Florid Inflammation Research Articles

Acute necrotizing duodenitis in diabetic ketoacidosis

Acute necrotizing esophagitis (ANE), acute necrotising duodenitis (AND), and Wishnesky’s lesions (WLs) are three peculiar upper gastrointestinal pathologies that can be seen in death from diabetic ketoacidosis (DKA). Amongst these three, AND has only been recently described. Morphologically, ANE and AND present as generalized black discoloration of the intestinal tract, and florid necrosis and inflammation. Whereas WLs are discrete black lesions in the stomach with necrosis and muted inflammation. We report a case of isolated AND with an unusual morphology not previously reported. A man in his 60s was found dead at home who died from pneumonia complicated by DKA. The gastrointestinal tract showed isolated patchy and discrete AND in which macroscopically resembled WLs, but microscopy resembled ANE with florid necrosis and acute inflammation. This case, together with the literature, documented AND can be macroscopically diffuse or discrete resembling ANE or WLs respectively but microscopically resemble ANE. Furthermore, the potential of these lesions being found in isolation in DKA raises the possibility of both general and local mechanisms playing a role on their morphology and presentation.

Diagnostic Challenges of Uncommon Paediatric Head and Neck MassesA Case Series

Paediatric head and neck masses pose diagnostic challenge to the clinicians owing to the wide spectrum of lesions including congenital (developmental), inflammatory and neoplastic lesions. In this case series, uncommon paediatric head and neck mass lesions that were diagnosed in a tertiary care hospital over a period of three years from January 2017 to December 2019, had been included, emphasizing on the diagnostic challenges encountered. First case was of Cervical Chondrocutaneous Branchial Remnant (CCBR) that was misdiagnosed as branchial cyst clinically. Second case was a lymphoepithelial cyst that masqueraded as an acute suppurative lymphadenitis in Fine Needle Aspiration Cytology (FNAC) due to florid inflammation. Third case was an aggressive poorly differentiated malignant neoplasm of left nasal cavity namely Nuclear protein in Testis (NUT) carcinoma that had to be differentiated from several other small round blue cell tumors. Fourth was a case of lipoblastoma which could be mistaken for myxoid liposarcoma. The last two cases were vascular tumors, one of them was juvenile capillary hemangioma with a benign clinical course while the other was an intermediate grade tumor namely kaposiform hemangioendothelioma. A wholesome clinical, radiological and pathological evaluation will help to solve the diagnostic dilemmas in this group of lesions.

Histopathological progression of hidradenitis suppurativa/acne inversa : Amorphological study with acloser look on the early changes of the folliculosebaceous apocrine apparatus.

It is generally acknowledged that the first morphological change of hidradenitis suppurativa/acne inversa (HS/AI) consists of infundibular plugging of the folliculosebaceous apocrine apparatus, which is followed by acute and chronic inflammation, cysts with sinus formation, and fibrosis. Alternatively, it has been hypothesized that HS/AI is primarily aneutrophilic autoinflammatory disease and that the follicular plugging typical of this disease is secondary to inflammation. To review the sequence of the changes that mark the disease development, we have performed ahistopathologic study on the surgical material from aseries of axillary and inguinal/perineal cases. The histologic material from surgery on Hurley's second and third stage HS/AI was retrieved and collected with the patients' clinical images. The virtually uninvolved skin peripheral to the lesions was studied together with the main inflammatory foci on vertical sections stained with hematoxylin-eosin and immunohistochemistry for the follicle sheaths. The fully developed lesions showed acute and chronic, suppurative and granulomatous inflammation overlapping fibrosis, cysts, and sinuses. Instead, the skin adjacent to florid inflammation showed plugging and dysmorphic alterations of the hair follicles associated with immunopathological changes of the inner root sheath keratin expression. Our observations coincide with the classical pathological studies on the progressive changes of HS/AI; however, in our specimens, the virtually normal skin peripheral to the fully developed lesions show seemingly initial follicular changes that suggest development error. This finding would support the hypothesis of combined mutation-induced epithelial differentiative defects and immunological derangement in HS/AI pathogenesis.

