- A Rare Presentation of Epstein-Barr Virus-induced Hepatitis With an Interesting Twist: A Case Report Involving a Clinical Pearl. [Journal Article]
- CCureus 2018 Jun 14; 10(6):e2808
- An Epstein-Barr Virus (EBV) infection generally presents with the classic infectious mononucleosis symptomatology-sore throat, lymph node enlargement, and fatigue. However, there are cases in which i...
An Epstein-Barr Virus (EBV) infection generally presents with the classic infectious mononucleosis symptomatology-sore throat, lymph node enlargement, and fatigue. However, there are cases in which induced hepatitis does occur. The liver enzymes leaked during the acute damage would be apparent in the serum as an elevation of transaminases and alkaline phosphatase. These elevations are almost always mild in nature. In addition, the associated presenting symptomatology is a generalized weakness, lethargy, and fatigue. Aside from the marked elevation of liver enzymes, what makes our case a rarity is the fact that the chief complaint was polydipsia and polyuria. Furthermore, an initial negative hepatitis A panel was found to be positive weeks later. The insight offered by this case is a true clinical pearl-namely, that the seroconversion of hepatitis A takes several weeks to occur.
- Double Trouble - Severe Hypernatremia Secondary to Central Diabetes Insipidus Complicated by Hypercalcemic Nephrogenic Diabetes Insipidus: A Case Report. [Journal Article]
- AJAm J Case Rep 2018 Aug 18; 19:973-977
- CONCLUSIONS: Our case emphasizes the importance of identification of causes and complications of electrolyte abnormalities associated with metastatic cancers. These electrolyte abnormalities can be primary or paraneoplastic and should be actively pursued and treated in such cases.
- Questions to ask a patient with nocturia. [Journal Article]
- AJAust J Gen Pract 2018; 47(7):465-469
- CONCLUSIONS: Nocturia results from the interplay between nocturnal polyuria, reduced bladder storage and sleep disruption. Changes in the function of the urinary bladder, kidneys, brain and cardiovascular system, and hormone status underlie the development and progression of nocturia. Medications commonly prescribed to older people can affect development or resolution of nocturia. The bother caused to a patient by waking to void relates to disturbance of slow-wave sleep, the physical act of getting out of bed and resulting chronic fatigue. An assessment process that identifies relevant and co-existing causes of an individual's nocturia will facilitate a targeted approach to treatment.
- A COMBINED OUTPATIENT AND INPATIENT OVERNIGHT WATER DEPRIVATION TEST IS EFFECTIVE AND SAFE IN DIAGNOSING PATIENTS WITH THE POLYURIA-POLYDIPSIA SYNDROME. [Journal Article]
- EPEndocr Pract 2018 Aug 14
- CONCLUSIONS: A combined outpatient and inpatient overnight WDT protocol is safe and feasible when the test is performed with special care at experienced centers. Newer diagnostic tools are expected to improve the accuracy of PPS diagnosis.
- SLC2A9 (GLUT9) mediates urate reabsorption in the mouse kidney. [Journal Article]
- PAPflugers Arch 2018 Aug 13
- Uric acid (UA) is a metabolite of purine degradation and is involved in gout flairs and kidney stones formation. GLUT9 (SLC2A9) was previously shown to be a urate transporter in vitro. In vivo, human...
Uric acid (UA) is a metabolite of purine degradation and is involved in gout flairs and kidney stones formation. GLUT9 (SLC2A9) was previously shown to be a urate transporter in vitro. In vivo, humans carrying GLUT9 loss-of-function mutations have familial renal hypouricemia type 2, a condition characterized by hypouricemia, UA renal wasting associated with kidney stones, and an increased propensity to acute renal failure during strenuous exercise. Mice carrying a deletion of GLUT9 in the whole body are hyperuricemic and display a severe nephropathy due to intratubular uric acid precipitation. However, the precise role of GLUT9 in the kidney remains poorly characterized. We developed a mouse model in which GLUT9 was deleted specifically along the whole nephron in a tetracycline-inducible manner (subsequently called kidney-inducible KO or kiKO). The urate/creatinine ratio was increased as early as 4 days after induction of the KO and no GLUT9 protein was visible on kidney extracts. kiKO mice are morphologically identical to their wild-type littermates and had no spontaneous kidney stones. Twenty-four-hour urine collection revealed a major increase of urate urinary excretion rate and of the fractional excretion of urate, with no difference in urate concentration in the plasma. Polyuria was observed, but kiKO mice were still able to concentrate urine after water restriction. KiKO mice displayed lower blood pressure accompanied by an increased heart rate. Overall, these results indicate that GLUT9 is a crucial player in renal handling of urate in vivo and a putative target for uricosuric drugs.
