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Cyclic vomiting syndrome (CVS) is a chronic digestive disorder characterized by recurrent episodes of severe nausea and vomiting. The perioperative management of patients with CVS undergoing general anesthesia is challenging, especially when combined with obesity. This case report describes the successful management of a patient with CVS and obesity who underwent dental surgery under general anesthesia. A 21-year-old woman with CVS, obesity (body mass index, 35), and intellectual disability was scheduled for tooth extraction and composite resin restoration under general anesthesia. The patient was diagnosed with CVS at the age of 20 years with frequent vomiting attacks requiring hospitalization. Surgery was scheduled during the CVS remission to reduce the risk of perioperative vomiting. Preoperative laboratory test results were normal, including serum adrenocorticotropic hormone (ACTH), anti-diuretic hormone (ADH), and cortisol levels. General anesthesia was induced using remifentanil and propofol. Nasal endotracheal intubation was performed after rocuronium administration. Local anesthesia (2% lidocaine with 1:80,000 epinephrine) was used for all dental procedures. Postoperatively, midazolam was administered to control agitation. No postoperative vomiting occurred. Serum ACTH, ADH, and cortisol levels showed no significant changes before and after anesthesia, suggesting that hypothalamic-pituitary-adrenal (HPA) axis activation due to surgical stress did not occur. This case highlights the importance of careful perioperative planning and monitoring stress-related hormone levels in patients with CVS or obesity. An anesthetic approach using midazolam may effectively suppress HPA axis activation and prevent postoperative vomiting.

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INTRODUCTION: Stimulated copeptin may provide an alternative to water deprivation testing (WDT) in the evaluation of polyuria-polydipsia syndrome (PPS). Though best studied, arginine stimulation alone produces a modest copeptin response in children. We investigated the effectiveness of the arginine + LevoDopa/Carbidopa stimulation test (ALD-ST) for copeptin. METHODS: 47 healthy short children (controls), 10 children with primary polydipsia, and 10 children with AVP deficiency received arginine hydrochloride (500 mg/kg intravenously over 30 min) and Levodopa/carbidopa (10:1 ratio; 175 mg of l-Dopa/m2 BSA) orally. Serum copeptin was measured at 0, 60, 90, and 120 min. RESULTS: In controls, ALD-ST increased copeptin from a median of 7.0 pmol/L (IQR 5.0-10.0) to a peak of 44.0 pmol/L (IQR 21.4-181.0) between 60 and 120 min (p < 0.001). Copeptin peak was higher in subjects who experienced nausea or vomiting (57%) than in those who did not (131.0 pmol/L [IQR 42.5-193.8] vs. 22.7 pmol/L [IQR 16.0-33.7], p < 0.001). While subjects with primary polydipsia had similar baseline (8.5 pmol/L [IQR 8.0-11.0]) and stimulated (125.2 pmol/L [IQR 87.6-174.0]) copeptin levels as controls, subjects with AVP deficiency had lower baseline (2.5 pmol/L [IQR 2.0-3.1]) and peak levels (4.6 pmol/L [IQR 2.4-6.0]). A peak copeptin of ≥9.3 pmol/L best predicted absence of complete or partial AVP deficiency with a sensitivity of 100% and specificity of 80%. CONCLUSIONS: ALD-ST induced a robust peak copeptin in healthy short children and children with primary polydipsia. Nausea/vomiting, a side effect of ALD-ST, amplified the copeptin response. The ALD-ST may be a suitable initial screening test in children with PPS.

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Syndrome of inappropriate anti-diuretic hormone (SIADH) can be presented as a paraneoplastic syndrome in primary malignancies involving the lung and brain. However, the development of SIADH in primary thymic carcinoma is poorly documented. We report a case of an elderly, with an initial presentation of symptomatic persistent hyponatremia as a paraneoplastic syndrome of SIADH with an incidental finding of anterior mediastinal mass confirmed on imaging. Further investigations are consistent with the diagnosis of poorly differentiated locally advanced thymic carcinoma with lung infiltration (T3N1Mx). The patient underwent an En-bloc total thymectomy and subsequently completed adjuvant chemotherapy and further follow-up showed a complete resolution of hyponatraemic SIADH. In conclusion, SIADH may be presented as a paraneoplastic syndrome in primary thymic carcinoma and early detection of thymic malignancy is paramount to ensure early diagnosis and prognostication.

