Summary Background : The diagnostic yield of the stool antigen test (HpSA) in evaluating the results of Helicobacter pylori eradication therapy is controversial, but many studies have used only the 13 C‐urea breath test ( 13 C‐UBT) as a gold standard which has greatly reduced their relevance. Aim : To compare the reliability of HpSA and 13 C‐UBT in patients post‐treatment using biopsy‐based methods as reference tests. Methods : A total of 100 consecutive dyspeptic patients (42 male and 58 female; mean age, 56 ± 18 years) were enrolled in our study. All patients were H. pylori positive on the basis of at least two biopsy‐based methods, and underwent 1 week of treatment with various triple therapies. They were again endoscoped 4 weeks after completing therapy and six biopsyspecimens were taken from the gastric antrum and corpus for rapid urease test, histology and culture. HpSA and 13 C‐UBT were also performed within 3 days of the second endoscopy. Results : On the basis of biopsy‐based tests, infection was eradicated in 77 patients but continued in 23. Three false negatives were observed with HpSA and two with 13 C‐UBT. In contrast, the number of false positives was significantly higher ( P < 0.01) with HpSA than with 13 C‐UBT (nine vs. one), confirming the lower specificity of the former test. The overall accuracy of HpSA was 88% vs. 97% for 13 C‐UBT ( P < 0.02). Conclusions : HpSA has lower diagnostic value than 13 C‐UBT in the evaluation of the outcome of anti‐ H. pylori therapy. 13 C‐UBT remains the first‐line diagnostic method to monitor eradication results. The use of HpSA should be reserved for those settings in which 13 C‐UBT is not available.
Wernicke’s encephalopathy (WE) is an acute neurological disorder, due to a lack of thiamin (vitamin B1) which is observed mainly in alcoholic patients. Unfortunately, the syndrome is underestimated in clinical practice and most often recognized only on autopsy, especially among non-alcoholics. The common clinical picture include mental status changes, ocular dysfunction, and gait ataxia. Treatment consists of timely thiamine replacement through intravenous infusion. We describe the case of two patients who developed a non-alcoholic WE post-surgical, regressed completely after intravenous infusion of thiamine. These cases suggest interesting diagnostic and therapeutic implications.
Pituitary adenylate cyclase activating polypeptide-38 (PACAP38) is a widely distributed neuropeptide involved in neuroprotection, neurodevelopment, nociception and inflammation. Moreover, PACAP38 is a potent inducer of migraine-like attacks, but the mechanism behind this has not been fully elucidated. Migraine is a neurovascular disorder, recognized as the second most disabling disease. Nevertheless, the antibodies targeting calcitonin gene-related peptide (CGRP) or its receptor are the only prophylactic treatment developed specifically for migraine. These antibodies have displayed positive results in clinical trials, but are not effective for all patients; therefore, new pharmacological targets need to be identified. Due to the ability of PACAP38 to induce migraine-like attacks, its location in structures previously associated with migraine pathophysiology and the 100-fold selectivity for the PAC1 receptor when compared to VIP, new attention has been drawn to this pathway and its potential role as a novel target for migraine treatment. In accordance with this, antibodies against PACAP38 (ALD 1910) and PAC1 receptor (AMG 301) are being developed, with AMG 301 already in Phase II clinical trials. No results have been published so far, but in preclinical studies, AMG 301 has shown responses comparable to those observed with triptans. If these antibodies prove to be effective for the treatment of migraine, several considerations should be addressed, for instance, the potential side effects of long-term blockade of the PACAP (receptor) pathway. Moreover, it is important to investigate whether these antibodies will indeed represent a therapeutic advantage for the patients that do not respond the CGRP (receptor)-antibodies. In conclusion, the data presented in this review indicate that PACAP38 and PAC1 receptor blockade are promising antimigraine therapies, but results from clinical trials are needed in order to confirm their efficacy and side effect profile.