- Neuroimaging of central diabetes insipidus-when, how and findings. [Review]
- NNeuroradiology 2018 Aug 10
- Central or neurogenic diabetes insipidus (CDI) is due to deficient synthesis or secretion of antidiuretic hormone (ADH), also known as arginine vasopressin peptide (AVP). It is clinically characteris...
Central or neurogenic diabetes insipidus (CDI) is due to deficient synthesis or secretion of antidiuretic hormone (ADH), also known as arginine vasopressin peptide (AVP). It is clinically characterised by polydipsia and polyuria (urine output > 30 mL/kg/day) of dilute urine (< 250 mOsm/L). It is the result of a defect in one of more sites involving the hypothalamic osmoreceptors, supraoptic or paraventricular nuclei of the hypothalamus, median eminence of the hypothalamus, infundibulum or the posterior pituitary gland. A focused MRI pituitary gland or sella protocol is essential. There are several neuroimaging correlates and causes of CDI, illustrated in this review. The most common causes are benign or malignant neoplasms of the hypothalamic-pituitary axis (25%), surgery (20%), head trauma (16%) or familial causes (10%). No cause is identified in up to 30% of cases. Knowledge of the anatomy and physiology of the hypothalamo-neurohypophyseal axis is crucial when evaluating a patient with CDI. Establishing the aetiology of CDI with MRI in combination with clinical and biochemical assessment facilitates appropriate targeted treatment. The aim of the pictorial review is to illustrate the wide variety of causes of CDI on neuroimaging, highlight the optimal MRI protocol and to revise the detailed neuroanatomy and neurophysiology required to interpret these studies.
- StatPearls [BOOK]
- BOOKStatPearls Publishing: Treasure Island (FL)
- Nocturia is often described as the most bothersome of all urinary symptoms and is also one of the most common symptoms. It affects 40 million people in the United States alone. One in 3 adults older ...
Nocturia is often described as the most bothersome of all urinary symptoms and is also one of the most common symptoms. It affects 40 million people in the United States alone. One in 3 adults older than age 30 make at least 2 trips to the bathroom every night, and about 70% of these individuals are bothered by this. Nocturia can be associated with long-term sleep deprivation in addition to the inconvenience that it causes. Nocturia is defined as the need for a patient to get up at night on a regular basis to urinate. The urinary episode must be preceded and followed by a period of sleep to count as a nocturnal void. This means the first-morning void is not considered when determining nocturia episodes. Nocturnal enuresis is a completely different disorder as patients are generally not aware of a full bladder and typically experience an involuntary void while in bed. Additionally, nocturnal frequency is very similar to nocturia except that in nocturia the voiding episodes are each preceded and followed by sleep periods. Nocturia frequently accompanies an overactive bladder not explainable by urinary tract infections or other identifiable disorders. About half of the patients with daytime urinary urgency will also have nocturia. Those with nocturia of 3 or more nocturnal voids per night have a significantly higher overall mortality rate than the general population. Nocturia affects overall health and daytime functioning from loss of sleep, risks falls and injuries at night, reduces the quality of life, lowers productivity, and may even affect the health of the partner whose sleep is often disrupted as well. In particular, older adults with nocturia who make multiple nocturnal trips to the bathroom are at substantially increased risk of potentially serious falls. A quarter of all the falls that occur in older individuals happen overnight. Of these, 25% are directly related to nocturia. Patients who make at least 2 or more nocturnal bathroom visits a night, have more than double the risk of fractures and fall-related traumas. Nocturia leads to sleep deprivation, which can cause exhaustion, mood changes, somnolence, impaired productivity, increased risk of falls and accidents, fatigue, lethargy, inattentiveness, and cognitive dysfunction. It is also associated with decreased physical health, obesity, diabetes, depression, and heart disease. There is a significant financial aspect associated with nocturia. The disorder costs an estimated $62.5 billion dollars to Americans each year due to lost productivity and sick leave associated with nocturia; primarily as a result of preventable falls, fractures, and associated injuries. Despite its relative frequency, nocturia is often underreported, poorly managed, and inadequately treated. Many patients are reluctant or too embarrassed to mention this problem to their physicians, or they mistakenly believe it just a normal part of aging. Compounding the problem, initial treatment of nocturia by physicians is often superficial and somewhat routine regardless of the actual underlying etiology; with men typically receiving alpha blockers and women prescribed overactive bladder medications without any diagnostic investigation. Further evaluation and management of nocturia are often lacking even when these initial measures fail. For these reasons, it may take 1 or even 2 years between the onset of significant symptoms and the beginning of physician-directed, effective nocturia treatment. This creates an obligation of physicians to ask patients about their nocturia, explain that it is an abnormal but treatable condition and offer appropriate help. Treatment should be based on the underlying cause, which requires further evaluation. The purpose of this review is to facilitate improved diagnosis and treatment of this common and bothersome urinary disorder that often requires additional diagnostic and therapeutic measures beyond simple drug treatment of benign prostatic hyperplasia (BPH) in men or bladder overactivity (OAB) in women. A simple evaluation, based on a good medical history, diabetes screening, voiding diary, urinalysis and post-void residual determination, can identify the underlying etiology (such as diabetes or nocturnal polyuria) leading to better treatment outcomes, improved quality of life scores, and substantial symptom resolution.