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Hypernatremia has been significantly associated with in-hospital mortality and discharge to long-term care facilities. The appropriate correction of electrolyte disturbances, especially sodium, is important to consider to prevent the addition of central nervous system disturbances, such as cerebral edema and eventual brain injury. The importance of maintaining a proper correction of hypernatremia has been well studied and used in clinical practice. Choosing to use a hypotonic solution is a key principle. It is of utmost importance to adjust the rate of correction based on the patient's symptoms, underlying etiology, and associated comorbidities. This case demonstrates how a correction formula was used and adjusted accordingly in an 81-year-old female with severe hypernatremia and metabolic encephalopathy with multiple comorbidities, including hypopituitarism. It is noteworthy to examine the correction rate, how it was calculated and delivered, and how the main cause of the hypernatremia was determined. Considering all these factors can help to properly administer any additional corrective medications, such as desmopressin (DDAVP) in a patient with diabetes insipidus (DI) secondary to hypopituitarism, or adjust the correcting rate based on signs, symptoms, and laboratory findings.

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Vasopressin (AVP) acts as a neurotransmitter and its activity can potentiate respiratory activity. Hypoglossal (XII) motoneurons that innervate the tongue express V1a vasopressin receptors, which are excitatory. Therefore, we hypothesized that V1a receptor activation at XII motoneurons would potentiate inspiratory bursting. We developed this study to determine whether AVP can potentiate inspiratory bursting in rhythmic medullary slice preparations in neonatal (postnatal, P0-5) mice. Bath or local application of AVP potentiated inspiratory bursting compared to baseline XII inspiratory burst amplitude. Antagonizing V1a receptors revealed significant attenuation of the AVP-mediated potentiation of inspiratory bursting, while antagonism of oxytocin receptors (at which AVP has similar binding affinity) revealed a trend to attenuate AVP-mediated potentiation of inspiratory bursting. Finally, we discovered that the AVP-mediated potentiation of inspiratory bursting increases significantly with postnatal maturation from P0-5. Overall, these data support that AVP potentiates inspiratory bursting directly at XII motoneurons.

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INTRODUCTION: Copeptin, co-secreted with arginine vasopressin, is regulated by osmotic and volume stimuli but also responds to intravenous arginine and insulin-induced hypoglycemia. The serum copeptin response to the latter agents has been studied in adults but only to a limited extent in children. The objective of this study was to describe the copeptin response to combined arginine and insulin in children with normal posterior pituitary function. METHODS: We conducted a prospective, single-arm assessment of serum copeptin concentrations in children (age 7-16 years, n = 38) undergoing growth hormone stimulation testing with an arginine-insulin tolerance test (AITT) for short stature or growth deceleration in a tertiary referral center. After overnight fasting, arginine (500 mg/kg) was administered between 0 and 30 min intravenously (IV) followed by insulin (0.1 units/kg IV) at 60 min. Copeptin serum concentrations were measured at baseline (0 min), at the post-arginine peak (60 min), and at the post-insulin peak (90 min; 30 min post-insulin), respectively. The main outcome was the peak copeptin concentration. RESULTS: Mean ± SD copeptin concentrations increased from 9.9 ± 5.0 pmol/L at 0 min to 13.2 ± 5.8 pmol/L at 60 min (p < 0.0001 vs. 0 min) and 27.7 ± 14.2 pmol/L at 90 min (p < 0.0001 vs. 0 and 60 min). There was no significant correlation between copeptin concentrations and age, BMI, pubertal status, cortisol, growth hormone, or glucose concentrations. DISCUSSION/CONCLUSION: Arginine and insulin appear to have an additive and consistent effect resulting in significant stimulation of copeptin secretion in children. The AITT may be a useful tool to evaluate for normal posterior pituitary function in this age-group, with potential implications for the evaluation of polyuria-polydipsia syndrome.

