Concomitant hemorrhagic fever with renal syndrome and COVID-19.

Udmurt Republic is an endemic region for hemorrhagic fever with renal syndrome (HFRS). An extremely high incidence of COVID-19 in 2020-2021 worldwide and in Udmurt Republic in particular suggests that patients might bear these two infections simultaneously. In this article, we report a case of mixed COVID-19 plus HFRS infection. Specific clinical manifestations of HFRS in a COVID-19-coinfected patient included long-term fatigue, thrombocytopenia, iso(hypo)sthenuria, polyuria, episodes of sinus tachycardia and hypertension. On the other hand, the main clinical characteristics of COVID-19 in a HFRS-coinfected patient included no clinical signs of respiratory failure and relatively high saturation despite a substantial lung damage. In general, mixed infection is a risk factor that aggravates the disease and can worsen outcome. However, simultaneous infection of a cell with more than one virus probably causes viral interference, which results in suppression of one or both viruses.Copyright © 2023, Dynasty Publishing House. All rights reserved.

Diabetic Ketoacidosis in Children Before and During COVID-19 Pandemic: A Cross-sectional Study

Background: Coronavirus disease 2019 (COVID-19) has spread quickly. Comorbidities, such as diabetes, have been determined as critical risk factors for COVID-19. Objective(s): This study aimed to determine the frequency and severity of diabetic ketoacidosis (DKA) in children before and during the COVID-19 pandemic. Method(s): This retrospective study examined children aged less than 18 years diagnosed with DKA hospitalized in Yazd Shahid Sadoughi Hospital from February 20, 2020, to November 21, 2021. The collected information was compared to those obtained during the same period in 2019 (pre-pandemic). According to the inclusion criteria, only children with suspected symptoms of COVID-19 or an infected family member underwent PCR. Result(s): The study included 70 children with confirmed DKA during the COVID-19 pandemic and 33 children hospitalized during the pre-pandemic period. The findings showed that the rate of DKA was higher during the pandemic than in the pre-pandemic period. In the DKA subgroups (during the COVID-19 pandemic vs. pre-pandemic), 35.7% vs. 21.2% were severe, 37.1% vs. 36.4% were moderate, and 27.1% vs. 42.4% were mild. Of 70 children, 30 underwent PCR tests for COVID-19, showing six positive cases. Among positive cases, five had mild symptoms, while one was hospitalized with signs of respiratory distress, polyuria, and polydipsia. All physical examinations of this patient were normal, except for the chest exam. Conclusion(s): A remarkable increase was observed in the frequency and severity of DKA in children during the pandemic.Copyright © 2023, International Journal of Endocrinology and Metabolism. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

New Onset Diabetes and Acute Pancreatitis- A Sequela of Long COVID?

Introduction: The association between worse COVID-19 outcomes and diabetes has been well-established in the literature. However, with more cases of new-onset diabetes and pancreatitis being reported with or after COVID-19 infection, it poses the question if there is a causal relationship between them. Case Description: 31 y/o female with COVID-19 infection 4-6 weeks ago with moderate symptoms (not requiring hospital admission or monoclonal ab), presented to ED with bandlike epigastric pain radiating to back, which is worsened with food, associated with nausea, vomiting, polyuria, and fatigue. Workup showed lipase 232, AST 180, ALT 256. Blood glucose was 281 and HbA1c was 12. CT A/P showed post cholecystectomy status, normal pancreas with mesenteric adenitis. MRCP showed hepatic steatosis with trace fluid around the pancreas s/o inflammation, and no evidence of choledocholithiasis or biliary dilatation. She denied alcohol use and autoimmune workup for pancreatitis was unremarkable. Islet cell antibodies were negative. The patient improved with fluid resuscitation and was discharged home on insulin with plans to transition to oral agents outpatient. Discussion(s): Long COVID is defined as a range of conditions or symptoms in patients recovering from COVID-19, lasting beyond 4 weeks after infection. A retrospective cohort study showed increased new-onset diabetes incidence in patients after COVID-19. This was redemonstrated in a systematic review and meta-analysis that showed a 14.4% increased proportion of new diagnoses of diabetes in patients hospitalized with COVID-19. Possible pathophysiology that have been attributed to this include undiagnosed pre-existing diabetes, hyperglycemia secondary to acute illness and stress from increased inflammatory markers during the cytokine storm, the effect of viral infections on the pancreas, and concurrent steroid use in patients with severe respiratory disease. The binding of SARS-CoV-2 to ACE2 receptors is thought to the other mechanism by which COVID can cause pancreatitis and hyperglycemia. Study showed increased lipase and amylase levels in patients with COVID and the increase in serum levels was proportional to the severity of the disease. Patients who died due to COVID-19 were also found to have degeneration of the islet cells. While, several studies have showed new onset diabetes and pancreatitis during an active COVID infections, we need larger cohort studies to comment on its true association or causation, especially in patients with long COVID symptoms. As more cases of new onset diabetes and pancreatitis with COVID-19 are being reported, there may be a need for more frequent blood sugar monitoring during the recovery phase of COVID-19.Copyright © 2023