Recurrent Granulomatous Myocarditis after Heart Transplant

<h3>Introduction</h3> Recurrent granulomatous myocarditis is an uncommon phenomenon after heart transplantation. We present a case of late recurrent granulomatous myocarditis after heart transplant. <h3>Case Report</h3> A previously healthy gentleman presented with complete heart block requiring placement of a permanent pacemaker. He subsequently developed reduced left ventricular function and progressive heart failure, prompting an endomyocardial biopsy which revealed granulomatous myocarditis. He was treated with steroids but his symptoms progressed and ultimately underwent orthotopic heart transplant. Pathologic examination of the explanted heart revealed "Florid granulomatous inflammation throughout the myocardium, with dense scar that is patchy and irregularly distributed." 7 Years after transplant he developed severe rapid onset heart failure symptoms. Transthoracic echocardiography revealed a newly reduced left ventricular ejection fraction of 35 %. Urgent catheterization and endomyocardial biopsy was performed revealing mild single vessel allograft vasculopathy, mildly elevated filling pressures and a cardiac index of 2 liters per minute per meter squared. Pathologic examination of the biopsy revealed myocardium with significant inflammation including numerous eosinophils and scattered multinucleated giant cells with myocyte damage. Cardiac magnetic resonance imaging (CMR) was performed revealing late gadolinium enhancement in the apical lateral, and basal anteroseptal walls [Figure] with prolonged T2 time suggestive of edema. He was treated with high dose steroids, intravenous diuretics were administered, and he clinically recovered symptomatically and continues to follow in clinic. <h3>Summary</h3> Granulomatous myocarditis caused by giant cell myocarditis or cardiac sarcoidosis can lead to end stage heart failure and necessity for heart transplant. Recurrence of the granulomatous inflammation can lead to graft dysfunction and can be identified by endomyocardial biopsy as well as noninvasive imaging with CMR.

Components of the joint-sparing, combined bony and soft tissue correction of the cavovarus foot

Combined bony and soft tissue correction of amild foot and flexible rearfoot deformity in cavovarus foot. Drop foot during swing phase and muscular imbalance in the stance phase in cavovarus foot, flexible cavovarus foot, accompanying symptoms such as recurrent calluses and ulcerations, compliance. Pes cavovarus of spastic genesis, mild deformities, fixed bony deformity, lack of compliance, florid inflammation in the foot area, severe peripheral artery disease (PAD), diabetes mellitus. Description of the gradual escalation of joint-sparing bony and soft tissue procedures. Postoperative lower leg cast. In cases of combined bony and soft tissue correction, first 6weeks of nonweight-bearing with lower leg cast, then 6weeks of lower leg walking cast. With adequate bony consolidation, cast removal after atotal of 12weeks. In cases of pure soft-tissue foot correction, 6weeks of lowerleg walking cast. It was shown that only 22.5% of the affected feet (40 preoperative patients with cavovarus foot deformity) had asevere hindfoot equinus due to shortened calf muscles. In astudy with 14patients, it was shown that the tibialis posterior tendon transfer corrects the drop foot component and the excessive medial arch of the feet is significantly reduced by combined soft tissue and bony procedures.

Observational analysis on inflammatory reaction to talc pleurodesis: Small and large animal model series review.

