PurposeTo determine the efficacy of mitomycin C in reducing the recurrence of anterior urethral stricture after internal optical urethrotomy (IOU).Materials and MethodsThis was a randomized controlled trial conducted in the Department of Urology at the Institute of Kidney Diseases Peshawar from March 2011 to December 2013. A total of 151 patients who completed the study were divided into two groups by the lottery method. Group A (cases) comprised 78 patients in whom mitomycin C 0.1% was injected submucosally in the stricture after conventional IOU. Group B (controls) comprised 73 patients in whom IOU only was performed. Self-clean intermittent catheterization was not offered in either group. All patients were regularly followed up for 18 months. Recurrence was diagnosed by use of retrograde urethrogram in all patients and flexible urethroscopy in selected cases. Data were collected on a structured pro forma sheet and were analyzed by SPSS.ResultsThe mean age of the patients in group A was 37.31±10.1 years and that in group B was 40.1±11.4 years. Recurrence of urethral stricture was recorded in 11 patients (14.1%) in group A and in 27 patients (36.9%) in group B (p=0.002). The mitomycin group also showed a delay in recurrence compared with the control group (p=0.002).ConclusionsRecurrence of urethral stricture is high after optical urethrotomy. Mitomycin C was found to be highly effective in preventing the recurrence of urethral stricture after IOU.
Background and AimTo investigate the quality of and reasons for referrals of patients with likely functional gastrointestinal disorders (FGID) and explore patients’ experience of clinical management.MethodsA cross sectional, mixed‐methods study was undertaken. Referrals (July 2013–2015) to one gastroenterology outpatient department triaged as “likely FGID”, the referred patients and their referring primary healthcare providers were examined.ResultsA total of 69% of patients reported not yet receiving an initial diagnosis, 52% reported persistent/distressing symptoms or reduced quality of life, 24% feared missed or worsening pathology, and 35% were seeking repeat specialist consultation. Most patients were dissatisfied (40%) or only partially satisfied (36%) with current management. Dissatisfaction was significantly related to the lack of provision of a diagnosis and effective treatment options (P < 0.001). Referral quality was poor and with the reason for referral clearly communicated in only 25%. Common referral reasons included repeat presentations (n = 32), diagnostic uncertainty (n = 19), to ensure nothing is missed (n = 19), patient request (n = 17), no response to treatment (n = 16), and to allay patient fears (n = 14). A total of 28/60 primary healthcare providers were confident that their patient had a FGID, yet sought confirmation (n = 16), second opinion (n = 8), or advice (n = 4).ConclusionCurrent management of FGID in usual care is suboptimal, as evidenced by the tertiary referral load, patient dissatisfaction, and the lack of provision of diagnoses and effective treatment options. Some clinicians lack confidence in effectively identifying and managing these conditions. Resources and supports to equip and assist clinicians to identify and manage FGID successfully may enhance patient care.
ObjectivesTo evaluate the role of apolipoprotein(Apo A-1) as a biomarker of coronary artery disease (CAD) and its comparison with the traditional marker high-density lipoprotein (HDL).MethodologyOne hundred patients proven to have coronary artery disease by angiography were recruited and their serum biomarkers were compared with 100 normal individuals adjusted for age and sex.ResultThe mean +/-standard deviation (SD) value of plasma Apo A-1 levels in the normal individuals were observed to be 207.42 +/- 41.35 (mg/dL) against 90.69 +/- 20.77 (mg/dL) in the cardiac patients. On the other hand the serum HDL levels were 52.93 +/-33.58 (mg/dL) in the normal individuals and 37.86 +/- 23.19 (mg/dL) in the cardiac patients. Both of these differences were statistically significant (p < 0.001). For Apo A-1, a large proportion of patients (85%) were found to be in the abnormal range when compared to the control group in which only 7% had an abnormal value. For HDL, a majority (70%) of the cardiac patients had abnormal values while 40% of the normal individuals also had abnormal values. The sensitivity of Apo A-1 for detecting CAD was 85%, while for HDL, it was only 69%. Similarly, the specificity of Apo A-1 for detecting CAD was 93%, while for HDL, it was 60%. When plotted on a receiver operating characteristic (ROC) curve, Apo A-1 had a much larger area under the curve when compared to HDL.ConclusionThis study suggests that Apo A-1 may, in fact, be more sensitive than HDL as a predictor of CAD. However, to completely elucidate its role as a biomarker, to set target serum levels and to increase its clinical use, further studies are required.
Gitelman syndrome is one of the few inherited causes of metabolic alkalosis due to salt losing tubulopathy. It is caused by tubular defects at the level of distal convoluted tubules, mimicking a thiazide-like tumor. It usually presents in late childhood or in teenage as nonspecific weakness, fatigability, polyuria, and polydipsia but very rarely with seizures. It is classically associated with hypokalemia, hypomagnesemia, hypocalciuria, hyperreninemia, and hyperaldosteronism. However, less frequently, it can present with normal magnesium levels. It is even rarer to find normomagnesemic patients of GS who develop seizures as the main complication since hypomagnesemia is considered the principal etiology of abnormal foci of seizure-related brain activity in GS cases. Interestingly, patients with GS are oftentimes diagnosed during pregnancy when the classic electrolyte pattern consistent with GS is noticed. Our case presents GS with normal serum magnesium in a patient, with seizures being the main clinical presentation. We also did a comprehensive literature review of 122 reported cases to show the prevalence of normal magnesium in GS cases and an overview of clinical and biochemical variability in GS. We suggest that further studies and in-depth analysis are required to understand the pathophysiology of seizures in GS patients with both normal and low magnesium levels.
Haemophagocytic lymphohistiocytosis (HLH) is a potentially fatal syndrome that is caused by an abnormal activation of the immune system. It can present as the primary syndrome or occur secondary to a variety of conditions such as malignancy, autoimmune diseases and infections. We present a case of a man who developed HLH secondary to Plasmodium vivax infection. He presented with symptoms of fever, chills and myalgias. Physical examination revealed significant hepatosplenomegaly. The presence of pancytopaenia, elevated ferritin levels and haemophagocytosis on bone marrow biopsy confirmed the diagnosis of HLH (based on HLH-2004 criteria). There was a significant improvement after the initiation of intravenous antimalarials. No relapses were documented on follow-up. It is imperative that physicians should promptly recognise and treat this rare condition, as a timely intervention can be lifesaving.
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