful surgical treatment of a phaeochromocytoma.

Open access

Antonella Corcillo, Zoe Kleinaki, Stella Kapnisi, Nikolaos Fountoulakis, Giuseppe Maltese, Stephen M Thomas, and Janaka Karalliedde

Summary

A 26-year-old Caucasian female with no past medical history or family history of auto-immune disease presented to the emergency department with new onset painless left foot drop. A panel of blood tests revealed blood glucose of 49.9 mmol/L and raised blood ketone levels. The patient was referred to the diabetes team who made a clinical diagnosis of type 1 diabetes (T1DM) and insulin treatment was initiated. Elevated levels of diabetes auto-antibodies were subsequently detected. Nerve conduction studies demonstrated a left common peroneal nerve lesion with conduction block at the fibular head. After 2 weeks of insulin treatment, a significant improvement of her foot drop was observed and after 8 weeks she was walking normally. The most probable cause of her foot drop was acute diabetic mononeuropathy. To our knowledge, there are no similar cases in adult patients reported in the literature. Our case highlights the importance of physicians being aware of atypical presentation of new onset T1DM.

Learning points:

  • There is an increasing incidence of T1DM with more than half of patients presenting after the age of 20.

  • Diabetic peripheral neuropathy can present both acutely and as a mononeuropathy.

  • Although rare, clinicians should be aware of mononeuropathy as a presenting symptom of T1DM to avoid delay in the treatment initiation.

  • This case highlights an unusual presentation of T1DM and illustrates the importance of the early diagnosis and management of T1DM.

Open access

Anthony Ramos-Yataco, Kelly Meza, Reyna Cecilia Farfán-García, Solange Ortega-Rojas, Isaac Salinas-Mamani, Ivonne Silva-Arrieta Ontaneda, and Ricardo Correa

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.

Open access

Shunsuke Shimazaki, Itsuro Kazukawa, Kyoko Mori, Makiko Kihara, and Masanori Minagawa

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.