Talc pleurodesis has been associated with pleuropulmonary damage, particularly long-term damage due to its inert nature. The present model series review aimed to assess the safety of this procedure by examining inflammatory stimulus, biocompatibility and tissue reaction following talc pleurodesis. Talc slurry was performed in rabbits: 200 mg/kg checked at postoperative day 14 (five models), 200 mg/kg checked at postoperative day 28 (five models), 40 mg/kg, checked at postoperative day 14 (five models), 40 mg/kg checked at postoperative day 28 (five models). Talc poudrage was performed in pigs: 55 mg/kg checked at postoperative day 60 (18 models). Tissue inspection and data collection followed the surgical pathology approach currently used in clinical practice. As this was an observational study, no statistical analysis was performed. Regarding the rabbit model (Oryctolagus cunicoli), the extent of adhesions ranged between 0 and 30%, and between 0 and 10% following 14 and 28 days, respectively. No intraparenchymal granuloma was observed whereas, pleural granulomas were extensively encountered following both talc dosages, with more evidence of visceral pleura granulomas following 200 mg/kg compared with 40 mg/kg. Severe florid inflammation was observed in 2/10 cases following 40 mg/kg. Parathymic, pericardium granulomas and mediastinal lymphadenopathy were evidenced at 28 days. At 60 days, from rare adhesions to extended pleurodesis were observed in the pig model (Sus Scrofa domesticus). Pleural granulomas were ubiquitous on visceral and parietal pleurae. Severe spotted inflammation among the adhesions were recorded in 15/18 pigs. Intraparenchymal granulomas were observed in 9/18 lungs. Talc produced unpredictable pleurodesis in both animal models with enduring pleural inflammation whether it was performed via slurry or poudrage. Furthermore, talc appeared to have triggered extended pleural damage, intraparenchymal nodules (porcine poudrage) and mediastinal migration (rabbit slurry).

Inositol 1,4,5-trisphosphate receptor type 1 autoantibodies in paraneoplastic and non-paraneoplastic peripheral neuropathy.

BackgroundRecently, we described a novel autoantibody, anti-Sj/ITPR1-IgG, that targets the inositol 1,4,5-trisphosphate receptor type 1 (ITPR1) in patients with cerebellar ataxia. However, ITPR1 is expressed not only by Purkinje cells but also in the anterior horn of the spinal cord, in the substantia gelatinosa and in the motor, sensory (including the dorsal root ganglia) and autonomic peripheral nervous system, suggesting that the clinical spectrum associated with autoimmunity to ITPR1 may be broader than initially thought. Here we report on serum autoantibodies to ITPR1 (up to 1:15,000) in three patients with (radiculo)polyneuropathy, which in two cases was associated with cancer (ITPR1-expressing adenocarcinoma of the lung, multiple myeloma), suggesting a paraneoplastic aetiology.MethodsSerological and other immunological studies, and retrospective analysis of patient records.ResultsThe clinical findings comprised motor, sensory (including severe pain) and autonomic symptoms. While one patient presented with subacute symptoms mimicking Guillain-Barré syndrome (GBS), the symptoms progressed slowly in two other patients. Electrophysiology revealed delayed F waves; a decrease in motor and sensory action potentials and conduction velocities; delayed motor latencies; signs of denervation, indicating sensorimotor radiculopolyneuropathy of the mixed type; and no conduction blocks. ITPR1-IgG belonged to the complement-activating IgG1 subclass in the severely affected patient but exclusively to the IgG2 subclass in the two more mildly affected patients. Cerebrospinal fluid ITPR1-IgG was found to be of predominantly extrathecal origin. A 3H-thymidine-based proliferation assay confirmed the presence of ITPR1-reactive lymphocytes among peripheral blood mononuclear cells (PBMCs). Immunophenotypic profiling of PBMCs protein demonstrated predominant proliferation of B cells, CD4 T cells and CD8 memory T cells following stimulation with purified ITPR1 protein. Patient ITPR1-IgG bound both to peripheral nervous tissue and to lung tumour tissue. A nerve biopsy showed lymphocyte infiltration (including cytotoxic CD8 cells), oedema, marked axonal loss and myelin-positive macrophages, indicating florid inflammation. ITPR1-IgG serum titres declined following tumour removal, paralleled by clinical stabilization.ConclusionsOur findings expand the spectrum of clinical syndromes associated with ITPR1-IgG and suggest that autoimmunity to ITPR1 may underlie peripheral nervous system diseases (including GBS) in some patients and may be of paraneoplastic origin in a subset of cases.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-016-0737-x) contains supplementary material.

