Nausea and vomiting are common symptoms with many possible causes, including the adverse effects of drugs. If a drug is indicated, the cause guides the choice of antiemetic drug.The main antiemetic classes include antagonists of the serotonin, dopamine, histamine, muscarinic and neurokinin systems, corticosteroids and benzodiazepines. Some antiemetics appear more effective for specific indications.Serotonin and neurokinin antagonists, such as ondansetron and aprepitant, are highly effective in treating chemotherapy-induced nausea and vomiting. Metoclopramide and antihistamines are first-line options for nausea and vomiting in pregnancy.Serotonin antagonists and some dopamine antagonists, such as metoclopramide, can prolong the QT interval on the ECG. Dopamine antagonists can cause extrapyramidal adverse effects, particularly in children. GastroenteritisAcute gastroenteritis is caused by viral, bacterial or protozoal infections. Therapeutic options available for adults with vomiting secondary to gastroenteritis include dopamine antagonists such as metoclopramide or prochlorperazine and serotonin antagonists such as ondansetron. 15 Nausea and vomiting resulting from acute gastroenteritis is particularly challenging in children. Until the early 2000s, antiemetics including promethazine, metoclopramide and prochlorperazine were widely used in children, however their use is now controversial due to reports of adverse events including sedation and extrapyramidal reactions. 16 When an antiemetic drug is indicated, serotonin antagonists such as ondansetron are now recommended in guidelines, such as those published by the Royal Children's Hospital Melbourne. 17 These guidelines recommend a single weight-based dose of oral ondansetron. Children weighing 8-15 kg should receive 2 mg, children weighing 15-30 kg should receive 4 mg and children weighing more than 30 kg should receive 8 mg. Ondansetron is not recommended in children under six months of age or less than 8 kg in weight. 17 A systematic review reported that oral ondansetron reduced vomiting, hospitalisation and the need for intravenous rehydration in children with acute gastroenteritis. 18 Intravenous ondansetron or metoclopramide also reduced vomiting and hospitalisation. A single study in the review reported that rectal dimenhydrinate was effective at reducing vomiting. 18
The burden of chronic kidney disease (CKD) is growing globally, particularly in low-and lower-middleincome countries (LLMICs) where access to treatment is poor and the largest increases in disease burden will occur. The individual and societal costs of kidney disease are well recognized, especially in developed health care systems where treatments for the advanced stages of CKD are more readily available. The consequences of CKD are potentially more catastrophic in developing health care systems where such resources are often lacking. Central to addressing this challenge is the availability of data to understand disease burden and ensure that investments in treatments and health resources are effective at a local level. Use of routinely collected administrative data is helpful in this regard, however, the barriers to developing a more systematic focus on data collection should not be underestimated. This article reviews the current tools that have been used to measure the burden of CKD and considers limitations regarding their use in LLMICs. A review of the literature investigating the use of registries, disease specific databases and administrative data to identify populations with CKD in LLMICs, which indicate these to be underused resources, is included. Suggestions regarding the potential use of administrative data for measuring CKD burden in LLMICs are explored.
Proteinuria, in particular albuminuria, is a potentially significant modifiable risk factor for cardiovascular disease and the progression of kidney disease. Current treatment guidelines for albuminuria recommend a single renin-angiotensin-aldosterone inhibitor. This can be an ACE inhibitor or an angiotensin receptor antagonist. The routine use of combined renin-angiotensin-aldosterone inhibition for albuminuria is not supported by current evidence. Combination therapy is associated with higher rates of adverse events such as hyperkalaemia and progressive renal impairment. In 2015 the Kidney Health Australia publication Chronic Kidney Disease Management in General Practice recommended a 50% reduction in albuminuria as a target of treatment. It advised against combination ACE inhibitor and angiotensin receptor antagonist therapy, 9 as did the NICE guidelines in the UK. 10 Efficacy Multiple trials have reported that ACE inhibitors are effective at reducing proteinuria in both diabetic and non-diabetic populations. 11-13 ACE inhibitors also reduce the rate of progression of kidney disease, and the risk of dialysis or transplantation by up to 50% in patients with proteinuria. 11-13 The angiotensin receptor antagonists are effective for reducing proteinuria in diabetic and non-diabetic populations. 14 Major trials have also reported that they slow the progression of kidney disease. 15-17 During the first 6-12 months of treatment, a 50% reduction in proteinuria is associated with a 40-50% reduction in the risk for progression of kidney disease. 18
Introduction: Urine drug screens (UDS) assist in clinical planning and assessment of adherence in opioid agonist treatment (OAT). Urine drug screens may also be used in criminal justice and child protection settings. Buprenorphine (BPN) UDS testing is complex. Immunoassay often does not detect BPN and gas chromatography-mass spectrometry (GC-MS) is needed. A limited understanding of testing can negatively influence UDS interpretation and clinical decision making.Objectives: The primary aim was to determine detection rates of BPN in UDS in participants on BPN or buprenorphine/naloxone (BNX) treatment. The secondary aim was to identify if comorbidities, sex, co-prescribed medications, or dosing site and observation were associated with BPN detection.Setting: Public outpatient clinic in a specialist addiction treatment service.Design/participants: In this retrospective observational study, records of clients on supervised BPN/BNX treatment between September 2017 and 2018 were reviewed.Measures: Data extracted included UDS results, age, sex, indication for BPN, frequency of observed doses, dose of BPN, dosing site, co-morbid medical conditions, and medications.Results: One hundred and sixty-one medical records were reviewed. Ninety-seven (60 percent) underwent screening urine immunoassay. Of these 97, 51 (53 percent) had further GC-MS testing for BPN of which 22 (43 percent) did not detect BPN despite directly observed OAT. Co-prescription of medications known to interact with cytochrome P450 3A4 was associated with nondetection of BPN (p 0.05). No significant association between median dose, dosing site, and observed dosing and BPN detection was identified.Conclusion: Urine drug testing for BPN is complex. Failure to detect BPN does not betoken nonadherence to treatment and is associated with co-prescription of drugs interacting with cytochrome P450 3A4.
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