New Onset of Type 1 Diabetes After Severe Acute Respiratory Syndrome Coronavirus 2 Vaccination

Introduction: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) poses the greatest threat of our times. SARS-CoV-2 vaccines are one of the most effective strategies against this infection. Diabetic ketoacidosis, hyperglycemic hyperosmolar syndrome, and new-onset diabetes as adverse effects of SARS-CoV-2 vaccination have been infrequently described in the literature. We hereby report a rare case of new-onset type 1 diabetes after SARS-CoV-2 vaccination. Case Description: An 18-year-old male presented to the outpatient office for evaluation of breast pain. On routine laboratory tests, he was noted to have fasting blood glucose of 200 mg/dL. On further questioning, he reported some polyuria, nocturia, and a 10-pound weight loss over the preceding month. He received the initial dose of Pfizer-BioNTech SARS-CoV-2 vaccine in May 2022 and the second dose in June 2022, approximately one month before the onset of symptoms. He denied any earlier viral infections and had no personal or family history of autoimmune conditions. On evaluation, his body mass index was 20 kg/m2, but otherwise, he had a normal physical exam, including a breast exam. Over the next few days, his blood glucose progressively increased to over 300 mg/dl. HbA1c was noted to be elevated at 8.6%, glutamic acid decarboxylase-65 (GAD-65) antibodies were remarkably high >250 IU/ml (normal 5 IU/ml), C-peptide was 1.51 ng/ml (normal 0.80 - 3.85 ng/ml), blood glucose 156 mg/dl, islet-cell antibody titer was 320 (< 1.25 JDF units) and insulin autoantibodies were negative. He was diagnosed with autoimmune Type 1 diabetes and a basal-bolus insulin regimen was initiated to improve glycemic control. On a one-month follow-up, his insulin requirements remained low but persistent and his glycemic control was acceptable. Discussion(s): Various viruses are known to play a fundamental role in the onset of type 1 diabetes via a variety of effects on pancreatic beta-cells because of either the direct lytic effects of viral replication or the inflammatory response to the virus, which is mediated by autoreactive T cells. The limited release of islet cell antigens induces molecular mimicry and paves the way for long-term autoimmunity and the development of type 1 diabetes mellitus. Our patient did not report any viral illnesses before the onset of his symptoms. He also did not have a family or personal history of autoimmune diseases. His onset of diabetic symptoms coincided temporally with receiving the SARS-CoV-2 vaccine. The detection of a considerable titer of GAD-65 antibodies proved autoimmunity. Clinicians must stay vigilant about this potential side effect of SARS-CoV2 vaccine so that a timely diagnosis can be made.Copyright © 2023

Massive polyuria associated with severe COVID-19-related pneumonia complicated by pulmonary embolism

