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Hyperammonemic encephalopathy (HE) refers to a clinical condition characterized by abrupt alteration in mental status (AMS) with markedly elevated plasma ammonia levels and frequently results in intractable coma and death. While hepatic cirrhosis is by far the most common etiology for hyperammonemia together with drugs such as valproic acid as well as urea cycle disorders, non-hepatic causes of hyperammonemia are rare and pose a clinical challenge. In this report, we describe a case of HE caused by obstructive urinary tract infection due to urease-producing bacteria in a 69-year-old man with two episodes of obstructive uropathy associated with AMS resolving with treatment with antibiotics and lactulose with normalization of ammonia level. We also provide a review of the literature with emphasis on the recognition of this serious entity of HE in the setting of obstructive uropathy to avoid the possible complications that include intractable coma and high mortality from this potentially treatable disorder.

Patients with systemic lupus erythematosus (SLE) and antiphospholipid antibody syndrome (APS) are at high risk of developing arterial or venous thromboembolism and a state of systemic hypercoagulability. Libman-Sacks endocarditis (LSE) is a type of non-bacterial endocarditis usually seen in patients with systemic lupus erythematosus and antiphospholipid antibody syndrome. These vegetations dislodge easily and can cause profound neurological and systemic complications in the form of emboli. We describe one such case of a young woman with known SLE who presented with an acute middle cerebral artery (MCA) stroke and was found to have APS with extensive mitral valve vegetation, indicating Libman-Sacks endocarditis on echocardiography. Recognizing the increasing frequency of both APS and LSE in patients with SLE and screening patients, especially the younger population with SLE, for APS is vital. Furthermore, in those patients presenting with embolic events, echocardiography plays a key role as it can help expedite the diagnosis of LSE. Our case report also reiterates that warfarin, when compared to direct oral anticoagulants (DOAC), is superior in decreasing future embolic events.Patients with systemic lupus erythematosus (SLE) and antiphospholipid antibody syndrome (APS) are at high risk of developing arterial or venous thromboembolism and a state of systemic hypercoagulability. Libman-Sacks endocarditis (LSE) is a type of non-bacterial endocarditis usually seen in patients with systemic lupus erythematosus and antiphospholipid antibody syndrome. These vegetations dislodge easily and can cause profound neurological and systemic complications in the form of emboli. We describe one such case of a young woman with known SLE who presented with an acute middle cerebral artery (MCA) stroke and was found to have APS with extensive mitral valve vegetation, indicating Libman-Sacks endocarditis on echocardiography. Recognizing the increasing frequency of both APS and LSE in patients with SLE and screening patients, especially the younger population with SLE, for APS is vital. Furthermore, in those patients presenting with embolic events, echocardiography plays a key role as it can help expedite the diagnosis of LSE. Our case report also reiterates that warfarin, when compared to direct oral anticoagulants (DOAC), is superior in decreasing future embolic events.

Brugada syndrome is an autosomal dominant channelopathy that usually affects healthy young males without apparent structural heart disease. It is associated with a spectrum of variable and dynamic clinical manifestations, high risk of life-threatening ventricular arrhythmias, and sudden cardiac death. Our patient demonstrated transient and dynamic EKG changes of both type 1 (coved) and type 2 (saddleback) ST elevation, suggestive of the Brugada pattern that was associated with physical chest trauma and stressful situations. While common triggers like fever and certain drugs are well-recognized, this case illustrates the potential for physical stress and trauma to unmask or aggravate Brugada syndrome, albeit without definitive evidence for a causal link. Ultimately, this report underscores the importance of considering a broad differential diagnosis, including Brugada syndrome, in patients presenting with unexplained syncope or characteristic EKG changes, even when traditional triggers are absent.

Tricuspid valve endocarditis is increasing in incidence owing to the prevalent use of intravenous substances. Although most patients respond well to intravenous antibiotics over the course of six weeks, some patients require surgical intervention. A multilayered approach to diagnosis with both transthoracic and transesophageal echocardiography (TEE) is recommended for optimal diagnosis and management. In this article, we report a case of septic shock resulting from tricuspid valve infective endocarditis in a young woman with a history of intravenous drug use who ultimately required cardiothoracic surgical intervention for tricuspid valve vegetation. The sensitivity and specificity of TEE for vegetation on the native valves are about 96% and 90%, respectively. Timely surgical intervention may increase the likelihood of tricuspid valve repair by preventing further destruction of leaflet tissue. Transthoracic echocardiogram (TTE) and TEE have complementary roles in the diagnosis and evaluation of endocarditis. With this case report, we emphasize the importance of multimodality imaging and early surgical intervention to prevent further embolism and destruction of tricuspid valve leaflet tissue.

