Syndrome Of Antidiuretic Hormone Research Articles

A recent ongoing effect: Hyponatremia in neurologically ill patients

Different variables altering the volume of extracellular fluid might result in hyponatremia, which is defined as a serum sodium content below 136 millimoles per liter. Depending on the volume status, it can be classified as hypovolemic, euvolemic, or hypervolemic. Hyponatremia is caused by a number of risk factors and drugs, such as diuretics, NSAIDs, and antidepressants. Hyponatremia is more common in patients with neurological conditions, especially those with head trauma, subarachnoid hemorrhage, or acute meningitis. Recent advancements in analysis for disorder of antidiuretic hormone syndrome (SIADH), a prevalent cause, include vasopressin-2 receptor antagonists. The intricate regulation of sodium and water balance by humoral, neurological, and renal mechanisms is a part of normal physiology. Hyponatremia may result from medications such as tramadol, sacubitril/valsartan, antidepressants, and anticonvulsants interfering with these mechanisms. Drug-induced hyponatremia is managed by stopping the offending agent, limiting fluid intake, and occasionally administering hypertonic saline. For chronic hyponatremia, the use of vaptans, like tolvaptan, in conjunction with urea therapy is growing. A risky complication of hyponatremia is osmotic demyelination syndrome, which can occur when the condition is treated too quickly. To avoid negative consequences, close observation and the right amount of fluids must be administered during treatment. To summarize, treating hyponatremia effectively entails determining the underlying causes, treating them, and making sure that serum sodium levels are carefully corrected to avoid consequences such as osmotic demyelination syndrome.

The Never-Ending Story of Hyponatremia: A Current Problem to Overcome.

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt-wasting syndrome (CSWS) are in general associated to refractory hyponatremia especially in patients with neurologic disorders.Extracellular fluid (ECF) assessment is the key to distinguish between SIADH and CSWS.Nevertheless, measurement of the ECF volume is not sufficient to determine the correct etiology and more established diagnostic algorithms are required.

Approach to Hyponatremia in the ICU: A review article

Hyponatremia is a common condition in clinical practice and a major cause of morbidity and mortality. Differentiating between its acute and chronic forms is challenging because of their variable symptoms. A thorough approach is necessary to diagnose hyponatremia. Proper interpretation of the numerous laboratory tests aids in the differentiation of hyponatremia types. In the ICU, management varies for acute and chronic cases to prevent neurological issues. While fluid restriction and hypertonic saline administration are two common forms of management, however, individualized strategies are essential for illnesses like cirrhosis or Syndrome of Inappropriate Anti Diuretic Hormone. To successfully treat hyponatremia, use vaptans and other protocols while monitoring the patient's condition closely. Monitoring acute and chronic cases must adhere to specific monitoring frequency and indices, and should cease only when Na+ levels are deemed safe. Balancing the diagnosis and therapy provides patient safety and avoids side effects.

¿Guillain Barre syndrome and inadequate secretion of antidiuretic hormone, is their relationship possible?

Guillain-Barré syndrome (GBS) is a polyradiculoneuropathy of acute onset and the most common cause of acute flaccid paralysis. It is characterized by the appearance of sensory and/or motor symptoms, accompanied by a decrease or absence of muscle stretch reflexes and other symptoms such as facial paralysis, altered eye movements, bulbar symptoms, altered wakefulness, dysautonomia and ataxia. On the other hand, hydroelectrolyte disorders are associated with serious neurological diseases as a poor prognostic factor; the most affected electrolyte is sodium; in fact, hyponatremia is the most common disorder in hospitalized patients, regardless of the cause; in GBS, it is a frequent finding on admission. It is important to recognize hyponatremia, due to its high morbidity and mortality; it is also a marker of an underlying disease. Syndrome of inappropriate secretion of antidiuretic hormone (SSIADH) is the most common cause of hyponatremia and has been associated with Guillain Barre syndrome; in this way, its diagnosis is a challenge for the doctor; finally, below we describe details of a 70-year-old male patient who was admitted to the intensive care unit, with hyponatremia with a SSIHAD, with good subsequent evolution.

