Introduction
Patients with nocturia have to face many hurdles before being diagnosed and treated properly. The aim of this paper is to: summarize the nocturia patient pathway, explore how nocturia is diagnosed and treated in the real world and use the Delphi method to develop a practical algorithm with a focus on what steps need to be taken before prescribing desmopressin.
Methods
Evidence comes from existing guidelines (Google, PubMed), International Consultation on Incontinence‐Research Society (ICI‐RS) 2017, prescribing information and a Delphi panel (3 rounds). The International Continence Society initiated this study, the authors represent the ICI‐RS, European Association of Urology, and Society of Urodynamics, Female Pelvic Medicine and Urogenital Reconstruction (SUFU).
Results
Diagnostic packages: consensus on, history taking for all causalities, intake diary (fluid, food) and bladder diary, not for its duration. Pelvic (women) or rectal (men) examination, prostate‐specific antigen, serum sodium check (SSC), renal function, endocrine screening: when judged necessary. Timing or empty stomach when SSC is not important. Therapeutic packages: the safe candidates for desmopressin can be phenotyped as no polydipsia, heart/kidney failure, severe leg edema or obstructive sleep apnea syndrome. Lifestyle interventions may be useful. Initiating desmopressin: risk management consensus on three clinical pictures.
Follow‐up of desmopressin therapy: there was consensus on SSC day 3 to 7, and at 1 month. Stop therapy if SSC is <130 mmol/L regardless of symptoms. Stop if SSC is 130 to 135 mmol/L with symptoms of hyponatremia.
Conclusion
A summary of the nocturia patient pathway across different medical specialists is useful in the visualization and phenotyping of patients for diagnosis and therapy. By summarizing basic knowledge of desmopressin, we aim to ease its initiation and shorten the patient journey for nocturia.
In utero transmission of HIV‐1 has been demonstrated and may account for around 10–20% of all materno–fetal HIV‐1 transmission. The possible routes for such transmission are transannexial or transplacental. In both cases, the microenvironment (cytokines and chemokines) at the placental interface could be an important regulatory factor in viral transmission.
We therefore performed explant cultures of placental villi, and isolated purified trophoblasts, from term placentae obtained from HIV‐1‐seropositive and HIV‐1‐seronegative women in order to assess and compare the cytokine and chemokine secretion profiles using ELISA and semiquantitative RT‐PCR.
No major differences could be seen in the secretions of cytokines and chemokines at the level of whole placental tissue in HIV‐1‐positive and HIV‐1‐negative women. However, variations were observed in the expression of inflammatory cytokines and chemokines from trophoblastic cells, depending on the status of HIV‐1 infection of the mothers but not the babies, all of which remained uninfected. The significance of these data is discussed.
Intravenous ZDV remains an effective tool to reduce transmission in cases of virological failure, even in cART-treated women. However, for the vast majority of women with low viral loads at delivery, in the absence of obstetrical risk factors, systematic intravenous ZDV appears to be unnecessary.
Further investigations are needed to better understand the pathophysiology of nocturia, to allow improvement in diagnosis, and to optimize treatment by increasing efficacy and reducing adverse events. Patient-oriented practical guidelines on nocturia are needed to help clinicians from different disciplines diagnose and treat nocturia.
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