There are a significant number of colonoscopies and esophagogastroduodenoscopies (EGDs) done in the United States every year and post-endoscopic infections are frequently seen. Data demonstrating causality between endoscopic procedures and infectious endocarditis (IE) or that antibiotic prophylaxis prior to endoscopic procedures protects against IE is still lacking. Here we have presented the case of a patient who underwent diagnostic colonoscopy as part of a malignancy workup and was later found to be septic with bacteremia and had IE. We hypothesized that the infection was most likely contracted during colonoscopy as a result of bacterial translocation from the perineal region to the bloodstream. This case report highlights the need for further studies investigating the efficacy of prophylactic antibiotics in reducing the risk of IE after colonoscopies.

Plasma cytokines are biomarkers of disease extent and mycobacterial burden in pulmonary tuberculosis (PTB). Whether chemokines can perform the same role in PTB is not known. We examined the plasma levels of chemokines in individuals with PTB, latent TB (LTB) or healthy controls (HC) and their association with disease severity and mycobacterial burdens in PTB. We also examined the chemokines in PTB individuals at the end of anti-tuberculous chemotherapy (ATT). PTB individuals exhibited significantly higher levels of CCL1, CCL3, CXCL1, CXCL2, CXCL9 and CXCL10 in comparison to LTB and/or HC individuals. PTB individuals with bilateral or cavitary disease displayed significantly elevated levels of CCL1, CCL3, CXCL1, CXCL10 and CXCL11 compared to those with unilateral or non-cavitary disease and also exhibited a significant positive relationship with bacterial burdens. In addition, PTB individuals with slower culture conversion displayed significantly elevated levels of CCL1, CCL3, CXCL1 and CXCL9 at the time of PTB diagnosis and prior to ATT. Finally, the chemokines were significantly reduced following successful ATT. Our data demonstrate that PTB is associated with elevated levels of chemokines, which are partially reversed followed chemotherapy. Our data demonstrate that chemokines are markers of disease severity, predicting increased bacterial burden and delayed culture conversion in PTB.

Background Ligands of the receptor for advanced glycation end products (RAGE) are key signalling molecules in the innate immune system but their role in tuberculosis-diabetes comorbidity (TB-DM) has not been investigated. Methods We examined the systemic levels of soluble RAGE (sRAGE), advanced glycation end products (AGE), S100A12 and high mobility group box 1 (HMGB1) in participants with either TB-DM, TB, DM or healthy controls (HC). Results Systemic levels of AGE, sRAGE and S100A12 were significantly elevated in TB-DM and DM in comparison to TB and HC. During follow up, AGE, sRAGE and S100A12 remained significantly elevated in TB-DM compared to TB at 2nd month and 6th month of anti-TB treatment (ATT). RAGE ligands were increased in TB-DM individuals with bilateral and cavitary disease. sRAGE and S100A12 correlated with glycated hemoglobin levels. Within the TB-DM group, those with known diabetes (KDM) revealed significantly increased levels of AGE and sRAGE compared to newly diagnosed DM (NDM). KDM participants on metformin treatment exhibited significantly diminished levels of AGE and sRAGE in comparison to those on non-metformin regimens. Conclusions Our data demonstrate that RAGE ligand levels reflect disease severity and extent in TB-DM, distinguish KDM from NDM and are modulated by metformin therapy.

Background Matrix metalloproteinases (MMPs) are considered to be key mediators of tuberculosis (TB) pathology but their role in tuberculosis – diabetes comorbidity (TB-DM) is not well understood. Methods To study the association of MMP levels with severity and extent of disease as well as bacterial burden in TB-DM, we examined the systemic levels of MMP-1, − 2, − 3, − 7, − 8, − 9, − 10, − 12 and − 13 in individuals with TB-DM and compared them to those with TB alone (TB) or healthy controls (HC). Results Circulating levels of MMP-1, − 2, − 3, − 7, − 10 and − 12 were significantly higher in TB-DM compared to both TB and HC and MMP -13 levels were higher in comparison to HC alone. To understand the effect of standard anti-tuberculosis therapy (ATT) on these MMP levels in TB-DM, we measured the levels of MMPs at the end of treatment (post-treatment). Our findings indicate that ATT is associated with a significant reduction in the levels of MMP-1, − 2, − 3, − 8 and − 13 post-treatment. Moreover, the levels of MMP-1, − 2, − 3, − 9 and − 12 were significantly higher in TB-DM individuals with cavitary disease and/or bilateral disease at baseline but not post-treatment. Similarly, the levels of MMP -1, − 2, − 3 and − 8 exhibited a significant positive relationship with bacterial burden and HbA1c levels at baseline but not post-treatment. Within the TB-DM group, those known to be diabetic before incident TB (KDM) exhibited significantly higher levels of MMP-1, − 2, − 10 and − 12 at baseline and of MMP-1 and -3 post-treatment compared to those newly diagnosed with DM (NDM). Finally, KDM individuals on metformin treatment exhibited significantly lower levels of MMP-1, − 2, − 3, − 7, − 9 and − 12 at baseline and of MMP-7 post-treatment. Conclusions Our data demonstrate that systemic MMP levels reflect baseline disease severity and extent in TB-DM, differentiate KDM from NDM and are modulated by ATT and metformin therapy.