Uncommon presentation of small cell lung carcinoma with ectopic adrenocorticotropic hormone secretion and resistant hypokalemia: A case report

Paraneoplastic syndromes can serve as initial indicators of malignancy, with small cell lung cancer accounting for 13% of new lung cancer diagnoses. The most prevalent paraneoplastic syndrome associated with small cell lung cancer is inappropriate antidiuretic hormone syndrome, followed by ectopic adrenocorticotropic hormone-mediated Cushing’s syndrome. Cushing’s syndrome manifests as hypercortisolemia and presents with diverse symptoms, including central obesity, plethora, menstrual irregularities, hypertension/diabetes mellitus, ecchymoses, osteoporosis, muscle weakness, virilization/hirsutism, skin atrophy, decreased libido, and infertility. This case report details the uncommon presentation of small cell lung carcinoma manifesting with ectopic adrenocorticotropic hormone secretion (EAS), leading to resistant hypokalemia and rhabdomyolysis. This case emphasizes the importance of considering EAS in severe cases of Cushing's syndrome and highlights the diagnostic and therapeutic challenges associated with this condition.

Response to: Hypouricaemia and acute kidney injury: a hereditary condition should be considered.

First, we would like to thank Dr Martin for his insightful comments. We agree that we should evaluate the mutations in the gene that caused renal hypouricemia (RHUC) in the patient in this report.1 The patient was of Japanese ethnicity with no family history of nephrolithiasis or exercise-induced acute kidney injury (EIAKI), and this was the first instance that they noticed symptoms suggesting EIAKI. At discharge, we recommended sufficient hydration during exercise and avoiding strenuous activity. After kidney function recovery, the patient’s uric acid (UA) level was as low as it was at hospitalization, but the fractional excretion of UA remained high. Although we did not mention it in our report, we diagnosed this case as RHUC and excluded diseases that could cause hypouricemia with increased UA excretion, such as the syndrome of inappropriate secretion of antidiuretic hormone and Fanconi syndrome.1 UA is excreted from the renal glomerulus into the renal tubules and reabsorbed via UA transporters, such as urate transporter 1 (encoded by the URAT1/SLC22A12 gene) and glucose transporter 9 (encoded by the GLUT9/SLC2A9 gene), expressed in the proximal tubular epithelium. Dysfunction of these transporters causes RHUC, and nephrolithiasis or EIAKI are known complications of RHUC; however, the exact frequencies of these complications remain unknown. It is postulated that there are genes other than URAT1/SLC22A12 and GLUT9/SLC2A9 that cause RHUC.2,3 The genetic test could have been performed to discover the causative gene. Although allopurinol might prevent EIAKI in patients with RHUC, its administration remains controversial, and the dosage and dosing period are unclear.2,4 Therefore, we did not administer allopurinol.

Metabolic and Endocrin Complications of Pediatric, Adolescent and Young Adult Acute Lymphoblastic Leukemia: Single Centre Experience

Introduction: Metabolic and endocrine complications are common complications in the treatment of Acute Lymphoblastic Leukemia (ALL). Inappropriate anti-diuretic hormone (ADH) syndrome, diabetes mellitus, hypoglycemia, surrenal failure, hypercalcemia may ocur during the treatment. Obesity, growth retardation or pause and osteopenia are the most common complications. These complications are usually due to combined chemotherapeutic agents used during the treatment. In this study, we present the metabolic/endocrine complications which are observed during treatment of ALL patients at our center.Material -Metod: One hundred and ten patients who were diagnosed with ALL and treated with the ‘Children's Oncology Group’ (COG) protocol and follow-up in the Pediatric Hematology / Oncology Department of the Istanbul University Institute of Oncology were included in the study. We retrospectively analyzed the demographic characteristics of the patients and presence of metabolic/endocrin problems (hyperglycemia, hypoglycemia, hypothyroidism, hypercholesterolemia, obesity) during all treatment stages were recorded. Forty-five (40.9%) of the patients were female and 65 (59.1%) were male. Ninety-seven (88.2%) patients were pre-B-cell ALL, 1 (0.9%) patients were mature B-cell ALL, 11 (10%) patients were T-cell ALL and 1 (0.9%) patients were biphenotypic ALL. The median age of the patients were 7 years (range:1,5-23).Results: One hundred of the 110 patients whose all clinical data were obtained were included for the evaluation of the metabolic and endocrin complications. The metabolic and endocrine problems were detected in 16 (16%) patients in any phases of the treatment and 84 (84%) patients did not have any metobolic or endocrine problems during the treatment. Twelve (12%) of the 16 patients with metabolic and endocrine problems were in 1 phase and 4 (4%) in 2 phases. Totally, 23 problems were detected. All metabolic / endocrine problems that arise during treatment are shown in Table 1. Seven of them (30.4%) were in induction, 2 of them were in consolidation (8.8%), no problems were found in interim maintenance 1, 7 (30.4%) were in delayed intencification, Interim maintenance 2 and delayed intencification 2 did not show any problems, and 7 (30.4%) were seen in maintenance.Conclusion: In the treatment of ALL, endocrine and metabolic problems are frequently seen during and after treatment. In our study, 23 metabolic problems (hyperglycemia, hypoglycemia, hypothyroidism, hypertriglyceridemia, hypercholesterolemia, osteoporosis, obesity, hyperferritinemia, metabolic syndrome) were recorded in 16 (16%) of the patients. Our resuts suggest that metabolic complications that may occur in ALL treatment should be considered as well as the remission of the disease. Therefore, patients should be carefully evaluated for metabolic and endocrin problems in ALL treatment. [Display omitted] DisclosuresNo relevant conflicts of interest to declare.

