Rejected

Mpox Virus (MPXV) is a zoonotic infectious disease first identified in 1970 in rural villages in rainforest areas of central and western Africa when smallpox was in the final stages of eradication. Since May 2022, cases and sustained transmission chains of monkeypox have been reported for the first time in countries where the disease is not endemic and without cases having direct or immediate epidemiological links to areas of West or Central Africa (travel, importation of mammals). On 23 July 2022, WHO declared monkeypox a "Public Emergency of International Concern" (PHEIC). In this paper, we report two cases of a Polymerase Chain Reaction (PCR)-confirmed MPXV infection. A 39-year-old Italian male came to our attention for a suspected herpetic infection, fever, headache, and malaise, which were followed by the development of an erythematous plaque covered by vesicles on the chin, an oval ulcer with a white peripheral border on the lower lip, and a central erosive area and three pustules on the arms and trunk. During the physical examination, cervical lymphadenopathy was also detected. PCR investigation of the patient and his partner confirmed the presence of MPXV infection. Our report describes a possible clinical feature of Mpox disease and illustrates the challenge of a disease that seems to present itself in different ways.

A 17-year-old previously healthy female presented with unilateral chest pain and dyspnea. Chest radiographs demonstrated a unilateral pleural effusion and pneumonia. Pleural fluid bacterial cultures were negative; acid-fast cultures grew Mycobacterium tuberculosis. Two months after starting appropriate therapy, she had a recrudescence of symptoms and reaccumulation of the pleural fluid. Her tuberculosis antibiotic regimen was expanded, the effusion drained, and systemic corticosteroids initiated, resulting in rapid clinical improvement. Cultures of the second pleural fluid collection were negative. Her clinical deterioration was due to immune reconstitution inflammatory syndrome (IRIS). IRIS can be seen within the first several months of starting tuberculosis therapy and can result in paradoxical worsening of symptoms or radiographic findings in adolescents who are on the appropriate therapy. IRIS is a diagnosis of exclusion after drug resistance and medication malabsorption, intolerance, and nonadherence are excluded. Therapy includes nonsteroidal anti-inflammatory agents for milder reactions and systemic corticosteroids for more severe IRIS cases.

A 27-year-old Nepalese male presented with recurrent abdominal pain accompanied by a lower stool consistency over the past 2 years. These episodes occurred several times a year, lasting 1 to 2 weeks, and resolved spontaneously, after adjustment of diet and/or medication for symptomatic control (e.g., antispasmodics, probiotics). Over the last year, the patient had undergone an extensive diagnostic investigation, which revealed no alterations in the laboratory workup, abdominal scan, esophagogastroduodenoscopy, and colonoscopy, including biopsies of the duodenum, and colon, so the symptoms have been attributed to irritable bowel syndrome. However, the symptoms had become more frequent, so the patient was referred to our gastroenterology department. We repeated and extended the work-up. Laboratory investigations showed an elevated erythrocyte sedimentation rate and faecal calprotectin. The remaining laboratory as well an extensive stool workup for infection were unremarkable. Esophagogastroduodenoscopy and ileocolonoscopy were normal. Small bowel capsule endoscopy revealed jejunal mucosa with lymphangiectasias, pseudopolypoids formations and superficial longitudinal ulcers, these findings were corroborated by the double-balloon enteroscopy, and biopsies showed marked architectural distortion, chronic inflammatory infiltrate, and an epithelioid granuloma. The clinical, endoscopic, biochemical, and histological findings were consistent with isolated jejunal Crohn's disease. The patient started adalimumab with complete remission after one year. We present this case given its exuberant endoscopic findings and due to the difficulty in making the diagnosis due to its rarity, location, and unspecific presentation.

For patients suffering from myofascial pain syndrome (MPS) affecting muscles of mastication, traditional trigger point therapy treatment regimens can prove inconvenient, due to the short duration of pain relief after each injection and expense of repeated visits which are often not covered by insurance. We present a case of a patient treated using an alternative technique that could develop into an additional modality for treating MPS patients who are refractory to conservative treatment. This technique involves identifying and marking the patient's trigger points and surgically cauterizing each location using a Bovie electrosurgical unit. While traditional trigger point injection therapy for myofascial pain syndrome is a well-described technique with acceptable pain relief expected for a period of 8-12 weeks, this technique provided up to 24 months of adequate pain relief in a patient. While further studies are indicated before widespread adoption can be recommended, this patient's response suggests that this technique may be useful in offering longer-term pain relief compared with trigger point injection therapy.