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Diabetes insipidus is a rarely encountered cause of hypernatremia, often presenting a diagnostic and therapeutic dilemma for the encountering physician. Patients are often asymptomatic for a number of years due to compensation of their polyuria with polydipsia, but may have dramatic presentations in situations where they lose access to hydration. Our case is of a 62-year-old woman who was found unconscious with signs and symptoms of a heat stroke, and later was found to have resistant hypernatremia that persisted despite extensive free water supplementation. She had dilute polyuria throughout her hospital course, eventually warranting testing for diabetes insipidus with a vasopressin challenge test. She responded well to therapy with intranasal desmopressin and currently remains asymptomatic. Because our patient was reported to have polyuria and polydipsia for a number of years presumed to be due to underlying diabetes mellitus, it is possible that she had pre-existing central diabetes insipidus that was exacerbated by the lack of access to free water while she was in her intubated and sedated state. Alternatively, she may have also developed new-onset diabetes insipidus due to severe hyperthermia. This case serves to highlight a dramatic presentation of diabetes insipidus, and the importance of careful consideration of its diagnosis in patients with persistent dilute polyuria despite signs of intravascular volume depletion.

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K+ balance in mammals relies on regulated renal K+ excretion matching unregulated fluctuating K+ intake. Upon a K+ rich meal, rapid and powerful K+ excretion is needed. Renal K+ secretion is stimulated by the increased tubular flow. We speculated that high K+ intake acutely increases urinary flow to stimulate K+ excretion. METHODS: Mice were K+ challenged through diets or gavage. Post K+ loading urinary output, osmolarity, [K+ ]u , [Na+ ]u , plasma osmolarity, [copeptin]p , [K+ ]p , and [Na+ ]p were measured. To locate the mechanism of K+ -induced diuresis in the glomerular/tubular system we measured creatinine excretion and assessed functional transport in isolated perfused TALs and CDs during an acute [K+ ]bl switch from 3.6 to 6.5 mM. Molecular adaptations of transport proteins involved in water reabsorption were investigated by immunoblotting. RESULTS: (1) Mice switched from a 1% to 2% K+ diet increased diuresis within 12 hours and reciprocally reduced diuresis when switched from 1% to 0.01% K+ diet. (2) A single K+ gavage load, corresponding to 25%-50% of daily K+ intake, induced 100% increase in diuresis within 30 minutes. This occurred despite augmented plasma osmolarity and AVP synthesis. (3) K+ gavage did not change GFR. (4) In isolated perfused TALs, shifting [K+ ]bl from 3.6 to 6.5 mM did not affect AVP-induced NaCl transport. (5) In sharp contrast, in isolated perfused CDs, shifting [K+ ]bl from 3.6 to 6.5 mM markedly reduced CD AVP sensitivity, ie inhibited water absorption. CONCLUSION: Dietary K+ loading induces a rapidly on-setting diuresis. The mechanism of K+ -induced diuresis involves desensitization of the CD to AVP.

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Atrial fibrillation is the most common sustained cardiac arrhythmia. While there have been reports of atrial fibrillation caused by the compression of pulmonary veins, we have not found reports of atrial fibrillation caused by the compression of the pulmonary artery. This report highlights the possible pathophysiology and management of atrial fibrillation in a patient with small cell lung cancer. The patient was admitted for hyponatremia secondary to syndrome of inappropriate antidiuretic hormone (SIADH) but subsequently developed tachycardia which progressed to atrial flutter and atrial fibrillation. Antiarrhythmics were ineffective until the patient received his first palliative chemotherapy for his small cell lung cancer. Subsequently, rate control was achieved with sotalol, with eventual conversion back to sinus rhythm. Management of atrial fibrillation is complex and sometimes depends on the underlying etiology. Early chemotherapy, in addition to antiarrhythmic drugs, may be beneficial in the management of patients with small cell lung cancer and atrial fibrillation. The CHA2DS2-VASc score does not take active malignancy into account and anti-coagulation should be evaluated on a case-by-case basis in this patient population.

