Stroke epidemiology and outcomes of stroke patients in Nepal: a systematic review and meta-analysis.

BACKGROUND: With an increasing burden of stroke, it is essential to minimize the incidence of stroke and improve stroke care by emphasizing areas that bring out the maximum impact. The care situation remains unclear in the absence of a national stroke care registry and a lack of structured hospital-based data monitoring. We conducted this systematic review and meta-analysis to assess the status of stroke care in Nepal and identify areas that need dedicated improvement in stroke care. METHODS: A systematic literature review was conducted to identify all studies on stroke epidemiology or stroke care published between 2000 and 2020 in Nepal. Data analysis was done with Statistical Package for Social Sciences (SPSS) and Comprehensive Meta-analysis (CMA-3). RESULTS: We identified 2533 studies after database searching, and 55 were included in quantitative and narrative synthesis. All analyses were done in tertiary care settings in densely populated central parts of Nepal. Ischemic stroke was more frequent (70.87%) than hemorrhagic (26.79%), and the mean age of stroke patients was 62,9 years. Mortality occurred in 16.9% (13-21.7%), thrombolysis was performed in 2.39% of patients, and no studies described thrombectomy or stroke unit care. CONCLUSION: The provision of stroke care in Nepal needs to catch up to international standards, and our systematic review demonstrated the need to improve access to quality stroke care. Dedicated studies on establishing stroke care units, prevention, rehabilitation, and studies on lower levels of care or remote regions are required.

Recent trends in cyclic vomiting syndrome-associated hospitalisations with liberalisation of cannabis use in the state of Colorado.

BACKGROUND: Currently, 33 states in the United States along with the District of Columbia have legalised cannabis in some forms. There is a paucity of data on the impact of legalisation of cannabis use on hospitalisations due to cyclic vomiting syndrome (CVS). AIM: To study the trends in CVS-related hospitalisations and cannabis use in CVS in relation to legalisation of recreational cannabis use in Colorado. METHODS: All hospital admissions in Colorado between 2010 and 2014 with the diagnosis of CVS were identified using the Colorado State Inpatient Database. Five-year trends in CVS-related hospitalisations along with the cannabis use were analysed. Multivariate logistic regression analysis was performed to determine predictors of cannabis use in CVS. RESULTS: There was a significant increase in CVS-related hospitalisations by 46% from 806 in 2010 to 1180 in 2014 when CVS was included as all-listed diagnoses (P < 0.001). The overall prevalence of cannabis use in CVS (13% with CVS as primary diagnosis and 17% with CVS as all-listed diagnoses) was much higher than non-CVS-related hospitalisations (1.7%) (P < 0.001 for both comparisons). Cannabis use increased dramatically in both CVS and non-CVS-related hospitalisations following legalisation of cannabis for recreational use in 2012. CONCLUSION: Our study shows a significant increase in CVS-related hospitalisations concomitant with an increase in cannabis use with its liberalisation in Colorado. Future studies on the relationship between cannabis use and hyperemesis are warranted, especially with its ongoing legalisation in the United States.

Cyclic vomiting syndrome: epidemiology, diagnosis, and treatment.

Cyclic-vomiting syndrome (CVS) is a chronic functional gastrointestinal disorder characterized by recurrent episodes of nausea and vomiting. Although once thought to be a pediatric disorder, there has been a considerable increase in recognition of CVS in adults. The exact pathogenesis is unknown and several theories have been proposed. Migraine and CVS share a similar pathophysiology as suggested by several studies. Since there are no specific biomarkers available for this disorder, physicians should rely on Rome criteria for the diagnosis. Due to the lack of randomized control trials, the treatment of CVS is primarily empirical.

Risk, Outcomes, and Predictors of Clostridium difficile Infection in Lymphoma: A Nationwide Study.