Hexabromocyclododecanes Are Dehalogenated by CYP168A1 from Pseudomonas aeruginosa Strain HS9.

Hexabromocyclododecanes (HBCDs) are widely used brominated flame retardants that cause antidiuretic hormone syndrome and even induce cancer. However, little information is available about the degradation mechanisms of HBCDs. In this study, genomic and proteomic analyses, reverse transcription-quantitative PCR, and gene knockout assays reveal that a cytochrome P450-encoding gene is responsible for HBCD catabolism in Pseudomonas aeruginosa HS9. The CO difference spectrum of the enzyme CYP168A1 was matched to P450 characteristics via UV visibility. We demonstrate that the reactions of debromination and hydrogenation are carried out one after another based on detection of the metabolites pentabromocyclododecanols (PBCDOHs), tetrabromocyclododecadiols (TBCDDOHs), and bromide ion. In the 18O isotope experiments, PBCD18OHs were only detected in the H218O group, proving that the added oxygen is derived from H2O, not from O2. This study elucidates the degradation mechanism of HBCDs by Pseudomonas. IMPORTANCE Hexabromocyclododecanes (HBCDs) are environmental pollutants that are widely used in industry. In this study, we identified and characterized a novel key dehalogenase, CYP168A1, that is responsible for HBCD degradation from Pseudomonas aeruginosa strain HS9. This study provides new insights into understanding biodegradation of HBCDs.

Posterior Reversible Encephalopathy Syndrome in Childhood Hematological/Oncological Diseases: Multicenter Results.

The aim of the study was to analyze the characteristics of posterior reversible encephalopathy syndrome (PRES) cases treated at 10 different institutions in our country. Fifty-eight patients diagnosed with PRES were included in this study. The data of PRES cases from 10 departments of pediatric hematology/oncology were analyzed. The mean age of the patients at the time of diagnosis of PRES was 8.95±3.66 years. Most patients (80.4%) had a primary diagnosis of acute leukemia. Patients received chemotherapy (71.4%) and/or used steroids within 14 days before the diagnosis of PRES (85.7%). Hypertension was found in 83.9% of the patients. Twenty-six patients had infections and 22 of them had febrile neutropenia. The most common electrolyte disorders were hypocalcemia, hypomagnesemia, and hypopotassemia. Six patients had tumor lysis syndrome and 4 had inappropriate antidiuretic hormone syndrome. Magnetic resonance imaging was used for diagnosis in all patients. The most commonly involved regions by magnetic resonance imaging were occipital (58%), parietal (51%), and frontal lobes (45%), respectively. Twenty-five patients required intensive care and 7 patients were intubated. In conclusion, PRES may develop during the follow-up and treatment of hematological diseases. In addition to steroid and intense combined chemotherapies, immunosuppressive agents and hypertension are also factors that may be responsible for PRES.

Fostamatinib, a Spleen Tyrosine Kinase (SYK) Inhibitor, for the Treatment of Warm Antibody Autoimmune Hemolytic Anemia (wAIHA): Final Results of the Phase 2, Multicenter, Open-Label Study

Fostamatinib, a Spleen Tyrosine Kinase (SYK) Inhibitor, for the Treatment of Warm Antibody Autoimmune Hemolytic Anemia (wAIHA): Final Results of the Phase 2, Multicenter, Open-Label Study