Coronavirus disease 2019 (COVID-19) predominantly manifests with signs of respiratory system injury;however, multi-systemic manifestations may occur. Renal pathology develops in up to 80% of patients with COVID-19. The aim of the study was to describe the case of isolated massive polyuria of unknown etiology in the patient with severe COVID-19-related pneumonia complicated by pulmonary embolism (PE). A 54-year-old male with bilateral pneumonia, related to COVID-19, developed PE. The next day after successful thrombolysis with alteplase (90 mg) the diuresis of the patient began to increase and fluctuated between 5000 mL and 8000 mL. The diuresis returned to normal ranges two weeks after PE episode. The rise of the diuresis was not accompanied by electrolyte disorders and elevation of serum creatinine. Changes in the urine tests were minimal, only once the urine protein was detected (0.25 g/L). The highest urine excretion was observed in evening hours (16.00-24.00). Chest CT on the day 14 after the patient's admission revealed 90% of lung tissue injury, cranial CT showed no brain abnormalities, including hypothalamus and pituitary gland. The patient's condition met neither diagnostic criteria of acute kidney injury, nor acute interstitial nephritis, nor pituitary gland damage. The course of the polyuria in the presented case was benign (self-limiting, no blood electrolyte abnormalities, compensated by oral rehydration only). Polyuria in patients with COVID-19 may not be a life-threatening condition that does not require active treatment.Copyright © 2021 EDIZIONI MINERVA MEDICA.

An Overview About Pediatric Type 1 Diabetes Mellitus

Background: Diabetes mellitus (DM) represents one of the most common metabolic diseases in the world, with rising prevalence in recent decades. Most cases are generally classified into two major pathophysiological categories: type 1 diabetes mellitus (DM1), which progresses with absolute insulin deficiency and can be identified by genetic and pancreatic islet autoimmunity markers, and type 2 diabetes mellitus (DM2), which is the most prevalent form and involves a combination of resistance to the action of insulin with an insufficient compensatory response of insulin secretion. In the last two decades, in parallel with the increase in childhood obesity, there has also been an increase in the incidence of DM2 in young people in some populations. Other forms of diabetes may affect children and adolescents, such as monogenic diabetes (neonatal diabetes, MODY – maturity onset diabetes of the young, mitochondrial diabetes, and lipoatrophic diabetes), diabetes secondary to other pancreatic diseases, endocrinopathies, infections and cytotoxic drugs, and diabetes related to certain genetic syndromes, which may involve different treatments and prognoses. DM1 is considered an immuno-mediated disease that develops as a result of gradual destruction of insulin-producing pancreatic beta cells that eventually results in their total loss and complete dependence on exogenous insulin. Clinical presentation can occur at any age, but most patients will be diagnosed before the age of 30 years

A rare case of central diabetes insipidus unmasked after renal transplantation in a young male

Background: The diagnosis of central Diabetes insipidus (DI) requires intact renal function to manifest polyuria. Therefore, it may not become evident in patients with oliguric or anuric renal failure such as in chronic kidney disease (CKD) or end stage renal disease (ESRD). This might get manifested after renal transplantation, however there are only 5 cases reported so far of Central DI post renal transplantation. Here we report a case of central DI that was unmasked in a patient with CKD after kidney transplantation leading to polyuria. Case Report: RV, 26-year-old male had one episode of febrile illness with hematuria at age of 20 years and was diagnosed IgA nephropathy by renal biopsy following which he recovered completely. Hypertension was detected in Feb 2021, and he has been on Cilnidipine 10 mg OD, Clonidine 0.1 mg TDS, Metoprolol XL 40 mg OD. At age of 25 years, he had covid illness and his kidney function deteriorated to ESRD for which he was started on twice weekly hemodialysis for 8 months and then underwent live donor renal transplantation in October 2021. Two months later, he was admitted for polyuria, polydipsia, and nocturia. After renal transplantation, his urine volume increased to 9-10 L/ d, while it had been less than 500 mL/day before the transplantation. His serum creatinine level improved from 3.2 mg/dL prior to transplant to 0.8 mg/dL after transplant. He had not been diagnosed with diabetes before, and his blood glucose levels were within the normal range. He showed no symptoms of polyuria or polydipsia before transplantation and had no history of head trauma or neurosurgery. Diagnosed to have primary hypothyroidism in Feb 2021 during pre-transplant workup, for which he was started on levothyroxine 50 ug and was euthyroid. The patient received prednisolone, tacrolimus, mycophenolate mofetil, and sulfamethoxazole/trimethoprim after the transplantation. During evaluation for polyuria, urine volume was >100 ml/kg in 24 Hour. Serum osmolality of 295 mOsm/kg, urine osmolality of 101 mOsm/kg, and serum sodium of 138 mEq/L, RBS 86 mg/dl, Urea 24 mg/dl. Anterior pituitary hormone profile workup was normal. To evaluate the cause of polyuria, water deprivation test was performed which confirmed complete central diabetes insipidus. He was started on oral desmopressin 120 ug in divided doses. His urine output subsequently decreased to about 2.5 L/d with resolution of excessive thirst and nocturia. MRI sella revealed normal anterior pituitary, infundibulum and diminished posterior pituitary bright spot in the T1-weighted image. Patient is continued on desmopressin therapy at 6 months with marked improvement in symptoms. Conclusion: In this case, the water deprivation test and diminished posterior pituitary bright spot-on MRI and the responsiveness to desmopressin therapy confirm the diagnosis of central DI. Hence, any case of polyuria after renal transplantation must be evaluated for Central Diabetes Insipidus.