OBJECTIVE: The risk of Clostridium difficile infection (CDI) has not been well studied in patients with lymphoma. We thus sought to determine the risk of CDI in hospitalizations with lymphoma along with its trend, outcomes, and predictors using a large database. METHODS: Hospital discharge data from the Nationwide Inpatient Sample (NIS) from 2007 to 2011 were used for the study. Using the International Classification of Diseases, Ninth Revision, Clinical Modification codes, all adult patients aged 18 years or older having a primary diagnosis of lymphoma were queried for the presence of CDI as any of the secondary diagnoses. The risk of CDI in lymphoma and its yearly trend were assessed. We performed multivariate logistic regression to determine the independent risk factors of CDI in lymphoma. Furthermore, we studied mortality and other adverse outcomes of CDI in patients with lymphoma. RESULTS: There were 236,312 discharges (weighted) with the primary diagnosis of lymphoma. CDI was present in 2.13% of patients with lymphoma versus 0.8% in the nonlymphoma group (P < 0.001). On multivariate analysis, the significant predictors of CDI in lymphoma were presence of infection (odds ratio [OR] 3.1, 95% confidence interval [CI] 2.7-3.6), stem cell transplant (OR 2.7, 95% CI 2.3-3.4), graft-versus-host disease (OR 1.9, 95% CI 1.4-2.8), race (Asian vs white, OR 1.6, 95% CI 1.1-2.4), chemotherapy (OR 1.6, 95% CI 1.4-1.8), gastrointestinal surgery (OR 1.4, 95% CI 1.2-1.7), and Charlson Comorbidity Index (CCI) (CCI of 2 vs 0-1: OR 1.2, 95% CI 1.1-1.4; CCI of 3 vs 0-1: OR 1.3, 95% CI 1.03-1.6). CDI in lymphoma was associated with worse hospital outcomes such as increased mortality (17% vs 8%), increased length of stay (23.6 vs 9.9 days), mean total hospital charges ($197,015 vs $79,392), rate of intubation (13% vs 4% vs 13%), and rate of total parenteral nutrition (11% vs 3%). CONCLUSIONS: Hospitalization with lymphoma was associated with an increased risk of CDI. The significant predictors for CDI in lymphoma were infection, stem cell transplant, graft-versus-host disease, race, chemotherapy, gastrointestinal surgery, and Charlson Comorbidity Index. CDI in lymphoma was associated with increased mortality and other adverse outcomes warranting a need of more vigilance for CDI in patients with lymphoma.

A Case of Optic Neuritis Secondary to Lyme Disease.

INTRODUCTION: Optic neuritis is a condition associated with various systemic diseases, such as multiple sclerosis, and is also considered a rare complication of Lyme disease. CASE: A 46-year-old white woman presented with sudden onset of bilateral vision loss. After extensive workup, she was diagnosed with Lyme optic neuritis based on the clinical presentation and positive serology. She was treated with doxycycline for 2 weeks. DISCUSSION: Lyme disease is caused by infection with the spirochete Borrelia burgdorferi. The most commonly affected areas include the skin, joints, heart, and nervous system. Lyme optic neuritis is a challenging diagnosis and therefore often underreported. Doxycycline or ceftriaxone for 2 weeks are recommended for treatment. CONCLUSION: We report this case to increase awareness among clinicians to include Lyme disease in the differential diagnosis of optic neuritis for unexplained cases of vision loss, particularly in Lyme endemic areas.

Treatment of bile acid amidation defects with glycocholic acid.

UNLABELLED: Bile acid amidation defects were predicted to present with fat/fat soluble vitamin malabsorption with minimal cholestasis. We identified and treated five patients (one male, four females) from four families with defective bile acid amidation due to a genetically confirmed deficiency in bile acid CoA:amino acid N-acyl transferase (BAAT) with the conjugated bile acid, glycocholic acid (GCA). Fast atom bombardment-mass spectrometry analysis of urine and bile at baseline revealed predominantly unconjugated cholic acid and absence of the usual glycine and taurine conjugated primary bile acids. Treatment with 15 mg/kg GCA resulted in total duodenal bile acid concentrations of 23.3 ± 19.1 mmol/L (mean ± SD) and 63.5 ± 4.0% of the bile acids were secreted in bile in the conjugated form, of which GCA represented 59.6 ± 9.3% of the total biliary bile acids. Unconjugated cholic acid continued to be present in high concentrations in bile because of partial intestinal deconjugation of orally administered GCA. Serum total bile acid concentrations did not significantly differ between pretreatment and posttreatment samples and serum contained predominantly unconjugated cholic acid. These findings confirmed efficient intestinal absorption, hepatic extraction, and biliary secretion of the administered GCA. Oral tolerance tests for vitamin D2 (1,000 IU vitamin D2/kg) and tocopherol (100 IU/kg tocopherol acetate) demonstrated improvement in fat-soluble vitamin absorption after GCA treatment. Growth improved in 3/3 growth-delayed prepubertal patients. CONCLUSION: Oral glycocholic acid therapy is safe and effective in improving growth and fat-soluble vitamin absorption in children and adolescents with inborn errors of bile acid metabolism due to amidation defects.