C1 Case series: managing desquamative inflammatory vaginitis in trans-men

Background/introduction Desquamative inflammatory vaginitis (DIV) is an uncommon condition characterised by florid vaginal inflammation causing vaginal discharge, vulval pain and dyspareunia. Microscopy typically shows absent vaginal flora, numerous polymorphs and immature parabasal cells with no mature epithelia. The pathogenesis of DIV is currently unknown but may involve tissue kallikrein-related peptidases which are regulated by sex hormones and corticosteroids. Case-1: 35-year-old trans-man on testosterone for 18-months presenting with yellow vaginal discharge, vestibular pain and dyspareunia. Examination revealed vaginal inflammation and mucopurulent discharge. Microscopy was typical of DIV. He was treated with intravaginal clindamycin reporting a good response. Case-2: 26-year-old trans-man on testosterone for 7-years presenting with vaginal discharge, dyspareunia and post-coital bleeding. Examination revealed inflamed friable vaginal mucosa. Microscopy findings were typical of DIV and he started treatment with intravaginal clindamycin (partial-response) and switched to intravaginal prednisolone. Case 3: 20-year-old trans-man with vaginal discharge and post-coital bleeding who started testosterone 6-months earlier. Examination and microscopy findings were typical of DIV. He commenced treatment with intravaginal clindamycin (partial-response) and switched to intravaginal prednisolone. Case 4: 19-year-old trans-man on testosterone for 9-months presenting with vaginal pain and bleeding. Examination and microscopy were typical of DIV. He started treatment with intravaginal clindamycin (partial-response) and switched to intravaginal prednisolone. Discussion We present four cases of DIV in trans-men possibly associated with androgens responding to intravaginal clindamycin and steroids. As well as causing significant morbidity DIV may increase transmission of sexually-transmitted-infections in trans-men: we need to understand more about its aetiology, management and long term outcomes.

Acute alcoholic hepatitis and cellular Th1 immune responses to alcohol dehydrogenase

BackgroundAlcoholic hepatitis is characterised by florid hepatic inflammation, liver failure, and death within 28 days in 35% of patients. We recently showed proliferative peripheral blood mononuclear cell (PBMC) responses to alcohol dehydrogenase (ADH) in patients with alcohol-related cirrhosis, associated with T-helper-type 1 (Th1) immunity and disease severity. We aimed to define whether ADH-specific cellular immunity is present in alcoholic hepatitis. MethodsPBMCs were collected from 15 patients with alcoholic hepatitis (modified Maddrey's discriminant function >32), nine with alcohol-related cirrhosis (long-term alcohol abstinence), and three healthy controls. 25 overlapping peptides, spanning the human ADH β1 subunit, were constructed. Proliferation to ADH peptides (1 × 105 cells per well, cultured with 10 mM peptides for 7 days) was assessed by 3H-thymidine incorporation. A stimulation index (SI) of 2·5 or more was regarded as positive. ELISA measured concentrations of interferon γ (IFNγ), interleukin (IL) 17, and IL4 from supernatant. FindingsPBMCs from seven of 15 patients with alcoholic hepatitis recognised one to three ADH peptides (SI ≤5·7). IFNγ (mean 390·9 pg/mL [SE 31·4]) was detected in 48% of wells, IL17 (20·1 [3 ·4]) in 15%, and IL4 (90·5 [9·3]) in 14%. PBMCs from six of the nine patients with alcohol-related cirrhosis recognised one to five peptides (SI ≤5·2). IFNγ (360·7 [58·9], p>0·05) was detected in 31% of wells, IL17 (57·7 [10·9], p=0·0006) in 19%, and IL4 (219·7 [11·2], p=0·0012) in 28%. PBMCs from two healthy controls recognised one to two peptides (SI ≤3·1); all cytokine levels were below baseline. InterpretationProliferative anti-ADH immune responses in alcoholic hepatitis focused on individual epitopic regions. Predominance of proinflammatory Th1 responses was more pronounced in alcoholic hepatitis than in alcoholic-related cirrhosis. This finding requires investigation of targeted therapies to inhibit Th1 immunity in alcoholic hepatitis. FundingWellcome Trust.

