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In virtue of precise clinical history, physical examinations, and biochemical/radiological investigations, pseudohypoparathyroidism can be effectively diagnosed, and its types can be differentiated even without exorbitant tests.
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Breast cancer is the most common malignancy affecting women worldwide, and early diagnosis of breast cancer is the key to its successful and effective treatment. Traditional imaging techniques such as mammography and ultrasound are used to detect and configure breast abnormalities; unfortunately, these modalities have low sensitivity and specificity, particularly in young patients with dense breast tissue, breast implants, or post-surgical scar/architecture distortions. Therefore, breast magnetic resonance imaging (MRI) has been superior in the characterization and detection of breast cancer, especially that with invasive features. This review article explores the importance of breast MRI in the early detection of invasive breast cancer versus traditional tools, including mammography and ultrasound, while also analyzing the use of MRI as a screening tool for high-risk women. We will also discuss the different MRI features for invasive ductal carcinoma and lobular carcinoma and the role of breast MRI in the detection of ductal carcinoma in situ with a focus on the utilization of new techniques, including MR spectroscopy and diffusion-weighted imaging.
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Acute ischemic stroke (AIS) patients arriving within a suitable time frame are treated with recanalization therapy i.e. intravenous thrombolysis (IVT) with alteplase and/or mechanical thrombectomy (MT). IVT with alteplase is indicated in AIS patients presenting within 4.5 hours of onset regardless of vascular territory involved. MT is indicated in AIS patients presenting within 24 hours of onset with large vessel occlusion in the anterior circulation. However, MT is ludicrously expensive and requires exorbitant setup, devices, and expertise which is not currently feasible in LMICs. Therefore, in LMICs the only feasible recanalization option left for AIS patients is IVT. The cost of IVT varies across the LMICs, however, most of them cost around 2000-5000 USD. Apart from IVT, patients with AIS often have other significant medical costs including those for neuroimaging, intensive care, and prolonged rehabilitative treatment. In LMICs, these costs can only be afforded by a handful of patients. The majority of the LMICs have health insurance in their infancy and family members of AIS patients opt-out IVT due to the economic burden. In general, the current treatment guidelines for AIS are not very useful in LMICs because of cost-related issues among several other factors. In this editorial, we discuss evidence for alternative treatment strategies that can help tackle the rising epidemic of AIS in poor countries by improvising on existing clinical guidelines and seeking alternative treatment regimens.
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Scrub typhus is endemic among farmers in the rural southern part of Nepal. It is grossly underdiagnosed due to a lack of clinical suspicion and inadequate testing facilities. The most common clinical features of the disease include fever, rashes, vomiting, myalgia, and eschar. The disease may present with ocular changes such as conjunctival injection, gastrointestinal features such as hepatitis and splenomegaly, acute kidney injury (AKI), or neurological findings in the form of meningoencephalitis. Herein, we present a report of three cases of scrub typhus from a rural part of South-west Nepal who failed to receive appropriate treatment initially. One of the patients recovered well with the treatment, the other developed AKI but recovered over the next few weeks. One of the patients died due to sepsis/multiorgan failure secondary to scrub typhus. While managing such cases in places with limited diagnostic facilities, the incorporation of early appropriate empirical therapy for scrub typhus after a careful clinical assessment prevents complications and saves lives.
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Cephalic tetanus is a rare clinical form of tetanus, clinically characterized by trismus and cranial nerve palsy involving one or more cranial nerves, facial nerve being the most common. We report a case of cephalic tetanus with left-sided lower motor facial nerve palsy in a 66-year-old non-immunized patient after an untreated laceration injury. The patient had dysphagia, spasm of the muscles of mastication, asymmetry of the left side of the face, cough, shortness of breath, and stiffness of neck muscles. The presentation was unique given that the facial nerve palsy appeared prior to the occurrence of trismus, which misled the initial diagnosis towards Bell's palsy. He was successfully treated with tetanus antitoxin without any adverse events. Although widespread use of tetanus vaccine has led to a dramatic decline in this fatal disease, sporadic disease occurrence is still possible, particularly in individuals without up-to-date vaccinations. In this case report we illustrate the importance of early recognition of cephalic tetanus prior to the development of the full clinical picture. The early initiation of therapy is the key to recovery from this deadly disease. Physicians are encouraged to include cephalic tetanus as a cause of facial nerve palsy in their differential. In particular, paying attention to cases manifesting early after head or neck injury.