Recent research suggests that mild traumatic brain injury (TBI) may exert deleterious effects on endogenous pain modulatory function, potentially underlying the elevated risk for persistent headaches following injury. Accumulating research also shows race differences in clinical and experimental pain, with African Americans (AA) generally reporting more severe pain, worse pain modulation, and greater pain sensitivity compared to Caucasians. However, race differences in pain-related outcomes following mild TBI have rarely been studied. The purpose of this study was to explore race differences in endogenous pain modulation, pain sensitivity, headache pain, and psychological factors among AA and Caucasian individuals with mild TBI in the first month following injury compared to healthy controls and across time. Patients with mild TBI were recruited from the local Emergency Department Trauma Centers. Sixty-three mild TBI participants (African Americans: n=23, Caucasians: n=40) enrolled in this study and completed study sessions at 1-2 weeks and 1-month post injury. Forty-one mild TBI-free control participants (African Americans: n=11, Caucasians: n=30), matched on age and sex, completed one study session. Assessments included a headache survey, Pain Catastrophizing Scale, CES-Depression Scale, and several quantitative sensory tests (QST) to measure endogenous pain modulatory function. The QST tests included conditioned pain modulation (CPM) to measure endogenous pain inhibitory function and temporal summation of pain and pressure pain thresholds (PPTs) of the head to measure pain sensitization and sensitivity. Two-way ANOVAs were used to determine whether the outcome measures differed as a function of race, mild TBI, and time. Mediation analysis was used to explore potential mediators for the race differences in headache pain intensity. The results showed that AA mild TBI participants reported significantly greater headache pain and pain catastrophizing and exhibited higher pain sensitivity and worse pain modulation on QST tests compared to Caucasian mild TBI participants. These same race differences were not observed among the healthy TBI-free control sample. The mediation analyses showed complete mediation for the relation between race and headache pain intensity by pain catastrophizing at 1-2 weeks and 1 month post injury. Overall, the results of this study suggest that African Americans compared to Caucasians are characterized by psychological and pain modulatory profiles following mild TBI that could increase the risk for the development of intense and persistent headaches following injury.

We describe the case of a 69-year-old male with Crohn's disease (CD), treated with infliximab and undergoing intestinal resection. The surgery and postoperative period were unremarkable, with no CD-related symptoms. Two months after surgery and two weeks after the introduction of infliximab, he was admitted due to acute onset diffuse abdominal pain, hematochezia and arthralgia. On physical observation on admission, he showed signs of arthritis of the left knee. Laboratory tests revealed renal failure with nephrotic proteinuria, slightly low complement (C3) and IgA elevation. Remaining autoimmunity and viral panel were negative. Abdominal examination showed duodenum and thickening of the proximal wall of the jejunum. Biopsies excluded active CD. Colon and ileum mucosa were normal. The patient met EULAR criteria for Henoch-Schönlein purpura and was started on prednisolone with response. Although no clear trigger was pointed out, we switched anti-TNF to ustekinumab. We present this case given its endoscopic exuberance, and because of the high index of suspicion to make the diagnosis in adult patients with previous inflammatory bowel disease. The distinction between this vasculitis and CD is of utmost importance, given the therapeutic implications.

To develop health literacy assessment instrument for patients with chronic pain.

Puumala hantavirus (PUUV) causes most cases of haemorrhagic fever with renal syndrome (HFRS) in Europe. PUUV infection is characterised by acute kidney injury, thrombocytopenia and increased capillary leakage. Typical symptoms are fever, headache, nausea, abdominal and back pain. This study aimed to evaluate the amount and distribution of intraperitoneal, retroperitoneal and pleural fluid and the association of fluid collections to the symptoms and clinical findings in patients with acute PUUV infection.

In self-revolving gram-negative infection, Resolvin D5 (RvD5) was found to enhance bacteria phagocytosis and reduce the production of inflammatory mediators, contributing to the resolution of infection. LPS (lipopolysaccharide) is a gram-negative bacterial structure product which activates the immune system and, at high doses, leads to endotoxemia. To our knowledge, the effect of RvD5 against LPS endotoxemia has not been investigated to date. Female Swiss mice received an i.p. treatment with RvD5 (0.1, 1 or 10 ng/animal). After 1 h, they were stimulated with LPS (10 mg/kg, i.v.), and samples were collected after additional 6 h. The resulting data demonstrated that RvD5 protected the kidneys (urea and creatinine serum levels) from tissue injury. These effects were related to an improvement in histopathological parameters and a reduction of enzymatic markers of leukocyte infiltration, pro-inflammatory cytokine (IL-1β, TNF-α, and IL-6) production, and oxidative stress. Antioxidant markers were also increased by RvD5, but IL-10 (an anti-inflammatory cytokine) levels were unaltered. We also observed that RvD5 reduced the infiltration of CD45 hematopoietic cells into the kidneys, reduced the activation of NFκB and promoted the Nrf2 pathway by reducing Keap-1 levels. Our data indicate that RvD5 may be a therapeutic possibility to reduce kidney lesions in LPS endotoxemia.