Different neurotransmitter systems are involved in the development of esophageal achalasia

Sigala, Sandra; Missale, Guido; Missale, Cristina; Villanacci, Vincenzo; Cestari, Renzo; Grigolato, Pier Giovanni; Lojacono, L; Spano, PierFranco

doi:10.1016/0024-3205(95)00082-8

Cited by 20 publications

(26 citation statements)

References 18 publications

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“…Dopamine receptors are divided into two categories, D‐1 and D‐2, later extended to at least five subtypes 24 . After activation, the two types of receptors may have opposite effects on the LES tension via different signal transduction mechanisms 25,26 . In addition to DA receptors, DA may also activate α‐ and β‐adrenoceptors.…”

Section: Discussionmentioning

confidence: 99%

Responses of human clasp and sling fibers to neuromimetics

Tian¹,

Liu²,

Wang

et al. 2004

J of Gastro and Hepatol

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Section: Discussionmentioning

confidence: 99%

Responses of human clasp and sling fibers to neuromimetics

Tian¹,

Liu²,

Wang

et al. 2004

J of Gastro and Hepatol

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“…Botox blocks the release of acetylcholine from skeletal motor end plates and has been shown to affect neuromuscular transmission in visceral organs. In achalasia there is selective loss of inhibitory neuronal activity that results in unopposed excitation of the LES by cholinergic neurons [4]. Botox selectively blocks the release of acetylcholine from presynaptic cholinergic nerve terminals in the myenteric plexus, thereby restoring the balance between inhibitory and excitatory neurotransmitters, resulting in reduced LES pressure which, in turn, correlates with symptom relief [5].…”

Section: Discussionmentioning

confidence: 99%

Gastrointestinal Dysmotility

et al. 2011

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Case Presentation and EvolutionA 42 year-old previously healthy man was admitted to Stanford University hospital because of severe nausea and vomiting. He had been well until 3 weeks before admission, when he first experienced nausea, vomiting, and profound sweating without chills or fever, lasting up to 24 h. The symptoms became progressively worse and occurred with any oral intake of solids or liquids. He also noted the sensation of food being stuck in his throat despite swallowing small bites.An upper endoscopy that had been performed at another hospital showed a small hiatal hernia, antral and gastric body erythema, and gastric food retention. At that time, an abdomen CT scan revealed mild bowel wall thickening in the distal ileum. His symptoms had gradually improved and he was discharged. However, soon thereafter, his symptoms worsened to the point that he could no longer tolerate either solids or liquids and he was admitted to Stanford hospital. In the course of the three weeks before admission, he had lost 25 pounds but did not experience any abdominal pain or diarrhea. The use of anti-emetics was only marginally helping his nausea. He did however, note significant constipation, with his last bowel movement being one week before his admission to Stanford hospital. He had no known sick contacts, and had not recently traveled.His past medical and surgical histories were negative. His father had died of colon cancer at age 70. His sister had cholelithiasis. He worked as a mechanic, did not smoke, and only consumed alcohol socially.On examination, he was afebrile with a pulse of 53, blood pressure of 118/69, and oxygen saturation of 99% on room air. He appeared frail with some temporal wasting but otherwise he did not have any lymphadenopathy and he was anicteric. His abdomen was soft and non-tender but hypoactive bowel sounds could be heard. No abdominal masses were palpable. There was no edema, rashes, or erythema.His laboratory values were: hemoglobin 12.9 with MCV of 92.4. His INR was 1.1 with sodium of 132. His liver enzymes were normal as was his thyroid stimulating hormone. Although a random serum cortisol was 2 lg/dl (normal range: 4-26 lg/dl), an ACTH stimulation test revealed appropriate response from 12 to 33 lg/dl.An esophagogram revealed reduced primary esophageal peristalsis and tertiary contractions in the distal esophagus (Fig. 1). There was delay of passage of contrast, with the barium column reaching the level of the thoracic inlet; delayed gastric emptying (Fig. 2) and a small sliding hiatal hernia were also noted. Gastric emptying scan showed severe gastroparesis, with 74% of the radioactive tracer still remaining in the stomach at the end of 4 h (normal range: 0-10%) (Fig. 3). Esophageal motility study was suspicious for vigorous achalasia versus severe nutcracker variant of diffuse esophageal spasm (Fig. 4).To further evaluate the etiology of his gastrointestinal dysmotility, a paraneoplastic workup was performed and it was negative. Head and body CT showed no masses. Systemic markers of ...

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“…Myenteric denervation of the distal oesophagus extending into the stomach is characteristically seen at histological examination (Csendes et al 1992) and is selective for inhibitory nitric oxide (Mearin et al 1993;De Giorgio et al 1999;Zarate et al 2006) and vasoactive inhibitory polypeptide (Aggestrup et al 1983;Sigala et al 1995) releasing motor neurons resulting in unopposed excitatory activity. Familial, infectious, genetic and autoimmune mechanisms have all been postulated to contribute to the development of achalasia (Park et al 2005).…”

Section: Idiopathic Achalasiamentioning

confidence: 99%

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

Hubball

Martin

Lang

et al. 2009

Progress in Neurobiology

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Dysfunction of the gastrointestinal neuromuscular apparatus (including interstitial cells ofCajal) is presumed to underlie a heterogeneous group of disorders collectively termed gastrointestinal neuromuscular diseases (GINMDs). Humoral (antibody)-mediated autoimmunity directed against ligand-or voltage-gated ion channels or associated proteins involved in neuromuscular transmission is associated with several acquired neuromuscular diseases of the periphery and is now implicated in an increasing number of less well-characterised diseases. Anti-channel antibodies have been reported in small numbers of patients with GINMD, particularly in those with GI dysfunction secondary to an underlying disease such as neoplasia or infection. However, little is known of humoral autoimmunity in primary GINMDs.This thesis investigated the association between anti-channel antibodies and GINMD, and the human GI tract as a potential target of anti-channel antibodies. The presence of antivoltage-and ligand-gated antibodies was investigated in the serum of patients with primary achalasia, enteric dysmotility and intestinal pseudo-obstruction, and in those with GINMD secondary to Chagas' disease. The functional effect of sera from some of these patients on colonic smooth muscle contractility was also characterised. Finally, the distribution of six voltage-gated potassium channels (VGKCs), which serve essential roles in the peripheral and central nervous systems and are known targets of pathological autoantibodies, were investigated in all layers of the human GI tract.Our findings suggest that currently recognised anti-channel antibodies are not a common pathogenic factor in primary GINMDs. Anti-channel antibodies, in particular anti-VGKC antibodies, were however found in a significant number of individuals with Chagas' disease. Furthermore, circulating factors in patients with chagasic GI disease altered GI smooth muscle contractility in vitro which may have pathological relevance to GI

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Different neurotransmitter systems are involved in the development of esophageal achalasia

Cited by 20 publications

References 18 publications

Responses of human clasp and sling fibers to neuromimetics

Responses of human clasp and sling fibers to neuromimetics

Gastrointestinal Dysmotility

The role of humoral autoimmunity in gastrointestinal neuromuscular diseases

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