Tandem mass spectrometric determination of atypical 3ß-hydroxy-Δ5-bile acids in patients with 3ß-hydroxy-Δ5-C27-steroid oxidoreductase deficiency: application to diagnosis and monitoring of bile acid therapeutic response.

BACKGROUND: 3ß-Hydroxy-Δ(5)-C27-steroid oxidoreductase (HSD3B7) deficiency, a progressive cholestatic liver disease, is the most common genetic defect in bile acid synthesis. Early diagnosis is important because patients respond to oral primary bile acid therapy, which targets the negative feedback regulation for bile acid synthesis to reduce the production of hepatotoxic 3ß-hydroxy-Δ(5)-bile acids. These atypical bile acids are highly labile and difficult to accurately measure, yet a method for accurate determination of 3ß-hydroxy-Δ(5)-bile acid sulfates is critical for dose titration and monitoring response to therapy. METHODS: We describe a electrospray ionization LC-MS/MS method for the direct measurement of atypical 3ß-hydroxy-Δ(5)-bile acid sulfates in urine from patients with HSD3B7 deficiency that overcomes the deficiencies of previously used GC-MS methods. RESULTS: Separation of sulfated 3ß-hydroxy-Δ(5)-bile acids was achieved by reversed-phase HPLC in a 12-min analytical run. The mean (SE) urinary concentration of the total 3ß-sulfated-Δ(5)-cholenoic acids in patients with HSD3B7 deficiency was 4650 (1711) µmol/L, approximately 1000-fold higher than in noncholestatic and cholestatic patients with intact primary bile acid synthesis. GC-MS was not reliable for measuring 3ß-hydroxy-Δ(5)-bile acid sulfates; however, direct analysis of urine by fast atom bombardment mass spectrometry yielded meaningful semiquantitative assessment of urinary excretion. CONCLUSIONS: The tandem mass spectrometry method described here for the measurement of 3ß-hydroxy-Δ(5)-bile acid sulfates in urine can be applied to the diagnosis and accurate monitoring of responses to primary bile acid therapy in HSD3B7 patients.

Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency.

BACKGROUND & AIMS: The final step in bile acid synthesis involves conjugation with glycine and taurine, which promotes a high intraluminal micellar concentration to facilitate lipid absorption. We investigated the clinical, biochemical, molecular, and morphologic features of a genetic defect in bile acid conjugation in 10 pediatric patients with fat-soluble vitamin deficiency, some with growth failure or transient neonatal cholestatic hepatitis. METHODS: We identified the genetic defect that causes this disorder using mass spectrometry analysis of urine, bile, and serum samples and sequence analysis of the genes encoding bile acid-CoA:amino acid N-acyltransferase (BAAT) and bile acid-CoA ligase (SLC27A5). RESULTS: Levels of urinary bile acids were increased (432 ± 248 µmol/L) and predominantly excreted in unconjugated forms (79.4% ± 3.9%) and as sulfates and glucuronides. Glycine or taurine conjugates were absent in the urine, bile, and serum. Unconjugated bile acids accounted for 95.7% ± 5.8% of the bile acids in duodenal bile, with cholic acid accounting for 82.4% ± 5.5% of the total. Duodenal bile acid concentrations were 12.1 ± 5.9 mmol/L, which is too low for efficient lipid absorption. The biochemical profile was consistent with defective bile acid amidation. Molecular analysis of BAAT confirmed 4 different homozygous mutations in 8 patients tested. CONCLUSIONS: Based on a study of 10 pediatric patients, genetic defects that disrupt bile acid amidation cause fat-soluble vitamin deficiency and growth failure, indicating the importance of bile acid conjugation in lipid absorption. Some patients developed liver disease with features of a cholangiopathy. These findings indicate that patients with idiopathic neonatal cholestasis or later onset of unexplained fat-soluble vitamin deficiency should be screened for defects in bile acid conjugation.

Follmann Balanitis: An Unusual Case of Syphilis.

