scholarly journals Lansoprazole – Induce Black Hairy Tongue- A Case Report

2017 ◽  
Vol 15 (1) ◽  
pp. 52-54 ◽  
Author(s):  
Eliz Aryal ◽  
M Rajbhandari ◽  
Sabina Bhattarai

Lansoprazole induced black hairy tongue has been rarely reported. The purpose of this paper is to report a case of lansoprazole induce black hairy tongue and review the literature. A 75 year man from eastern part of Kathmandu presented with black hairy fine growth from tongue along with discomfort, burning and halitosis from oral cavity after taking lansoprazole for acute peptic disease(APD) from over the counter and after discontinuation of lansoprazole, black hairy tongue was resolving. Clinically and histopathologically: lansoprazole induced black hairy tongue was confirmed. Black hairy tongue is characterized by abnormal hypertrophy and elongation of filliform papillae. Lansoprazole is a proton-pump inhibitor (PPI) with a racemic 1:1 mixture of the enantiomers dexlansoprazole which inhibits the stomach’s production of gastric acids.

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 128-129
Author(s):  
A LAGROTTERIA ◽  
A W Collins ◽  
A Someili ◽  
N Narula

Abstract Background Lymphocytic esophagitis is a new and rare clinicopathological entity. It is a histological pattern characterized by lymphocytic infiltrate without granulocytes. Its etiology and clinical significance remains unclear. The clinical manifestations are typically mild, with reflux and dysphagia the most commonly reported symptoms. Aims We describe a case report of spontaneous esophageal perforation associated with lymphocytic esophagitis. Methods Case report Results A previously well 31-year-old male presented to the emergency department with acute food impaction. His antecedent symptoms were acute chest discomfort and continuous odynophagia following his most recent meal, with persistent globus sensation. The patient had no reported history of allergies, atopy, rhinitis, or asthma. A previous history of non-progressive dysphagia was noted after resuscitation. Emergent endoscopy revealed no food bolus, but a deep 6 cm mucosal tear in the upper-mid esophagus extending 24 to 30 cm from the incisors. Chest computed tomography observed small volume pneumoperitoneum consistent with esophageal perforation. The patient’s recovery was uneventful; he was managed conservatively with broad-spectrum antibiotics, proton pump inhibitor therapy, and a soft-textured diet. Endoscopy was repeated 48 hours later and revealed considerable healing with only a residual 3-4cm linear laceration. Histology of biopsies taken from the mid and distal esophagus demonstrated marked infiltration of intraepithelial lymphocytes. There were no eosinophils or neutrophils identified, consistent with a diagnosis of lymphocytic esophagitis. Autoimmune indices including anti-nuclear antibodies and immunoglobulins were normal, ruling out a contributory autoimmune or connective tissue process. The patient was maintained on a proton pump inhibitor (pantoprazole 40 mg once daily) following discharge. Nearly six months following his presentation, the patient had a recurrence of symptoms prompting representation to the emergency department. He described acute onset chest discomfort while eating turkey. Computed tomography of the chest redemonstrated circumferential intramural gas in the distal esophagus and proximal stomach. Conclusions Esophageal perforation is a potentially life-threatening manifestation of what had been considered and described as a relatively benign condition. From isolated dysphagia to transmural perforation, this case significantly expands our current understanding of the clinical spectrum of lymphocytic esophagitis. Funding Agencies None


2017 ◽  
Vol 17 (4) ◽  
pp. 662-663 ◽  
Author(s):  
Suguru Mabuchi ◽  
Risa Suzuki ◽  
Mari Sasaki ◽  
Marie Nakamura ◽  
Norihiko Izumimoto ◽  
...  

2009 ◽  
Vol 72 (3) ◽  
pp. 166-167 ◽  
Author(s):  
Javier Molina-Infante ◽  
Moises Hernandez-Alonso ◽  
Belen Perez-Gallardo ◽  
Elisa Martin-Noguerol

2009 ◽  
Vol 6;12 (6;12) ◽  
pp. 1013-1023
Author(s):  
Howard Smith

There may be a relationship between proton pump inhibitors (PPIs) and iron absorption. PPIs may decrease the amount of iron absorbed gastrointestinally specifically due to alteration of the pH in the duodenum. Restless legs syndrome (RLS) is a sensorimotor disorder that includes an urge to move legs, accompanied or caused by uncomfortable and unpleasant sensations in the legs; the urge to move begins or worsens during periods of rest or inactivity, the urge to move is partially or totally relieved by movement, and the urge is worse or only occurs at night. In the majority of the restless leg syndrome population, the sensation is deep seated, often described as being in the shin bones, and most commonly felt between the knee and ankle. It may be described as a creepy, shock-like, tense, electric, buzzing, itchy, or even numb sensation. A subpopulation of this restless leg syndrome patient population experiences restless leg syndrome associated pain (RLSAP) that has been described as a deep “achy pain.” This pain has not been found to be relieved by many of the typical over the counter analgesics. Often, constant movement of the legs appears to be the only remedy, as these sensations usually appear during periods of rest. Furthermore, there appears to be an association between iron deficiency and those suffering from Restless Leg Syndrome (RLS). The authors theorize that there may be a possible correlation between PPIs and the symptoms (e.g. pain) associated with RLS. The authors propose that PPIs, such as omeprazole, may interfere with iron absorption in certain patients and that a subpopulation of patients who develop significant iron deficiency characterized by low serum ferritin levels while on PPIs may also develop RLS-like symptoms (including RLSAP). While there is no robust direct evidence to support any associations of PPIs and iron deficiency or PPIs associated with RLS-like symptoms (including RLSAP), it is hoped that this manuscript may spark research efforts on this issue. Key words: Proton pump inhibitor (PPI), Restless Leg Syndrome (RLS), iron deficiency, pain, iron absorption, Restless Leg Syndrome Associated Pain (RLSAP)


2017 ◽  
Vol 9 (1) ◽  
pp. 137-139 ◽  
Author(s):  
Anjan Adhikari ◽  
Rania Indu ◽  
Moumita Ray ◽  
Sangita Bhattacharya ◽  
Rahul Biswas ◽  
...  

2010 ◽  
Vol 106 (2) ◽  
pp. 294-295 ◽  
Author(s):  
Emilio Jesús Alegre-del Rey ◽  
Jesús Sierra-Sánchez ◽  
Rocío Castaño-Lara ◽  
Ramón Díaz-Alersi

2018 ◽  
Vol 68 (12) ◽  
pp. 706-711 ◽  
Author(s):  
Masahide Fukuda ◽  
Hirohito Ishigaki ◽  
Hiromitsu Ban ◽  
Mitsushige Sugimoto ◽  
Eri Tanaka ◽  
...  

2015 ◽  
Vol 11 (2) ◽  
pp. 543-546 ◽  
Author(s):  
ZHIHONG QIU ◽  
HONGTAO LIU ◽  
LIEN HE ◽  
YINLING MA ◽  
HAOJING SONG ◽  
...  

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