- [Nocturia in men with benign prostatic hyperplasia]. [Journal Article]
- AUAktuelle Urol 2018; 49(4):319-327
- Nocturia, defined as nocturnal micturition with a frequency of at least once per night, is one of the most frequent lower urinary tract symptoms in men with benign prostatic hyperplasia (BPH) and oft...
Nocturia, defined as nocturnal micturition with a frequency of at least once per night, is one of the most frequent lower urinary tract symptoms in men with benign prostatic hyperplasia (BPH) and often causes them to consult a physician. Nocturia is often bothersome and responsible for increased morbidity and mortality. Nocturia can be caused by increased fluid intake, increased diuresis or decreased bladder capacity, either alone or in combination. The underlying pathophysiology of nocturia can only be detected by methodical evaluation of the patient. Bladder diaries for 3 days are an essential part of the assessment. Treatment goals include reducing the nocturnal voiding frequency to less than 2 episodes per night, increasing the duration of undisturbed sleep to more than 4 hours, restoring quality of life, and reducing morbidity as well as mortality. In patients with reduced functional bladder capacity, α-blockers, 5α-reductase inhibitors, phosphodiesterase type-5 inhibitors, plant extracts or prostate operations (e. g. TURP) have shown to significantly reduce nocturnal voiding frequency. If nocturnal polyuria causes or contributes to nocturia, as shown in up to 80 % of BPH patients with nocturia, the treatment goal is to reduce urine production during the night. Low nocturnal serum concentration of the antidiuretic hormone can be treated with desmopressin to be taken at bedtime. The risk of hyponatremia is reduced with the new low-dose desmopressin formulation, which can be used even in men older than 65 years of age. Drug combinations may be useful in men with a mixed pathophysiology of nocturia.
- Comparative proteomics analysis of myocardium in mouse model of diabetic cardiomyopathy using the iTRAQ technique. [Journal Article]
- ACAdv Clin Exp Med 2018 Aug 07
- CONCLUSIONS: These results suggest that DCM shows differences in its proteomics compared to normal controls. Our quantitative proteomic analysis may provide a new insight into the distinct molecular profile of DCM.
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- Four Japanese Patients with Congenital Nephrogenic Diabetes Insipidus due to the AVPR2 Mutations. [Journal Article]
- CRCase Rep Pediatr 2018; 2018:6561952
- Almost 90% of nephrogenic diabetes insipidus (NDI) is caused by mutations in the arginine vasopressin receptor 2 gene (AVPR2) on the X chromosome. Herein, we reported clinical and biochemical paramet...
Almost 90% of nephrogenic diabetes insipidus (NDI) is caused by mutations in the arginine vasopressin receptor 2 gene (AVPR2) on the X chromosome. Herein, we reported clinical and biochemical parameters in four cases of three unrelated Japanese families and analyzed the status of the AVPR2. Two of the four patients had poor weight gain. However, in the male and female sibling cases, neither had poor weight gain while toddlers, but in the male sibling, episodes of recurrent fever, polyuria, and polydipsia led to the diagnosis of NDI at 4 years of age. Analysis of AVPR2 identified two nonsense mutations (c.299_300insA; p.K100KfsX91 and c.296G > A; p.W99X) and one missense mutation (c.316C > T; p.R106C). These mutations were previously reported. The patient with c.316C > T; p.R106C had milder symptoms consistent with previous reports. Of the familial cases, the sister was diagnosed as having NDI, but a skewed X-inactivation pattern in her peripheral blood lymphocytes was not identified. In conclusion, our study expands the spectrum of phenotypes and characterized mutations in AVPR2 in NDI.