Strongyloidiasis Mimicking Carcinoid Syndrome in an Immunocompetent Host.

Strongyloidiasis is a parasitic infection caused by Strongyloides stercoralis which commonly presents as an asymptomatic infection in immunocompetent patients but may cause non-specific gastrointestinal and pulmonary complaints. Here, we report the atypical presentation of strongyloidiasis in a 72-year-old Vietnamese male with shortness of breath and flushing. This case is notable for the unique presentation of cutaneous flushing, the absence of eosinophilia, and negligible microscopic findings on stool examination. Despite insignificant laboratory findings, clinicians should consider strongyloidiasis in patients from endemic areas with unexplained gastrointestinal and pulmonary findings.

Multiple Thrombotic, Infectious, and Cardiopulmonary Complications Following Laparoscopic Converted to Open Colectomy Procedure: A Case Report and Literature Review.

All surgeries, from minor procedures, such as sutures, to major surgeries, such as open abdominal surgery, carry with them risk for complications. Among the most frequently encountered complications are surgical site infections and thrombotic complications. Less frequently, cardiac complications such as atrial fibrillation are seen. In this case report, we discuss the various complications encountered during the hospital stay of a 61-year-old male following a laparoscopic converted to open colectomy procedure for the treatment of a colorectal mass. Following surgery, a surgical pathology report revealed a newly diagnosed stage 3b colorectal adenocarcinoma. Multiple abscesses in the abdominopelvic cavity were discovered on computed tomography (CT), revealing a major surgical site infectious process. These findings warranted emergent surgical intervention and placement of multiple Jackson-Pratt drains. Due to previously untreated carcinoma promoting a prothrombotic state, the patient developed numerous thrombotic complications such as segmental pulmonary embolism, superior mesenteric vein thrombosis, and superficial thrombophlebitis of the saphenous veins. He also developed new-onset paroxysmal atrial fibrillation secondary to postoperative pain, as well as bilateral pleural effusions. Here, we shed light on the mechanisms of development of such complications, as well as the management and methods for prevention.

An Uncommon Case of Atrial Fibrillation due to a Lung Mass Invasion of the Left Atrial Cavity.

Atrial fibrillation remains one of the most common conditions that clinical physicians encounter on a daily basis in the inpatient setting. This arrhythmia brings with it numerous complications if not treated properly and leads to intensive analysis of its primary etiology which is unique to every patient. In this case, we present a previously asymptomatic individual who presented to the hospital with respiratory complaints and was found to have a large lung mass, consistent with neuroendocrine lung cancer with direct compression of the left atrium leading to new-onset atrial fibrillation.

Reversal of motor-skill transfer impairment by trihexyphenidyl and reduction of dorsolateral striatal cholinergic interneurons in Dyt1 ΔGAG knock-in mice.

DYT-TOR1A or DYT1 early-onset generalized dystonia is an inherited movement disorder characterized by sustained muscle contractions causing twisting, repetitive movements, or abnormal postures. The majority of the DYT1 dystonia patients have a trinucleotide GAG deletion in DYT1/TOR1A. Trihexyphenidyl (THP), an antagonist for excitatory muscarinic acetylcholine receptor M1, is commonly used to treat dystonia. Dyt1 heterozygous ΔGAG knock-in (KI) mice, which have the corresponding mutation, exhibit impaired motor-skill transfer. Here, the effect of THP injection during the treadmill training period on the motor-skill transfer to the accelerated rotarod performance was examined. THP treatment reversed the motor-skill transfer impairment in Dyt1 KI mice. Immunohistochemistry showed that Dyt1 KI mice had a significant reduction of the dorsolateral striatal cholinergic interneurons. In contrast, Western blot analysis showed no significant alteration in the expression levels of the striatal enzymes and transporters involved in the acetylcholine metabolism. The results suggest a functional alteration of the cholinergic system underlying the impairment of motor-skill transfer and the pathogenesis of DYT1 dystonia. Training with THP in a motor task may improve another motor skill performance in DYT1 dystonia.

Evolution of Knowledge in the Treatment of Long-Standing Atrial Fibrillation in a UK Tennis Champion.

During the last several decades, there have been major advances in the evolution of drug therapies for the rate management of atrial fibrillation (AF). Initially, the drug of choice was digoxin but currently, the drug of choice is beta-adrenergic blockers. Drug therapies for stroke prevention in AF have also evolved. Initially, the drug of choice was aspirin, then became warfarin, and now in the current era, there are newer oral anticoagulants, such as apixaban, which are the preferred drugs. In this case report, we present the details of a 79-year-old athletic man who developed palpitations due to rapid AF at age 31. At the time of his initial presentation, he was treated with digoxin and aspirin and has remained on these drugs to the present. In 1973, 28 years after his initial presentation, he became the United Kingdom (UK) amateur tennis champion in the 55 and over division at age 59.  At present, the clinical applications of advances in the management of AF should include quality of life considerations in the context of patient preferences. This patient is an active and vigorous 79-year-old man who plays competitive tennis and pickleball. He steadfastly adheres to an antediluvian regimen for the management of his AF, but this may be viewed in the context of the famous quotation by Bert Lance, Director of the Office of Management and Budget in the US under President Carter who said "sometimes, if it ain't broke, don't fix it." In addition to the evolution of drug therapies from digoxin to beta-adrenergic blockers for rate control as well as from aspirin to warfarin to apixaban for the prevention of stroke, there have been other recent remarkable advances. For example, recent promising findings from randomized trials include that early rhythm control was more effective than rate control as well as that cryoballoon ablation was superior to drug therapies. These findings require confirmation in additional randomized trials designed a priori to test these promising but unproven hypotheses.

Decreased number of striatal cholinergic interneurons and motor deficits in dopamine receptor 2-expressing-cell-specific Dyt1 conditional knockout mice.

DYT1 early-onset generalized torsion dystonia is a hereditary movement disorder characterized by abnormal postures and repeated movements. It is caused mainly by a heterozygous trinucleotide deletion in DYT1/TOR1A, coding for torsinA. The mutation may lead to a partial loss of torsinA function. Functional alterations of the basal ganglia circuits have been implicated in this disease. Striatal dopamine receptor 2 (D2R) levels are significantly decreased in DYT1 dystonia patients and in the animal models of DYT1 dystonia. D2R-expressing cells, such as the medium spiny neurons in the indirect pathway, striatal cholinergic interneurons, and dopaminergic neurons in the basal ganglia circuits, contribute to motor performance. However, the function of torsinA in these neurons and its contribution to the motor symptoms is not clear. Here, D2R-expressing-cell-specific Dyt1 conditional knockout (d2KO) mice were generated and in vivo effects of torsinA loss in the corresponding cells were examined. The Dyt1 d2KO mice showed significant reductions of striatal torsinA, acetylcholine metabolic enzymes, Tropomyosin receptor kinase A (TrkA), and cholinergic interneurons. The Dyt1 d2KO mice also showed significant reductions of striatal D2R dimers and tyrosine hydroxylase without significant alteration in striatal monoamine contents or the number of dopaminergic neurons in the substantia nigra. The Dyt1 d2KO male mice showed motor deficits in the accelerated rotarod and beam-walking tests without overt dystonic symptoms. Moreover, the Dyt1 d2KO male mice showed significant correlations between striatal monoamines and locomotion. The results suggest that torsinA in the D2R-expressing cells play a critical role in the development or survival of the striatal cholinergic interneurons, expression of striatal D2R mature form, and motor performance. Medical interventions to compensate for the loss of torsinA function in these neurons may affect the onset and symptoms of this disease.