Candesartan-Induced Enteropathy That Mimics Celiac Disease in a 90-Year-Old Patient.

Sprue-like enteropathy (SLE) is a clinical syndrome similar to celiac disease and has been associated with the use of various angiotensin receptor blockers (ARBs), a class of medications frequently used in the management of hypertension. Currently, there has only been one documented case report which has observed this occurrence with the use of the ARB candesartan. A 90-year-old female patient presented with chronic diarrhea and weight loss of unclear etiology. Diagnostic esophagogastroduodenoscopy and ileocolonoscopy were macroscopically unremarkable, but histological samples revealed complete villous atrophy, chronic mucosal inflammation, and intraepithelial T-lymphocytic infiltration. However, serological studies could not confirm celiac disease as a cause for the patient's symptoms of malabsorption. After exclusion of other intestinal inflammation etiologies with noted ongoing candesartan use, the diagnosis of SLE was made, and candesartan therapy was discontinued. Additionally, we decided to initiate a lactose-free diet. Clinical remission was achieved without any recurrences. Candesartan is a commonly prescribed therapeutic agent in the treatment of hypertension. Our case underlines the importance of considering it as a potential cause for unexplained symptoms of malabsorption.

The diagnostic challenge of abdominal tuberculosis in nonendemic countries: A case series from a tertiary hospital in Germany.

Abdominal tuberculosis is a rare clinical condition in nonendemic countries and should be included as differential diagnosis by unspecific abdominal complaints, especially in patients with immigration background from high-prevalence regions.

[Off-label use of Budesonide suspensions to treat a patient with lymphocytic esophagitis]. / Off-label Anwendung einer budesonidhaltigen Suspension für die Behandlung einer lymphozytären Ösophagitis.

BACKGROUND: Lymphocytic esophagitis (LyE) is a rare chronic inflammatory disease of the esophagus, which shares clinical characteristics with the eosinophilic esophagitis. The most important part of its treatment is proton pump inhibitors (PPIs). Referring to locally acting steroids, evidence-based treatment strategies are missing. CASE REPORT: A 62-year-old patient presented for evaluation of his chronic dysphagia with previously diagnosed multiple oesophageal stenoses. Endoscopy revealed diffusely distributed esophageal rings and furrows and the diagnosis of LyE was established after immunohistochemical analysis of multiple mucosal biopsies. We initiated therapy with budesonide in the form of capsules (Entocort 3 × 3 mg Hartkapseln® once daily). During the course of the treatment, we initiated the off-label use of suspensions (Budenobronch® 0.5 mg twice daily) routinely used in the treatment of patients with asthma or COPD to increase the patient΄s acceptance of this therapy which was diminished because of his dysphagia. Under this therapy, clinical and later histological remission was achieved. CONCLUSION: Our case report is meant to describe an empirical therapeutic concept, which led to clinical and histological remission of chronic LyE.

[Off-label use of Budesonide suspensions to treat a patient with lymphocytic esophagitis]. / Off-label Anwendung einer Budesonidhaltigen Suspension für die Behandlung einer lymphozytären Ösophagitis.

Background Lymphocytic esophagitis (LyE) is a rare chronic inflammatory disease of the esophagus, which shares clinical characteristics with the eosinophilic esophagitis. The most important part of its treatment is proton pump inhibitors (PPIs). Referring to locally acting steroids, evidence-based treatment strategies are missing. Case Report A 62-year-old patient presented for evaluation of his chronic dysphagia with previously diagnosed multiple oesophageal stenoses. Endoscopy revealed diffusely distributed esophageal rings and furrows and the diagnosis of LyE was established after immunohistochemical analysis of multiple mucosal biopsies. We initiated therapy with budesonide in the form of capsules (Entocort 3 × 3 mg Hartkapseln® once daily). During the course of the treatment, we initiated the off-label use of suspensions (Budenobronch® 0.5 mg twice daily) routinely used in the treatment of patients with asthma or COPD to increase the patient΄s acceptance of this therapy which was diminished because of his dysphagia. Under this therapy, clinical and later histological remission was achieved. Conclusion Our case report is meant to describe an empirical therapeutic concept, which led to clinical and histological remission of chronic LyE.

Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes.

Recent investigation has focused on identifying signaling pathways that inhibit cardiac hypertrophy, a major risk factor for cardiovascular morbidity and mortality. In this context, nitric oxide (NO), signaling via cGMP and cGMP-dependent protein kinase type I (PKG I), has been recognized as a negative regulator of cardiac myocyte (CM) hypertrophy. However, the underlying mechanisms are poorly understood. Here, we show that PKG I inhibits CM hypertrophy by targeting the calcineurin-NFAT signaling pathway. Calcineurin, a Ca2+-dependent phosphatase, promotes hypertrophy in part by activating NFAT transcription factors which induce expression of hypertrophic genes, including brain natriuretic peptide (BNP). Activation of PKG I by NO/cGMP in CM suppressed NFAT transcriptional activity, BNP induction, and cell enlargement in response to alpha(1)-adrenoreceptor stimulation but not in response to adenoviral expression of a Ca2+-independent, constitutively active calcineurin mutant, thus demonstrating NO-cGMP-PKG I inhibition of calcineurin-NFAT signaling upstream of calcineurin. PKG I suppressed single L-type Ca2+-channel open probability, [Ca2+]i transient amplitude, and, most importantly, L-type Ca2+-channel current-induced NFAT activation, indicating that PKG I targets Ca2+-dependent steps upstream of calcineurin. Adenoviral expression of PKG I enhanced NO/cGMP inhibitory effects upstream of calcineurin, confirming that PKG I mediates NO/cGMP inhibition of calcineurin-NFAT signaling. In CM overexpressing PKG I, NO/cGMP also suppressed BNP induction and cell enlargement but not NFAT activation elicited by constitutively active calcineurin, which is consistent with additional, NFAT-independent inhibitory effect(s) of PKG I downstream of calcineurin. Inhibition of calcineurin-NFAT signaling by PKG I provides a framework for understanding how NO inhibits cardiac myocyte hypertrophy.