Transient diabetes insipidus in critically ill COVID19 patients.

PURPOSE: Vasopressin has become an important vasopressor drug while treating a critically ill patient to maintain adequate mean arterial pressure. Diabetes insipidus (DI) is a rare syndrome characterized by the excretion of a large volume of diluted urine, inappropriate for water homeostasis. We noticed that several COVID19 patients developed excessive polyuria suggestive of DI, with a concomitant plasma sodium-level increase and/or low urine osmolality. We noticed a temporal relationship between vasopressin treatment cessation and polyuria periods. We reviewed those cases to better describe this phenomenon. METHODS: We retrospectively collected COVID19 ECMO patients' (from July 6, 2020, to November 30, 2021) data from the electronic medical records. By examining urine output, urine osmolality (if applicable), plasma sodium level, and plasma osmolality, we set DI diagnosis. We described the clinical course of DI episodes and compared baseline characteristics between patients who developed DI and those who did not. RESULTS: Out of 37 patients, 12 had 18 episodes of DI. These patients were 7 years younger and had lower severity scores (APACHE-II and SOFA). Mortality difference was not seen between groups. 17 episodes occurred after vasopressin discontinuation; 14 episodes were treated with vasopressin reinstitution. DI lasted for a median of 21 h, with a median increase of 14 mEq/L of sodium. CONCLUSIONS: Temporary DI prevalence after vasopressin discontinuation in COVID19 ECMO patients might be higher than previously described for vasopressin-treated patients.

Socio-economic Barriers to Care and Medical Complexity Leading to a 5-year Diagnostic Delay of Untreated Chronic Diabetes Insipidus and Rapidly Progressive Puberty in a 10-year-old Venezuelan Immigrant

Introduction: Germ cell tumors, including germinomas, account for 10% of pediatric chronic Diabetes Insipidus (DI) cases. Delays in diagnosis of germinomas are generally longer than six months, however, no reported cases of suprasellar germinomas causing chronic DI and precocious puberty have been known to exceed a 5-year delay in both treatment of DI symptoms and a definitive diagnosis. Case Description: A 10-year-old Hispanic male presented with a 5-year history of polydipsia and polyuria. He underwent evaluation in Venezuela, where DI was reportedly 'ruled out';however, no head MRI was performed. After two years in the US struggling to acquire insurance, he presented to his pediatrician with worsening symptoms. A head MRI, ordered to evaluate dilute high-volume urine output, revealed a suprasellar mass. He was admitted for diagnostic evaluation and met the criteria for DI. Notably, he had an elevated Beta-Human Chorionic Gonadotropin (B-HCG) level. Biopsy confirmed the diagnosis of a Central Nervous System (CNS) germinoma. He was treated with DDAVP and proton therapy with subsequent remission of his tumor. Discussion: Throughout the patient's disease course, there were multiple delays in seeking and receiving care. These include a 5-year delay in seeking care despite worsening symptoms, a one-month delay in completing a 24-hour urine collection, a one-month delay in consulting pediatric nephrology, and another month delay before completing a retroperitoneal ultrasound. Multiple medical and socio-economic factors led to these delays. The patient did not present with symptoms more typical of CNS Germinomas like headaches, nausea, and vomiting. He had no visual disturbances despite mass effect on his optic chiasm. His increased stretched penis length and Tanner staging, which were identified later in his disease course, were contradicted by his pre-pubertal testicular volume and bone age. The patient is from a Spanishspeaking/Limited English Proficiency (SSLEP) household. While Spanish interpreters were present at each appointment, the language barrier proved to be a consistent issue. Initially, the child's mother indicated that the diagnosis of DI was 'ruled out' in Venezuela. In reality, the recommended imaging was never performed. Mychart messages left by his father further highlighted communication difficulties. Without access to an interpreter, he was forced to use broken English to relay his concerns. These frantic messages indicated misunderstandings regarding scheduling with various services and completing vital labs. Care only proceeded after significant physician intervention. Poverty in Venezuela, lack of insurance, and anxiety regarding COVID-19 also contributed to these delays. Conclusion: To our knowledge, this is the first case report of a pediatric patient presenting with a 5-year history of untreated polyuria and polydipsia due to undiagnosed DI with a B-HCG secreting CNS germinoma, without spinal metastasis. This study also illustrates the importance of supporting SSLEP families as they grapple with the complicated process of navigating our healthcare system. Sagittal T1 post gadolinium contrast image (A) and axial T2 FLAIR image (B) show an enigmatic, homogeneous, briskly enhancing mass in the suprasellar cistern (red arrow) with mass effect on the optic chiasm which is displaced upward and anteriorly (green arrow).