A 33-year-old man presented with suprapubic abdominal pain and small vesicular lesions on the foreskin of the penis. Based on the presentation, he was empirically treated for genital herpes, although the herpes simplex virus swab was negative. He returned to the emergency department 4 months after his initial presentation with worsening symptoms that were consistent with balanoposthitis and cystitis. He was tachycardic and febrile on presentation. He denied any sexual contact for the last 3 months, with previous negative screening tests for sexually transmitted infections. Syphilis was eventually diagnosed during this admission. The incidence rates of syphilis have increased in recent years, and the infection is often undiagnosed given atypical manifestations. Here we present an atypical manifestation of syphilis that was initially misdiagnosed as herpes simplex virus.

Vitamin B12 deficiency presenting as neck pain and cervical radiculopathy.

Vitamin B12 is required for the formation of haematopoietic cells and the synthesis of myelin. Deficiency typically presents with fatigue and megaloblastic anaemia. Prolonged deficiency can cause neurological symptoms such as paresthesia, which can progress to subacute combined degeneration of the spinal cord. We describe an unusual presentation of B12 deficiency in a young man who was initially diagnosed and treated for cervical radiculopathy. This case highlights the challenges of diagnosing B12 deficiency in patients with neurologic but without haematologic, abnormalities. While the current incidence of B12 deficiency in developed countries is low, cases are likely to rise with the increased adoption of veganism. Clinicians should be aware of the variable presentations of B12 deficiency because delayed diagnosis and treatment increases morbidity and can cause irreversible neurological deficits.

Severe Thrombocytopenia in Decompensated Liver Disease: An Example of Accelerated Intravascular Coagulation and Fibrinolysis.

INTRODUCTION: Advanced liver disease can present with severe thrombocytopenia that can be difficult to delineate and manage. Here we describe a unique entity of accelerated intravascular coagulation and fibrinolysis (AICF) in a patient with decompensated liver disease. CASE PRESENTATION: A 56-year-old male with a history of alcoholic cirrhosis was admitted for weakness, nausea, metabolic derangement, and acute kidney injury determined to be secondary to decompensated liver disease. During admission, his platelet count declined to <10 000/µL requiring 8 total platelet transfusions. Laboratory and clinical evaluation supported a diagnosis of AICF, and the patient gradually improved with supportive management. DISCUSSION: AICF can present similarly to disseminated intravascular coagulation, and careful evaluation of specific laboratory values is required for accurate diagnosis. Appropriate management minimizes the associated increased risk of bleeding and prevents delay in procedural intervention. CONCLUSIONS: This case highlights the importance of early clinical and laboratory correlation, multidisciplinary care, and supportive treatment in the management of AICF.

Interaction of Semaglutide and Ziprasidone in a Patient With Schizophrenia: A Case Report.

Semaglutide (Ozempic), a GLP-1 receptor agonist effective in weight management, and ziprasidone (Geodon), an antipsychotic with a lower risk of metabolic side effects, are well-established in treating type 2 diabetes and schizophrenia, respectively. However, their interactions and effects on psychiatric symptoms are less understood. In this study, we report a case of a 43-year-old male with schizophrenia and diabetes with exacerbated paranoid delusions upon semaglutide administration for weight loss; symptoms peaked at higher doses and subsided after dose reduction. Concurrently, serum ziprasidone levels were significantly elevated at the dose reduction, suggesting a pharmacokinetic interaction likely due to semaglutide-induced slowed gastric emptying affecting ziprasidone's absorption and metabolism. This study illustrates the need for careful monitoring of psychiatric symptoms and drug levels when these medications are used together. Additionally, further research into their interactions to optimize treatment for patients with coexisting metabolic and psychiatric conditions is warranted.

Olmesartan-Induced Enteropathy: A Case Report.

Patients with olmesartan-induced enteropathy, a rare illness, frequently endure prolonged diarrhea and weight loss with no apparent cause. Because this adverse event's clinical and histological characteristics mimic those of other small intestine illnesses, it can be challenging to recognize it in a timely manner. We report a case of olmesartan-induced enteropathy in a 58-year-old male who had been on olmesartan for several years. Recently, during his travel to Greece, he developed diarrhea lasting several weeks. This was accompanied by a significant weight loss of 35 lbs, acute kidney injury, and hypokalemia. Extensive negative workup, including esophagogastroduodenoscopy (EGD) with normal biopsy of esophagus, stomach, duodenum, and terminal ileum, and colonoscopy with biopsies, autoimmune serologies, and infectious disease workup, led to a diagnosis of olmesartan-induced enteropathy as a diagnosis of exclusion. Diarrhea improved/resolved within a few days after stopping olmesartan in our patient.