Abdominal Epilepsy, a Rare Cause of Abdominal Pain: The Need to Investigate Thoroughly as Opposed to Making Rapid Attributions of Psychogenic Causality Giuliano Lo Bianco,1– 3 Simon Thomson,3 Simone Vigneri,4 Hannah Shapiro,5 Michael E Schatman6,7 1Università di Catania, Dipartimento di Scienze Biomediche e Biotecnologiche (BIOMETEC), Catania, Italy; 2I.R.C.C.S. CROB Centro di Riferimento Oncologico Basilicata, Rionero in Vulture, Potenza, Italy; 3Basildon and Thurrock University Hospitals NHSFT, Orsett Hospital, Pain Management and Neuromodulation, London, Essex, UK; 4Pain Medicine Department, Santa Maria Maddalena Hospital, Occhiobello, Rovigo, Italy; 5Department of Biopsychology, Tufts University, Medford, MA, USA; 6Department of Diagnostic Sciences, Tufts University School of Dental Medicine, Boston, MA, USA; 7Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston, MA, USACorrespondence: Michael E Schatman Tel +1425647-4880Email Michael.Schatman@tufts.edu Abdominal pain is a nonspecific symptom which can be caused by myriad pathologies, resulting in frequent misdiagnosis.1 Some pathological conditions can cause paroxysmal gastrointestinal symptoms, such as porphyria, cyclical vomiting, intestinal malrotation, peritoneal bands, and abdominal migraine.2 Furthermore, emotional and psychological factors may also play an important role in the presentation of certain patients with gastrointestinal disorders, and accurate diagnosis can be confounded by these. An accurate diagnosis may be delayed or even abandoned due to the attribution of “functional” or “psychogenic” causality.3 Physicians in numerous fields of practice too often respond in such a fashion when the more common causes of pain conditions are ruled out,4 which potentially puts patients with rare pain disorders that are challenging to diagnose at considerable risk for needless, prolonged suffering. Further, the stigma associated with being diagnosed with a Somatoform Disorder or a Medically Unexplained Symptom (MUS) should not be understated.5
Background and Objective Neurophysiological studies in migraine have reported conflicting findings of either cortical hyper‐ or hypoexcitability. In migraine with aura ( MwA ) patients, we recently documented an inhibitory response to suprathreshold, high‐frequency repetitive transcranial magnetic stimulation (hf‐ rTMS ) trains applied to the primary motor cortex, which is in contrast with the facilitatory response observed in the healthy subjects. The aim of the present study was to support the hypothesis that in migraine, because of a condition of basal increased cortical responsivity, inhibitory homeostatic‐like mechanisms of cortical excitability could be induced by high magnitude stimulation. For this purpose, the hf‐ rTMS trains were preconditioned by transcranial direct current stimulation ( tDCS ), a noninvasive brain stimulation technique able to modulate the cortical excitability state. Methods Twenty‐two MwA patients and 20 patients with migraine without aura ( MwoA ) underwent trains of 5‐Hz repetitive transcranial magnetic stimulation at an intensity of 130% of the resting motor threshold, both at baseline and after conditioning by 15 minutes of cathodal or anodal tDCS . Motor cortical responses to the hf‐ rTMS trains were compared with those of 14 healthy subjects. Results We observed abnormal inhibitory responses to the hf‐ rTMS trains given at baseline in both MwA and MwoA patients as compared with the healthy subjects ( P < .00001). The main result of the study was that cathodal tDCS , which reduces the cortical excitability level, but not anodal tDCS , which increases it, restored the normal facilitatory response to the hf‐ rTMS trains in both MwA and MwoA . Conclusions The present findings strengthen the notion that, in migraine with and without aura, the threshold for inducing inhibitory mechanisms of cortical excitability might be lower in the interictal period. This could represent a protective mechanism counteracting cortical hyperresponsivity. Our results could be helpful to explain some conflicting neurophysiological findings in migraine and to get insight into the mechanisms underlying recurrence of the migraine attacks.