An Unusual Case of Autoantibody-Negative KetosisProne Diabetes (KPD) Secondary to Marked Insulin Resistance

KPD is classically regarded as an atypical form of diabetes caused by near-complete beta-cell failure. A 37-year-old Egyptian man (BMI: 27.7 Kg/m2) presented with hyperglycemia (362 mg/dL) and DKA (arterial pH 7.20, ketonemia 5.0 mmol/L, ketonuria 80 mg/dL) . He was afebrile, with recent polyuria, polydipsia and weight loss. HbA1c was 107 mmol/mol (11.9%) and blood tests excluded diabetes secondary to endocrinopathies. SARS-CoV-2 RT-PCR test was negative. IV insulin infusion (0.1 IU/kg/h) and IV fluid therapy were started. He was shortly transitioned to a sc basal-bolus insulin regimen (0.7 IU/kg/day) . Mixed-meal tolerance test (MMTT) revealed a peak 120-min stimulated C-peptide of 12.3 ng/mL, suggesting marked insulin resistance. Islet autoantibodies (ICA, IAA, GADA, IA-2A, ZnT8A) and insulin receptor autoantibodies (IgG/IgM) were negative. HLA genotyping detected the following haplotypes: DRB1∗01, ∗04;DQA1∗01:01P, ∗03:01P;DQB1∗03:02P, ∗05:01P. Insulin dose was gradually reduced and insulin therapy was discontinued after 4 months in favor of metformin (2550 mg/day) plus sc semaglutide (up to 1 mg/week) . After one year, MMTT revealed a peak 60-min stimulated C-peptide of 8.25 ng/mL. During the 18-month follow-up period, fasting capillary beta-hydroxybutyrate values were <0.2 mmol/L and HbA1c remained <48 mmol/mol (<6.5%) , indicating disease remission. This case suggests the existence of an autoantibody-negative KPD subtype driven by marked insulin resistance rather than by insulinopenia.

A Fatal Case of Intraparenchymal Hemorrhage Masquerading as Central Diabetes Insipidus