Unusual Presentation of Disseminated Histoplasmosis in an Immunocompetent Host.

Histoplasmosis, a fungal infection caused by the inhalation of Histoplasma capsulatum conidia spores, has been shown to cause disseminated disease in immunocompromised individuals. Disseminated histoplasmosis manifests as multi-system involvement including pulmonary and/or neurological disease. Imaging findings, such as pulmonary focal infiltrates, cavitary nodules, mediastinal, and hilar lymphadenopathy, are common. Here, we report a rare case of disseminated histoplasmosis in a 58-year-old immunocompetent male with no occupational exposure. This patient presented with primary adrenal insufficiency, and a subsequent CT-guided biopsy of the adrenal gland was performed and revealed numerous spores containing Histoplasma capsulatum. This patient also suffered from numerous pulmonary and neurological derangements, which are likely sequelae of the disseminated fungal infection. Ultimately, the patient succumbed to their illness and died. Preventing such outcomes relies on early detection and prompt management, which are crucial in treating disseminated histoplasmosis. Increased awareness of atypical presentations can enhance patient outcomes and alleviate the impact of this severe fungal infection. This case not only underscores the importance of considering disseminated histoplasmosis in an immunocompetent patient presenting with unexplained weight loss and adrenal insufficiency but also contributes to the limited literature on disseminated histoplasmosis in immunocompetent individuals.

Babesiosis: An Atypical Cause of Respiratory Failure.

Babesiosis is a parasitic infection of the Babesia protozoa, which has been increasing in incidence in endemic areas of the United States. Symptoms of babesiosis can occur on a wide spectrum, from a mild flu-like illness to a fulminant disease course. Known complications of severe cases include intravascular hemolytic anemia and may involve the coagulation system, heart, spleen, kidneys, and in some cases, the lungs. This case report describes an 81-year-old, asplenic female in northern Wisconsin who presented to a hospital with shortness of breath and a non-productive cough. Definitive diagnosis of babesiosis, which was made through both a nucleic acid panel and blood smear, was initially delayed given the rare pulmonary manifestation of babesiosis. When the lungs are involved in the disease course, non-cardiogenic pulmonary edema leading to acute respiratory distress syndrome is among the most commonly seen complications. The pathophysiology of pulmonary involvement has not been made entirely clear but is most likely multifactorial, including the sequelae of changes to both the patient's red blood cells and pulmonary vasculature. This report highlights that atypical tick-borne illnesses like babesiosis should be considered as a cause of acute respiratory failure, particularly in the setting of sepsis and fever. The threshold for parasitic testing should be low in patients in endemic regions with risk factors, including increased age and history of asplenia, as babesiosis frequently has no localizing symptoms to suggest a protozoan infection. As babesiosis incidence continues to rise, prompt diagnosis and proper treatment can prevent severe complications and death in patients.

Legionella-Induced Hepatitis: A Case Report.

Legionnaires' disease is caused by a potentially life-threatening infection with the opportunistic Gram-negative bacilli species Legionella pneumophila, which is transmitted via inhalation or aspiration of water droplets. Legionnaires' commonly presents as atypical community-acquired pneumonia with accompanying diarrhea. Although hepatic and renal involvement are relatively uncommon, in this report, we present a case of Legionella pneumonia with acute hepatitis.

Crohn's Disease Initially Presenting With Anterior Sclerouveitis.

This report examines the case of a 32-year-old male who initially presented with symptoms of eye pain, redness, and vision changes, and was subsequently diagnosed with anterior sclerouveitis. One week after his initial visit, the patient presented to the emergency department (ED) with daily bloody stools and left lower quadrant (LLQ) pain. Further workup and examination revealed a diagnosis of Crohn's disease. This report expands on ocular manifestations of Crohn's disease and touches on the importance of early gastrointestinal examination in patients who present with ocular symptoms.

Post-embolization Syndrome Following Yttrium-90 Radiation Segmentectomy.

Post-embolization syndrome (PES) is a complication that commonly occurs after treatment with transarterial embolization for hepatocellular carcinoma (HCC). Patients with PES often present with clinical symptoms such as fever, nausea, abdominal pain, and elevated liver enzymes typically 24-72 hours after the procedure. While cases of PES have been documented in patients treated with transarterial chemoembolization, here, we present an unusual case of delayed onset PES in a 70-year-old male with HCC following treatment with a form of transarterial radioembolization.