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BACKGROUND: Patients with sellar masses undergoing transsphenoidal surgery (TSS) frequently develop endocrine dysfunction; therefore, in-hospital endocrinology consultation (IHEC) is recommended. However, we wondered whether routine endocrinology assessment of all TSS patients is always necessary. METHODS: We developed an IHEC Physician's Guide to identify patients who would require peri-operative IHEC. An analysis of all patients undergoing TSS for a sellar mass over a 4-year period was conducted to assess the predictive value of the IHEC Physician's Guide in identifying patients who required IHEC. RESULTS: A total of 116 patients underwent TSS; 24 required IHEC. As expected, the risk of endocrine complications requiring peri-operative endocrine management was significantly higher in the IHEC group versus no-IHEC group (96% vs. 1%; p < 0.001). The negative predictive value of the IHEC Physician's Guide in identifying patients who did not require IHEC was 0.99 (95% CI 0.9409-0.9997); Fisher's exact test, p < 0.001), meaning that the IHEC Physician's Guide successfully identified all but one patient who truly required IHEC. CONCLUSION: Results from our study show that most patients do not need IHEC after TSS and that those patients requiring IHEC can be reliably predicted at surgery by using a simple IHEC Physician's Guide.

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BACKGOUND: Novel corona virus(SARS-CoV-2) which emerged from Wuhan, China, has spread to whole worlds very rapidly causing enormous health effect and death. Current publications worldwide showed that COVID-19 is a disease involving multiple system of the body with many unusual presentations. So physicians face the challenges to manage it in the hospital. CASE REPORT: The syndrome of inappropriate secretion of anti diuretic hormone (SIADH) is one of the most common causes of hyponatremia accounts for approximately one-third of all cases. In the diagnosis of SIADH it is important to ascertain the euvolemic state of extra cellular fluid volume, both clinically and laboratory measurement. Several infections associated with SIADH have been reported. Howover, Coronavirus disease 2019(COVID-19) associated with SIADH were only few cases reported. We are presenting a case of 70 year old female admitted with unconsciousness later diagnosed as severe hyponatremia along with COVID-19 complicated with severe pneumonia.

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Nephrogenic diabetes insipidus (NDI), which can be congenital or acquired, results from the failure of the kidney to respond to the anti-diuretic hormone (ADH). This will lead to excessive water loss from the body in the form of urine. The kidney, therefore, has a crucial role in maintaining water balance and it is vital to restore this function in an artificial kidney. Herein, an ultrasensitive and highly selective aptameric graphene-based field-effect transistor (GFET) sensor for ADH detection was developed by directly immobilizing ADH-specific aptamer on a surface-modified suspended graphene channel. This direct immobilization of aptamer on the graphene surface is an attempt to mimic the functionality of collecting tube V 2 receptors in the ADH biosensor. This aptamer was then used as a probe to capture ADH peptide at the sensing area which leads to changes in the concentration of charge carriers in the graphene channel. The biosensor shows a significant increment in the relative change of current ratio from 5.76 to 22.60 with the increase of ADH concentration ranging from 10 ag/mL to 1 pg/mL. The ADH biosensor thus exhibits a sensitivity of 50.00 µA· ( g / mL ) - 1 with a limit of detection as low as 3.55 ag/mL. In specificity analysis, the ADH biosensor demonstrated a higher current value which is 338.64 µA for ADH-spiked in phosphate-buffered saline (PBS) and 557.89 µA for ADH-spiked in human serum in comparison with other biomolecules tested. This experimental evidence shows that the ADH biosensor is ultrasensitive and highly selective towards ADH in PBS buffer and ADH-spiked in human serum.