This is 32-year-old women presented to us on postpartum day 10 with severe covid-19 pneumonia. Hercomplaints were dyspnea and headache which she described as, frontally located, 8/10 in intensity, non-radiating and not associated with any posture. She had no prior history of migraines. She was afebrile, tachycardiac and hypoxic on exam. Physical examination was unremarkable. Patient failed trial of non-invasive ventilation following which she was intubated. CT head on admission was unremarkable.For COVID 19 ARDS, she was started on dexamethasone, tocilizumab, paralysis was achieved withcisatracurium and prone protocol was followed for refractory hypoxia. Patient was placed on DVTprophylaxis with heparin. Her pneumonia and oxygenation improved. However, on hospital day 8, herlab results were suspicious of Diabetes insipidus (DI). Her serum sodium was 152mEq/L with serumosmolarity of 360 and polyuria (more than 2L of urine in one hour). A full neurological examinationcould not be obtained as she was paralyzed, however, pupils were equal in size and reactive to light. With high clinical suspicions of diabetes insipidus she received a one-time dose of 16mcg of DDAVP andMRI of pituitary gland was ordered to delineate etiology. Subsequent improvement in polyuria wasnoted. Despite DDAVP her serum sodium continued to worsen. We continued to monitor serumsodium levels every four hours. Her serum sodium levels remained labile with a precipitous drop notedfrom 174mEq/L to 152mEq/L. Review of Pituitary MRI revealed multiple intraparenchymal hemorrhageson bilateral frontal lobes along with trans tentorial and cerebellar tonsillar herniation. Subsequently, patient underwent a brain death exam and declared brain dead. We suspect the development of intracranial hemorrhage in our patient was secondary to covid-19. Onliterature review, an incidence of 0.2% in covid-19 patients with a mortality of 48% is reported. In ourpatient, inability to perform a full neurological exam due to paralysis limited early recognition andintervention. This case highlights the need for increased awareness in patients with features of central diabetesinsipidus and the urgency to obtain CT head immediately after a diagnosis has been established. Promptconsideration of neuroimaging should be made when features of central diabetes mellitus are noted with limited neurological exam.

Severe hypernatremia in soft drink ketoacidosis and hyperglycemic hyperosmolar state at the onset of type 2 diabetes mellitus: a case series of three adolescents

Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are diabetic emergencies. Some patients with a hyperglycemic crisis can present with an overlap of DKA and HHS. The coexistence of DKA and HHS is associated with higher mortality than in isolated DKA and HHS. In addition, electrolyte derangements caused by global electrolyte imbalance are associated with potentially life-threatening complications. Here, we describe three cases of mixed DKA and HHS with severe hypernatremia at the onset of type 2 diabetes mellitus. All patients had extreme hyperglycemia and hyperosmolarity with acidosis at the onset of diabetes mellitus. They consumed 2 to 3 L/d of high-carbohydrate drinks prior to admission to relieve thirst. They showed severe hypernatremia with renal impairment. Two patients recovered completely without any complications, while one died. Severe hypernatremia with mixed DKA and HHS is rare. However, it may be associated with excess carbohydrate beverage consumption. Reduced physical activity during the COVID19 pandemic and unhealthy eating behaviors worsened the initial presentation of diabetes mellitus. We highlight the impact of lifestyle factors on mixed DKA and HHS.

Diabetes Insipidus in Severe COVID-19 Pneumonia

Coronavirus disease 2019 (COVID-19) usually presents as a respiratory infection, and may progress to multiple organ failure and eventually death. In COVID-19 patients, kidney dysfunctions reported proteinuria, elevated markers of blood urea nitrogen, plasma creatinine, uric acids, and D-dimer. We present here the case of a 49-year-old male who was admitted to the intensive care unit (ICU) with COVID-19 pneumonia and respiratory failure. Diabetes insipidus (DI) developed during intensive care follow-up without electrolyte imbalance or kidney failure. A contrast-enhanced brain and pituitary MRI was performed to identify the etiology of the central DI, but revealed no pathological findings. The drugs used to treat our patient had no polyuria side effects. No electrolyte imbalance was identified from a blood test of our patient, and there were no findings of other diseases in the differential diagnosis that could lead to nephrogenic DI. We present here a case of COVID-19 infection complicated by nephrogenic diabetes insipidus, given the lack of reports in literature indicating the occurrence of diabetes insipidus alongside COVID-19 infection.

P.0680 Hypernatremia secondary to kidney injury after long-term lithium therapy during COIVD-19 pandemic