Pollution and biodegradation of hexabromocyclododecanes: A review

Hexabromocyclododecanes (HBCDs) are the most common brominated flame-retardants after polybrominated diphenyl ethers. HBCDs can induce cancer by causing inappropriate antidiuretic hormone syndrome. Environmental contamination with HBCDs has been detected globally, with concentrations ranging from ng to μg. Methods to degrade HBCDs include physicochemical methods, bioremediation, and phytoremediation. The photodegradation of HBCDs using simulated sunlight or ultraviolet lamps, or chemical catalysts are inefficient and expensive, as is physicochemical degradation. Consequently, bioremediation is considered as the most cost-effective and clean approach. To date, five bacterial strains capable of degrading HBCDs have been isolated and identified: Pseudomonas sp. HB01, Bacillus sp. HBCD-sjtu, Achromobacter sp. HBCD-1, Achromobacter sp. HBCD-2, and Pseudomonas aeruginosa HS9. The molecular mechanisms of biodegradation of HBCDs are discussed in this review. New microbial resources should be explored to increase the resource library in order to identify more HBCD-degrading microbes and functional genes. Synthetic biology methods may be exploited to accelerate the biodegradation capability of existing bacteria, including modification of the degrading strains or functional enzymes, and artificial construction of the degradation microflora. The most potentially useful method is combining microdegradation with physicochemical methods and phytoremediation. For example, exogenous microorganisms might be used to stimulate the adsorption capability of plants for HBCDs, or to utilize an interaction between exogenous microorganisms and rhizosphere microorganisms to form a new rhizosphere microbial community to enhance the biodegradation and absorption of HBCDs.

The HBCDs biodegradation using a Pseudomonas strain and its application in soil phytoremediation

Hexabromocyclododecanes (HBCDs) are the second-most widely used brominated flame retardants. They cause inappropriate antidiuretic hormone syndrome and can induce cancer. However, little information is available about bacterial degradation of HBCDs. In this study, HBCDs (α-, β- and γ-HBCD) degrading strain Pseudomonas aeruginosa HS9 was isolated, identified, and characterized. The strain HS9 could remove 69% (± 0.05%) of 1.7 mg/L HBCDs in 14 days. Based on identification of metabolites, this bacterium could oxidize HBCDs by two pathways. In the first, HBCDs are sequentially debromized to tetrabromocyclododecene, dibromocyclododecadiene, and then debromized once more to cis, trans, trans-1, 5, 9-cyclododecatriene (CDT). After that, CDT is then oxidized to 1,2-epoxy-5,9-cyclododecadiene. The second identified pathway is a simultaneous debrominating and hydroxylating process based on the detection of 2,5,6,9,10-pentabromocyclododecanols, which were newly identified. The strain's effects on plant-maize growth were tested and bioremediation evaluation trials were performed. The addition of strain HS9 could decrease HBCDs of 4.08 mg/g (87.6% removed) and 0.1 mg/g (25% removed) in soil and plants, respectively. Microbial diversity analysis shows that the addition of strain HS9 can promote the abundance of plant-beneficial bacteria, such as Methylobacillus, Nitrosomonas, Plancoccus, Bacillus, and Rhodococcus. The results provide insights for the bioremediation of HBCDs-contaminated soils.

An Inappropriate ADH Syndrome and Lung Cancer Diagnosis in A Patient with Isolated Hyponatremia

Hyponatremia is generally considered to have a plasma sodium concentration less than 135 mEq / L.It is the most common electrolyte abnormality which is important in clinical practice. It can be caused by many etiological factors. İnappropriate antidiuretic hormone syndrome (SIADH) is the one of the causes of normovolemic hyponatremia. On the other hand SIADH is responsible for 30% of hyponatremias due to cancer. It appears as a paraneoplastic syndrome especially and most offen in the lung carcinoma. The World Health Organization (WHO) reported that lung cancer is 12.9% of all cancers. It may manifest itself with specific symptoms, but may also show only the paraneplastic syndrome. Therefore, it should be kept in mind that the cause of hyponatremia must be determined and may be a symptom of SIADH and lung cancer.

SINDROM HORMON ANTIDIURETIK BERLEBIH

Syndrome of Inappropiate Antidiuretic Hormone (SIADH) is a condition caused by excessive antidiuretic hormone (ADH) secretion.High level of ADH increse water reabsorption in the kidney. This syndrome is characterized by hyponatremia, plasma hypo-osmolality,urine osmolality less than 100 mOsm/kg, elevated urine sodium, euvolemia, with normal renal, adrenal, and thyroid function. SIADHcould be the result of ectopic ADH caused by malignant cells, drug-induced, baroreceptor lesion, and other problems. Main treatmentfor SIADH is intended to overcome the underlying diseases. Other approaches are by fluid restriction, salt supplementation, and the useof drugs inducing diabetes insipidus or V2 receptor antagonist.