Assuntos
Tétano/diagnóstico , Idoso , Antibacterianos/administração & dosagem , Armênia , Paralisia de Bell/diagnóstico , Diagnóstico Diferencial , Paralisia Facial/etiologia , Humanos , Masculino , Metronidazol/administração & dosagem , População Rural , Tétano/complicações , Tétano/tratamento farmacológico , Trismo/etiologiaRESUMO
Cryptococcal meningitis (CM) is mostly seen in immune-compromised patients and rarely occurs in immune-competent individuals. Immunocompetent individuals with CM present with indolent neurological disease and have better clinical outcomes after treatment. However, misdiagnosis is common and these patients may suffer from serious complications with high mortality.
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Transthyretin amyloid cardiomyopathy disease burden is increasing daily due to advancements in diagnostic and imaging modalities in the modern world. Tafamidis is one of many therapeutic options. The main objective of this review is to study the role of Tafamidis in slowing the progression of transthyretin cardiomyopathy (TTR-CM) by analyzing randomized controlled trials (RCTs) and non-RCTs of Tafamidis. We searched for published papers of Tafamidis in the English language in electronic databases like Google Scholar, PubMed, Cochrane Library, and PubMed Central. We imported the resulting articles from our search to Mendeley software. Four reviewers removed the duplicates and performed title and abstract screening of the articles. The same reviewers obtained the full-text of relevant articles and did full-text screening based on eligibility criteria. Finally, five reviewers performed a quality assessment of RCTs using the Cochrane risk of bias assessment and of non-RCTs by a checklist prepared by Downs and Black. Any disagreements about any process were resolved by a discussion with other authors. One RCT and five non-RCTs of Tafamidis were included in this systematic review. From the non-RCTs, stability was observed in different parameters like echocardiographic findings, cardiac biomarkers, and ECG in patients with transthyretin cardiomyopathy during the study duration with Tafamidis. ATTR-ACT (Tafamidis in Transthyretin Cardiomyopathy Clinical Trial) trial demonstrated reduction of cardiovascular events and all-cause mortality in the Tafamidis group in comparison to placebo. In both RCT and non-RCTs, Tafamidis was established as a safe and tolerable drug for patients with TTR-CM. Our study proved the role of Tafamidis in reducing cardiovascular events, all-cause mortality, and the progression of cardiac disease in TTR-CM patients. In addition to five non-RCTs, current evidence is based on the findings of only one RCT of Tafamidis. Hence, evidence from additional RCTs is required to strongly support the stability of parameters like echocardiographic findings, cardiac biomarkers, and ECG with Tafamidis use.
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Tularemia is a zoonotic infection caused by Francisella tularensis. Oropharyngeal tularemia, one of the several clinical forms of tularemia identified, is typically characterized by fever, sore throat, cervical buboes, and rarely, cutaneous lesions. Here we describe an uncommon clinical manifestation of oropharyngeal tularemia with erythema nodosum, an inflammatory condition that causes tender nodules to form on the lower legs. A 45-year-old woman with fever, sore throat, unilateral cervical buboes, and erythema nodosum on both legs was diagnosed with oropharyngeal tularemia based on clinical manifestations and positive latex agglutination testing. We prescribed a 14-day course of intramuscular streptomycin, which resulted in the complete recovery of the patient. It is unusual for tularemia to manifest with erythema nodosum as a primary symptom, particularly one that persists throughout the illness. Although the cause of erythema nodosum is unknown in nearly half of cases, it is important to identify or exclude possible infectious causes of this condition, including tuberculosis, Valley fever, cat scratch disease, and, as illustrated in the case described herein, tularemia.
