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All Journal International Journal of Health and Pharmaceutical (IJHP)
I Made Suma Wirawan
Faculty of Medicine, Universitas Mahasaraswati Denpasar, Bali, Indonesia
Nursing Public Health

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Dysphagia Improvement Following Sublingual Nifedipine Administration in Long-Segment Esophageal Stricture: A Case Report Steven Jonathan; I Putu Bayu Triguna; Gde Giri Prathiwindya; I Made Suma Wirawan
International Journal of Health and Pharmaceutical (IJHP) Vol. 6 No. 1 (2026): February 2026
Publisher : CV. Inara

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.51601/ijhp.v6i1.504

Abstract

Dysphagia is a difficulty in swallowing either solid food or liquid. Esophageal stricture being one of the most common causes of dysphagia can be caused by inflammation, fibrosis, or neoplasia damaging the esophageal lumen. If left untreated, dysphagia can lead to malnutrition, aspiration, and decreased quality of life. Another common cause of dysphagia is esophageal motility disorder, an impairment in peristalsis of the esophageal. Calcium channel blockers such as nifedipine have been reported to improve dysphagia and may serve as alternative therapy while waiting for endoscopic intervention. A 27-year-old man presented with a two-month history of progressive dysphagia to solids, semisolids, and liquids, after an episode of hematemesis. Esophagogram showed esophageal stricture with impaired peristaltic. Contrast-enhanced CT result was suggestive of an intraluminal esophageal stricture. The patient was given sublingual nifedipine before meals as an alternative therapy while waiting for endoscopic intervention, and showed gradual sympomatic improvement. Dysphagia caused by long-segment esophageal stricture can be exacerbated by secondary motility disorder. While definitive treatment requires endoscopic intervention, sublingual nifedipine offered effective short-term symptomatic relief by reducing esophagogastric junction pressure and improving bolus transit through the narrowed lumen.
Altered Level of Consciousness in Metabolic Disease: An Emphasis on the Pathomechanism of Hepatic Encephalopathy Steven Jonathan; I Ketut Suryana; I Made Suma Wirawan
International Journal of Health and Pharmaceutical (IJHP) Vol. 6 No. 2 (2026): May 2026
Publisher : CV. Inara

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.51601/ijhp.v6i2.548

Abstract

Altered level of consciousness (ALOC) is a common clinical presentation in emergency and inpatient settings, with metabolic diseases representing as major etiologic causes. Among these, hepatic encephalopathy (HE) is one of the most frequent causes due to its high prevalence, morbidity, and mortality. HE has a complex pathophysiology mechanism involving neurotoxic substances such as ammonia. This narrative literature review discusses ALOC associated with metabolic disease, with emphasis on the underlying pathophysiological mechanisms of HE. Metabolic encephalopathy arises from systemic disturbances rather than primary structural brain injury and may progress to irreversible neuronal damage if untreated. HE develops in the context of acute liver failure, portosystemic shunting, or cirrhosis. Its pathogenesis reflects a multifactorial interaction involving hyperammonemia, systemic inflammation, gut microbiome dysbiosis, electrolyte disorders, malnutrition, sarcopenia, and manganese accumulation. Ammonia remains a central neurotoxin in HE, contributing to astrocytic swelling, glutamine accumulation, and cytotoxic edema. Inflammatory response further neuronal impairment through cytokine-mediated oxidative stress and blood–brain barrier disruption. Gut dysbiosis promotes bacterial translocation and endotoxemia, exacerbating systemic inflammation and worsening neurocognitive impairment. Given the broad differential diagnosis of ALOC, a structured clinical approach and early identification of metabolic causes especially HE is essential. Understanding the complex
Co-Authors Gde Giri Prathiwindya I Ketut Suryana I Putu Bayu Triguna Steven Jonathan Steven Jonathan