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INTRODUCTION: Hyponatremia, defined as a serum sodium concentration ([Na+]) <135 mEq/L. It is not a disease but rather a pathophysiologic process indicating disturbed water homeostasis. Hyponatremia should be further classified to provide directions for diagnosis and treatment. It is a heterogeneous disorder. The classifications of hyponatremia are commonly based on tonicity and volume status. The initial differentiation in hypotonic and non-hypotonic hyponatremia is important because management is different. Several studies have been conducted previously to measure the incidence of hyponatremia in medically ill patients. Several studies have demonstrated an increased prevalence of hyponatremia in the presence of co-morbid conditions. We conducted this study to bring out various causes of hyponatremia; their relation with sex, age and outcome and hyponatremia's classification and incidence in our hospitalised population. MATERIALS AND METHODS: This study was conducted to find out etiology, classification, prevalence and outcome and its relation with age and sex in patients of hyponatremia admitted in our institution. A total number of 106 patients were studied. RESULTS: Hospital-based incidence of hyponatremia was found to be 1.17%. Mean age of patients in study was 62.25 ± 17.7 years. Male to female ratio was 1.25:1. Altered sensorium was the most common neurological symptom. Ninety-five (90%) patients were hypo-osmolar. Out of ninety four patients, 38 (40%) were euvolemic. Chronic obstructive pulmonary disorder (COPD) with cor pulmonale with right-sided heart failure (n = 9, 31%) was the most common cause in hyper-volemic hyponatremia. Acute gastroenteritis (n = 13, 48%) was the most common cause in hypo-volemic hyponatremia. Syndrome of inappropriate anti-diuretic hormone secretion (SIADH) was the most common cause (n = 20, 53%) of euvolemic hyponatremia. Out of 106 patients, 11 (10.38%) patients expired. CONCLUSION: Hyponatremia acts as a poor prognostic marker of the primary disease. It is important to recognise it early because of the potential morbidity and mortality, economic impact on the patients and health care associated with it. Early management of hyponatremia, which includes determination of the rate of correction, the appropriate interventions and the presence of other underlying disorders, may help in improving the outcome and shortening the hospital stay of the patients.

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RATIONALE & OBJECTIVE: First-line therapy for syndrome of inappropriate antidiuresis (SIAD) is fluid restriction. Additional treatment for patients who do not respond to fluid restriction are water restriction with furosemide or water restriction with furosemide and salt supplementation. However, the efficacy of these treatments has never been tested in a randomized controlled study. The objective of this study was to investigate whether, combined with fluid restriction, furosemide with or without sodium chloride (NaCl) supplementation was more effective than fluid restriction alone in the treatment of hyponatremia in SIAD. STUDY DESIGN: Open-label randomized controlled study. SETTING & PARTICIPANTS: Patients with serum sodium concentrations ([Na+]) ≤ 130mmol/L due to SIAD. INTERVENTION(S): Random assignment to 1 of 3 groups: fluid restriction alone (FR), fluid restriction and furosemide (FR+FM), or fluid restriction, furosemide, and NaCl (FR+FM+NaCl). Strictness of fluid restriction (<1,000 or<500mL/d) was guided by the urine to serum electrolyte ratio. Furosemide dosage was 20 to 40mg/d. NaCl supplements were 3g/d. All treatments were continued for 28 days. OUTCOMES: The primary outcome was change in [Na+] at days 4, 7, 14, and 28 after randomization. RESULTS: 92 patients were recruited (FR, n=31; FR+FM, n=30; FR+FM+NaCl, n=31). Baseline [Na+] was 125±4mmol/L, and there were no significant differences between groups. Mean [Na+] on day 4 in all treatment groups was significantly increased from baseline by 5mmol/L (P<0.001); however, the change in [Na+] was not significantly different across groups (P=0.7). There was no significant difference in percentage of patients or time to reach [Na+] ≥ 130 or≥135mmol/L across the 3 groups. Acute kidney injury and hypokalemia (potassium≤3.0mmol/L) were more common in patients receiving furosemide. LIMITATIONS: Open-label treatment. CONCLUSIONS: In patients with SIAD, furosemide with NaCl supplement in combination with fluid restriction did not show benefits in correction of [Na+] compared with treatment with fluid restriction alone. Incidences of acute kidney injury and hypokalemia were increased in patients receiving furosemide. FUNDING: None. TRIAL REGISTRATION: Registered at the Thai Clinical Trial Registry with study number TCTR20170629004.