Renal Allograft Rejection

Renal Allograft Rejection

Differential response to bacteria, and TOLLIP expression, in the human respiratory tract

ObjectivesThe observation that pathogenic bacteria are commonly tolerated in the human nose, yet drive florid inflammation in the lung, is poorly understood, partly due to limited availability of primary human...

Intrauterine Candida albicans infection elicits severe inflammation in fetal sheep

BackgroundPreventing preterm birth and subsequent adverse neonatal sequelae is among the greatest clinical challenges of our time. Recent studies suggest a role for Candida spp. in preterm birth and fetal injury, as a result of their colonization of either the vagina and/or the amniotic cavity. We hypothesised that intraamniotic C. albicans would cause a vigorous, acute fetal inflammatory response.MethodsSheep carrying singleton pregnancies received single intraamniotic (IA) injections of either saline (control) or 107 CFU C. albicans 1 or 2 d prior to surgical delivery and euthanasia at 124 ± 2 d gestation.ResultsColonization of the amniotic cavity by C. albicans resulted in a modest inflammatory response at 1 d and florid inflammation at 2 d, characterised by fetal thrombocytopenia, lymphopenia and significant increases of inflammatory cytokines/chemokines in the fetal membranes skin, lung and the amniotic fluid.ConclusionAcute colonization of the amniotic cavity by C. albicans causes severe intrauterine inflammation and fetal injury. C. albicans is a potent fetal pathogen which can contribute to adverse pregnancy outcomes.

Die Behandlung periprothetischer Femurfrakturen nach Hüft-TEP-Implantation mittels sonderangefertigten retrograden Hohlnagels

Treatment of periprosthetic fractures by implantation of a specially constructed, retrograde hollow nail which fits over the tip of the prosthesis and becomes locked on it. Periprosthetic femoral fractures with firmly anchored prosthesis shaft after total hip arthroplasty of types B1 and C according to the Vancouver classification. Loosened prosthesis (type B2/B3) and trochanteric fractures (type A). Broken or damaged prosthesis, florid inflammation and soft tissue injuries in the operation field, contracted knee joint, advanced deformation in the knee joint and distal femur, enclosed prosthesis and general contraindications. In a supine position the periprosthetic fracture is exposed via a lateral access. For cemented prostheses the cement is removed around the tip of the prosthesis (at least 2-3 cm) and medullary cavity. Arthrotomy with flexion of the knee joint and marking of the nail entry point. Drill the medullary cavity, retrograde introduction of the nail, visually fit the nail over the tip of the prosthesis and lock the nail with the prosthesis. If necessary use additional spongiosaplasty or also placement of additional cerclages depending on fracture type and size of the defect zone. Lock the nail distally. Use intraoperative radiological imaging to control correct positioning and length of the nail. Close the wound layer by layer with placement of suction drainage devices and dressing. Partial loading for 6 weeks with a subsequent pain-adapted loading gradient until full loading is possible. If selective partial loading is not possible, a decision must be made in individual cases as to whether the intraoperative findings allow immediate full loading. From 2004 to 2011 a total of 25 periprosthetic femoral fractures in 25 patients were treated in 2 locations using specially constructed slotted hollow nails. Within the framework of a retrospective study 20 of these patients (16 female and 4 male; average age 77.2 [72-84] years) were clinically and radiologically re-examined on average 19.3 (7-31) months postoperatively. No postoperative bleeding, wound healing disorders and infections. In all patients there was a loading stable consolidation of the fracture in the correct femoral axis, length and rotation with no evidence for radiological signs of loosening of the prosthesis or dislocation of the nails. In one case there was loosening of the prosthesis which had obviously occurred during the operative procedure. After consolidation of the fracture it was necessary to exchange the prosthesis for a long shafted prosthesis. A comparable situation to the preoperative degree of mobility was found in 12 out of the 20 patients, a moderate deterioration in 5 patients, a substantial residual impairment in 2 patients and an improvement of the situation in 1 patient.