Introduction: As bipolar disorder often requires long-term lithium treatment, assessment of adverse effects is critical. Long-term treatment with lithium induces functional and / or structural disturbances in the kidneys. Nephrogenic diabetes insipidus (NDI) occurs in up to 40% of lithium users and leads to a 2-3 times increased risk of chronic kidney disease. Polyuria-associated fluid imbalances and NDI, increase the risk of hypernatremia. Without appropriate and quick treatments, hypernatremia can easily lead to life-threatening consequences. A major adverse effect, hypernatremia secondary to kidney injury induced by lithium should not be misdiagnosed. We report cases of three patients with mood disorders treated with long-term lithium therapy. They presented to our hospital during the state of emergency declared by the Japanese government in response to curb the coronavirus disease (COVID-19) pandemic. They showed hypernatremia and disturbance of consciousness. All three patients had been taking lithium for more 10 years and had dehydration and / or renal damage on admission. The main cause of clinically significant hypernatremia is not drug-induced kidney injury after long-term lithium treatment, but lithium is one of the most common causes of acquired NDI. Case Report: Case 1 A 65-year-old man with a history of bipolar disorder and presented with polyurea, dehydration, and altered consciousness. He had been on lithium carbonate (800 mg twice daily) for over 20 years. Case 2 A 58-year-old woman with recurrent depressive disorder presented with high fever, drowsiness, spasms, and a highly serum creatine phosphokinase. She was admitted to the emergency department to rule out neuroleptic malignant syndrome. She was prescribed lithium carbonate (800 mg twice daily), but was not fully compliant with the treatment. Case 3 A 72-year-old-woman with bipolar disorder and history of hospitalizations at a mental-health rehabilitation institution presented with disturbance of consciousness and psychomotor retardation. She had been on lithium carbonate (400 mg twice daily) for 16 years. Oral dyskinesia and dysarthria were observed as were high fever and confusion. Of the three patients, one was a COVID-19 patient, while the others were not: however, all of them showed hypernatremia. A cohort study showed that infection, intoxication other than lithium, and dehydration were the main causes of hypernatremia. Lithium intoxications only accounted for 1% of all hypernatremia episodes. Probably the COVID-19 infection may directly cause hypernatremia, and dehydration may indirectly cause hypernatremia owing to a close ward, delirium, and physical restraint because they cannot complain about thirst. The COVID-19 pandemic affects the mental health of patients with bipolar disorder. Amounts of alcohol, soft drinks, and food can potentially trigger symptoms of kidney injury and diabetes. Conclusion: These patients with mood disorders after long-term lithium therapy must be carefully monitored their mental condition, including delirium, their complaints, and laboratory data to avoid overlooking severe conditions. [1,2]

Concomitant presence of COVID-19 infection and inaugural diabetic ketoacidosis in children and adolescents

Introduction: The COVID-19 pandemic, which has left its mark all over the world, has led to a decrease in the addressability to health care professionals, due to people's fear of becoming infected with COVID-19. This delays a correct diagnosis that can have lifethreatening consequences. Objectives: To establish if type 1 diabetes is triggered by COVID-19 Methods: We will present 3 cases pf type 1 diabetes at onset with ketoacidosis, triggered by the COVID-19 infection, diagnosed between December 2020 and April 2021. The diagnosis of SARSCoV2 infection was established based on RT-PCR (a reversetranscription polymerase-chain-reaction) positive for SARS-CoV2. Results: Case 1: 14 years old, boy, presented with Kussmaul breathing, abdominal pain, polyuria, polydipsia, weight loss (5 kg in 2 weeks), fever (38 C). The laboratory test showed a bicarbonate: 5 mEq/L, pH: 7.08, alkaline reserve: 6 mmol/l, glucose: 454 mg/dl, HbA1c: 14.5%. Case 2: 7 years old, boy presented with Kussmaul breathing, shock hypovolemic, hypotensive (Blood pressure 60/30 mmHg), fever, tachypnea, polyuria, polydipsia. The laboratory test showed a bicarbonate: 3 mEq/L, pH: 6,95, alkaline reserve: 2 mmol/l, glucose: 567 mg/dl, HbA1c: 12.6 %. Case 3: 10 years old, boy presented with similar clinical findings. The laboratory test showed a bicarbonate: 5 mEq/L, pH: 6,90, alkaline reserve: 3 mmol/l, glucose: 457 mg/dl, HbA1c: 16.6 %. All patients received treatment according to the diabetic ketoacidosis protocol treatment and switched to basal-bolus insulin treatment after an average of 48 hours. In all 3 cases the SARS-CoV2 infection was mild, with no changes in the lungs (lung x-rays being within normal limits). Conclusions: Due to the general fear of appearing in a hospital during the COVID-19 pandemic, there are delays in the diagnosis of lifethreatening conditions, such as ketoacidosis. The link between SARSCoV2 infection and type 1 diabetes in children and adolescents remains unknown and further studies are needed to gather more data.