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Diabetes mellitus (DM) is the most common chronic metabolic disease. Parkinson's disease (PD) is considered one of the most common neurodegenerative diseases. There are many similarities between both conditions. Both disorders are chronic diseases. Both diseases result from a decrease in a specific substance: dopamine in PD, and insulin in DM. Besides, both disorders arise due to the destruction of particular cells, dopaminergic cells in PD, and pancreatic beta-cell in DM. Recently, many epidemiological and experimental studies showed a connection between DM and PD. There are common underlying mechanisms in the pathophysiology of both diseases. These underlying mechanisms include mitochondrial dysfunction, oxidative stress, hyperglycemia, and inflammation. Insulin resistance is indeed the hallmark of DM, especially type 2 diabetes mellitus (T2DM), which plays a significant role in these pathophysiological and molecular mechanisms. Besides, many studies revealed that anti-diabetic drugs have a beneficial effect on PD. In this current literature review, we aim to explore the standard pathophysiological and molecular linkages between these two disorders as well as how DM could affect the incidence and progression of PD. We also review how anti-diabetic drugs impact PD. In the future, further experimental and expanded clinical studies are needed to fully understand the exact pathophysiological connections between the two disorders and the efficacy of insulin and other anti-diabetic drugs in the treatment of PD in diabetic patients. Fully understanding and targeting these pathophysiological and molecular links could result in de novo curative therapy for PD and DM.
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Stem cell therapy is emerging as a promising treatment strategy to treat patients with stroke. While there are established modes of treatment for stroke patients such as thrombolysis and endovascular intervention, most of the stroke patients frequently end up with major residual deficits or even death. The use of stem cells to treat stroke has been found to be beneficial in the animal models but strict evidence for the same in humans is still lacking. We reviewed 13 clinical trials of stem cell therapy in stroke patients conducted between 2014 and 2020 based on the search using the database PubMed, and the clinical trial registry (www.clinicaltrials.gov). We aimed to assess the safety and efficacy of stem cell treatment in stroke patients who participated in the trials. Quality assessment of the clinical trials revealed a sub-optimal score. We found mixed results regarding the efficacy of stem cells in the treatment of ischemic stroke although we could not do a quantitative analysis of the effect outcomes. Assessment for safety revealed promising results as there were only minor side effects related to cell therapy. Although stem cell therapy seems to be a promising strategy to treat stroke patients in the future, we concluded that the field needs more evidence regarding the safety and efficacy of the use of stem cells in stroke patients before we use them in the clinic.
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High altitude pulmonary edema (HAPE) occurs in individuals rapidly ascending at altitudes greater than 2,500 m within one week of arrival. HAPE is characterized by orthopnea, breathlessness at rest, cough, and pink frothy sputum. Several mechanisms to describe the pathophysiology of HAPE have been proposed in different kinds of literature where most of the mechanisms are reported to be activated before a drop in oxygen saturation levels. The majority of the current studies favor diffuse hypoxic pulmonary vasoconstriction (HPV) as a pathophysiological basis for HAPE. However, some of the studies described inflammation in the lungs and genetic basis as the pathophysiology of HAPE. So, there is a major disagreement regarding the exact pathophysiology of HAPE in the current literature, which raises a question as to what is the exact pathophysiology of HAPE. So, we reviewed 23 different articles which include clinical trials, review articles, randomized controlled trials (RCTs), and original research published from 2010 to 2020 to find out widely accepted pathophysiology of HAPE. In our study, we found out sympathetic stimulation, reduced nitric oxide (NO) bioavailability, increased endothelin, increased pulmonary artery systolic pressure (PASP) resulting in diffuse HPV, and reduced reabsorption of interstitial fluid to be the most important determinants for the development of HAPE. Similarly, with the evaluation of the role of inflammatory mediators like C-reactive protein (CRP) and interleukin (IL-6), we found out that inflammation in the lungs seems to modulate but not cause the process of development of HAPE. Genetic basis as evidenced by increased transcription of certain gene products seems to be another promising hypoxic change leading to HAPE. However, comprehensive studies are still needed to decipher the pathophysiology of HAPE in greater detail.