Valproic acid (VPA), an antiepileptic medication, is known to cause hyperammonemia, which may be asymptomatic or can present with encephalopathy. VPA-induced hyperammonemic encephalopathy (VHE) is a serious but reversible condition, which requires high clinical suspicion for diagnosis. It may occur acutely or after chronic use of VPA. We present the case of a 44-year-old male who was on long-term VPA therapy for a seizure disorder. He presented to the emergency department with the complaint of two episodes of seizures two days before admission. On arrival, the patient was confused and tearful and was unable to recollect the events leading to the seizure. The initial complete metabolic panel, liver function tests, urinalysis, and serum VPA levels were observed to be normal. However, there was a marked elevation in ammonia levels. VPA was suspected to be the inciting agent of hyperammonemic encephalopathy, and, therefore, it was discontinued. The patient was started on oral lactulose and prescribed a different antiseizure medication (i.e., lamotrigine). His ammonia levels decreased gradually, and his condition improved. Thus, it was concluded that the patient had developed VHE. At the time of discharge, he was stable and had no confusion or seizures. This case report evaluates his presentation and discusses the possible pathogenesis of VHE.
Background: Biliary calculi are one of the most common problems affecting the digestive tract. Need for the study is to evaluate age, sex, incidence, most common etiopathological factors for the formation of biliary calculi and to illustrate varying clinical presentation with various modes of management adopted in the institution as well as to analyse biochemical types of stones prevalent in the region.Methods: A prospective study of 50 patients with clinical diagnosis of biliary colic was conducted in a tertiary center for a period of one year. Clinical presentation, etiology, and management of biliary calculi were studied.Results: Biliary calculi affect most commonly in fourth to the fifth decade with a higher preponderance in females (72%). Right hypochondriac pain is the commonest presentation (84%). Ultrasonography is sensitive and specific, and hence considered the investigation of choice. Open surgical procedures such as cholecystectomy, choledochotomy with T-tube drainage, choledochoduodenostomy were done in these subjects. Postoperative complications such as wound infection noted in 8% of the subjects. Most of the histopathological specimens (90%) revealed chronic cholecystitis.Conclusions: Biliary calculus disease is multifactorial in origin with slight female preponderance. The most common presentation is a right hypochondriac pain. This can be diagnosed accurately with the aid of ultrasonography and Endoscopic Retrograde Cholangio-pancreatography. Biliary calculus is managed according to the location of the calculus, whether intrahepatic or extrahepatic. Most of the patients presented with chronic cholecystitis.
Purpose: Viral infections had been historically observed in chronic disease development and complications including although not limited to hepatitis C, influenza A, cytomegalovirus (CMV), Epstein bar virus (EBV), HIV and herpes simplex. Epidemiologic data had implicated CMV, herpes simplex and hepatitis C in type II diabetes (T2D). With the observed increased incidence T2D in COVID-19 among children and adults, this review aimed to examine scientific literature on immune and endocrine systems dysregulation in T2D and pancreatic neoplasm. Materials & Method: A qualitative systematic review (QSR) was utilized in assessing the immune system deregulation and endocrine system involvement in chronic disease development such as T2D. The PubMed was the main search engine in studies identification with several search terms such as “SARS-CoV-2 and T2D”, “COVID-19 and T2D”, SARS-CoV-2 and insulin resistant”, etc. Results: Viral pathogens such as CMV, influenza A, and herpes simplex and hepatitis C infections have been implicated in decreased insulin sensitivity (IS) and increased insulin resistant (IR). Similarly, these pathogenic microbes increased the T2D incidence and complications. SARS-CoV-2 a COVID-19 causative pathogen had been observed in increased risk and incidence of T2D among children and adults. While data are not currently available on the precise mechanistic process, SARS-CoV-2 viral infection in T2D incidence may be explained by excess pro-inflammatory cytokines elaboration (cytokine storm) resulting in increased IR and decreased IS, leading to glucose intolerance and T2D. Further COVID-19 may increase pancreatic neoplasm in populations with increased incidence of COVID-19, due to pancreatic beta cells and insulin receptors dysregulation and cellular dysfunctionality as abnormal cellular proliferation. Conclusions/Recommendation: SARS-CoV-2 a causative pathogen in COVID-19 morbidity is associated with increased incidence of T2D, which is explained in part by immune and endocrine system integration dysregulation, resulting in cytokine storm, decreased IS and increased IR, implying glucose intolerance and T2D. Additionally this pathogenic microbe may result in increasing incidence of pancreatic neoplasm, a malignant neoplasm with the worst prognosis and excess mortality due to late stage at diagnosis and marginalized biomarkers of susceptibility and morbidity.
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