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Overall body fluid concentration is regulated within a narrow range by the concerted action of the hypothalamic-pituitary axis to influence water intake through thirst and water excretion via the effect of vasopressin, or antidiuretic hormone, on renal collecting duct water permeability. Sodium is the principal extracellular cation; abnormalities in overall effective body fluid concentration, or tonicity, manifest as disturbances in serum sodium concentration. Depending on its severity and chronicity, hyponatremia can lead to significant symptoms, primarily related to central nervous system function. Failure to correct hyponatremia can lead to permanent neurologic damage, as can over rapid correction. It is thus essential to stay within specific limits for correction, particularly for chronic hyponatremia. Hypernatremia also leads to central nervous system dysfunction, although goals for its correction rate are less well established. This Core Curriculum article discusses the normal regulation of tonicity and serum sodium concentration and the diagnosis and management of hypo- and hypernatremia.

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OBJECTIVE: To investigate the sex differences in clinical features, including salivary flow rate, psychological distress and hypothalamic-pituitary-adrenal axis response and their inter-relationships in patients with burning mouth syndrome. SUBJECTS AND METHODS: Eighteen men and 37 postmenopausal women with burning mouth syndrome underwent a comprehensive questionnaire evaluation, psychological evaluation and salivary flow rate measurement. Laboratory tests were performed to investigate the function and integrity of the hypothalamic-pituitary-adrenal axis. RESULTS: Both unstimulated and stimulated salivary flow rates were higher in men than in women (unstimulated: 0.58 ± 0.32 vs. 0.37 ± 0.15 ml/min, p < .01; stimulated: 1.83 ± 0.63 vs. 1.22 ± 0.31, p < .001). Symptom severity scored on a visual analogue scale negatively correlated with anti-diuretic hormone levels in both sexes. The visual analogue scale scores negatively correlated with unstimulated (r = -.652, p < .01) and stimulated (r = -.376, p < .05) salivary flow rates in men and women, respectively. Unstimulated salivary flow rates positively correlated with anti-diuretic hormone (r = .453, p < .05) and progesterone (r = .402, p < .05) levels only in women. CONCLUSIONS: Our results suggest that clinicians should consider hypothalamic-pituitary-adrenal axis response, as well as sex and salivary flow rates, when identifying the aetiology of patients with burning mouth syndrome, as it may enable more accurate and effective treatment.

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Carbamazepine-induced hyponatremia is a rare condition. The patients may or may not be symptomatic. Epilepsy is considered a social taboo. Hence, patients do not reveal history of being on antiepileptic agents. Carbamazepine is a known antiepileptic and psychotropic agent. It is commonly used for the treatment of seizures and psychiatric disorders. We present a case of a 60-year-old female patient presenting in emergency department with history of carbamazepine-induced hyponatremia. It raises antidiuretic hormone (ADH) levels. This leads to increased sensitivity of renal tubules to ADH levels. She was diagnosed as a case of syndrome of inappropriate ADH and was treated accordingly. She was asymptomatic and was ambulatory. She recovered significantly. Hence, it is essential to monitor sodium levels in patients on carbamazepine therapy and also on drugs with similar mechanism of action.

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@#Introduction: Hyponatraemia is one of the most frequent laboratory findings in hospitalised patients. We present an unusual case of hyponatraemia in a 23-year-old female secondary to acute intermittent porphyria (AIP), a rare inborn error of metabolism. Case Report: The patient presented with upper respiratory tract infection, fever, seizures and abdominal pain. An initial diagnosis of encephalitis was made. In view of the unexplained abdominal pain with other clinical findings such as posterior reversible encephalopathy syndrome by CT brain, temporary blindness as well as hyponatraemia, acute intermittent porphyria was suspected. Urine delta aminolaevulinic acid (δ-ALA) and porphobilinogen were elevated confirming the diagnosis of AIP. Genetic studies were done for this patient. The patient had a complete resolution of her symptoms with carbohydrate loading and high caloric diet. Conclusion: Although rare, AIP should be considered as a cause of hyponatraemia in a patient who presents with signs and/or symptoms that are characteristic of this disease.