Disseminated herpes zoster involving bladder and severe inappropriate antidiuretic hormone in a immunocompetent elderly patient - A case report -

Disseminated herpes zoster commonly occurs in patients with decreased immunity, but rarely in patients without any evidence of immunosuppression. We reported a case of disseminated herpes zoster with visceral organ involvement in a non-immunocompromised patient. An 83-year-old man visited our pain center, with chief complaints of painful rashes on the L3-L4 and S2-S4 due to acute herpes zoster. Even though intravenous antiviral therapy was initiated immediately upon hospitalization, his lesion deteriorated and systemic cluster formed. Urinary retention and hyponatremia occurred, and he was diagnosed with zoster cystitis and severe inappropriate antidiuretic hormone syndrome. Conservative treatment, including Foley catheter insertion and correction of hyponatremia with antiviral therapy, was initiated, and he was discharged without any complications at the 33rd day of hospitalization. Old age can be a risk factor of disseminated herpes zoster, and visceral organ involvement should also be considered. Keywords: Cystitis; Herpes zoster; Hyponatremia; Immunocompetence; Inappropriate ADH Syndrome; Urinary retention

A rare cause of acute severe hyponatraemia secondary to the syndrome of inappropraite anti-diuretic hormone (SIADH) secretion

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

A Case of Effective Correction of SIADH with Low Dose Tolvaptan: No Trade of for an Economic Benefit

Hyponatremia is a common electrolyte abnormality in the hospital setting and can cause significant morbidity and mortality. Syndrome of anti diuretic hormone (SIADH) secretion can pose management difficulties particularly if the etiology is not easily reversed. Fluid restriction as a treatment option is complicated in the acutely unwell patient, and fluid restriction is of limited treatment value once urine osmolarity exceeds 500 mosmo/kg. The “Vaptan” class of drugs has provided another therapeutic option in the management of euvolemic hyponatremia secondary to SIAD. The therapeutic use of this drug is sometimes limited by the associated expense of the drug. We present the case of a patient who was successfully treated with Tolvaptan for SIAD using a reduced dose, highlighting the role of dose reduction of Tolvaptan as an effective therapeutic option for SIAD with an associated economic benefit.

Randomized, double blinded, placebo-controlled trial to evaluate the efficacy and safety of tolvaptan in Chinese patients with hyponatremia caused by SIADH.

To study the effect of tolvaptan on non-acute, non-hypovolemic hyponatremia in inappropriate secretion of antidiuretic hormone (SIADH) syndrome in Chinese patients. Hyponatremic SIADH patients received placebo (N = 18) or tolvaptan (N = 19) at an initial dose of 15 mg/day with further titration to 30 mg/day and 60 mg/day based on serum sodium concentrations. Randomized, double-blind, placebo-controlled trial. Primary endpoint was the change of the serum sodium from baseline to days 4 and 7. Analysis of covariance (ANCOVA) was used for statistical analysis. At day 4, average daily changes in serum sodium levels from baseline was 1.9 ± 2.9 mmol/L (1.9 ± 2.9 mEq/L) in the placebo group and 8.1 ± 3.6 mmol/L (8.1 ± 3.6 mEq/L) in the tolvaptan group; at day 7, the values were 2.5 ± 3.9 mmol/L (2.5 ± 3.9 mEq/L) and 8.6 ± 3.9 mmol/L (8.6 ± 3.9 mmEq/L) for the placebo and tolvaptan groups (ANCOVA, P < 0.001). At days 4 and 7, daily urine output and proportions of patients with normalized serum sodium were significantly superior in the tolvaptan group. The most common adverse events occurring in the tolvaptan group were dry mouth and thirst. Tolvaptan demonstrated superiority to placebo in the treatment of Chinese SIADH patients with hyponatremia by elevating serum sodium concentration with acceptable safety profile.

Syndrome of Inappropriate Antidiuretic Hormone Secretion Associated With Olfactory Neuroblastoma

This study reports a patient having olfactory neuroblastoma complicated by syndrome of inappropriate antidiuretic hormone secretion. Olfactory neuroblastoma is a rare tumor that begins in the olfactory membrane. Only 10 cases have been reported previously. Because of having nonspecific symptoms, most patients manifest at an advanced stage at the time of diagnosis. Olfactory neuroblastoma may show local invasion and/or distant metastasis. We demonstrated preoperatively clinical and biochemical parameters consistent with antidiuretic hormone syndrome turned to normal ranges after the treatment. Surgery, chemotherapy, and radiotherapy are the choices of treatment; among these, surgery is an indispensible treatment.

Inappropriate secretion of antidiuretic hormone syndrome in a patient with systemic lupus erythematosus: What are the causes?

Introduction: The syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH) is defined by the hyponatremia and hypo-osmolality resulting from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume, which results in impaired water excretion. Causes of SIADH are numerous and variable. Reports of SIADH in patients with systemic lupus erythematosus (SLE) are scarce. We report here a case of SIADH in a young female lupic patient and try to analyze its possible causes.