The Biology of IL-15: Implications for Cancer Therapy and the Treatment of Autoimmune Disorders

IL-15 has a pivotal role in life and death of natural killer (NK) and CD8 memory T cells. IL-15 signals through a heterotrimeric receptor involving the common gamma chain (γc) shared with IL-2, IL-4, IL-7, IL-9, and IL-21, IL-2/IL-15 receptor β (IL-15Rβ) shared with IL-2 and a private IL-15Rα subunit. IFN- or CD40 ligand-stimulated dendritic cells coordinately express IL-15 and IL-15Rα. Cell surface IL-15Rα presents IL-15 in trans to cells that express IL-2/IL-15Rβ and γc. IL-15 is being used to treat patients with metastatic malignancy. However, IL-15 is an inflammatory cytokine involved in immunological memory including that to self, thereby playing a role in autoimmune diseases. These insights provide the scientific basis for clinical strategies directed toward diminishing IL-15 action. Dysregulated IL-15 expression was demonstrated in patients with rheumatoid arthritis, inflammatory bowel disease, psoriasis, celiac disease, and alopecia areata. The monoclonal antibody Hu-Mik-β-1 targets the cytokine receptor subunit IL-2/IL-15Rβ (CD122), blocks IL-15 transpresentation, and is being used in clinical trials in patients with autoimmune diseases. In parallel, clinical trials have been initiated involving the Jak2/3 (Janus kinase-2/3) inhibitor tofacitinib and Jak1/2 inhibitor ruxolitinib to block IL-15 signaling.

The role of dynamic contrast-enhanced MRI in differentiation of local recurrence and residual soft-tissue tumor versus post-treatment changes

To evaluate the reliability of dynamic contrast-enhanced MRI in the diagnosis of local recurrence of malignant soft-tissue tumors after receiving treatment. From March 2002 till December 2009 we performed dynamic contrast enhanced MRI in 95 patients with soft-tissue tumor after receiving treatment (surgery, radiotherapy, chemotherapy). Patients were classified according to five types of TIC. The recurrent disease was suspected in 47 patients and the biopsy was recommended. In 8 cases (TIC II), the biopsy was performed due to long-term post-treatment changes. Histological results proved STT recurrence in 45 patients; in 10 patients (8 with TIC II), biopsy revealed hypervascular granulation tissue, florid inflammation and reactive changes. The sensitivity for dynamic contrast-enhanced MR examination was 100 %, specificity 80 %, positive predictive value (PPV) 95.7 % and negative predictive value (NPV) 100 %. Our results indicate that TICs III, IV and V raise high suspicion of local tumor recurrence and require percutaneous imaging-guided biopsy. TIC of type II usually represents a pseudomass and the biopsy should be performed only in selected cases with increased risk of recurrent disease based on multidisciplinary approach. On the basis of literature review as well as our experiences we created a reliable algorithm proposed for diagnosing the residual or recurrent soft-tissue tumors (Tab. 2, Fig. 6, Ref. 20).

Gastrointestinal involvement in langerhans cell histiocytosis: consider treatment as for multi-system disease

Aims Langerhans cell histiocytosis (LCH) is a rare disorder characterised by abnormal proliferation of the Langerhans cell.1 While single system disease has a good prognosis, multisystem disease often requires intensive combination chemotherapy.23 Gastrointestinal (GI) involvement in LCH remains rare4 and its presence alone does not fit criteria for such treatment.3 The clinical picture can vary but most often consists of bloody diarrhoea, non bloody diarrhoea or constipation, protein losing enteropathy, hypoproteinaemia and anaemia.45 It almost exclusively affects children below two years of age and it has been noted that over half of patients with LCH and GI involvement die within one and a half years of diagnosis.45 Here we describe the case of a young female who required combination chemotherapy to control her GI disease. Methods A six month old female infant initially presented with a non-blanching erythematous rash involving the abdomen and groin, later developing bloody diarrhoea, intermittent bilious vomiting and failure to thrive. She was pale, wasted and developmentally delayed with a painless cystic lump on the occiput. There was lymphadenopathy and an enlarged spleen. Investigations revealed anaemia, thrombocytosis, elevated fibrinogen, a raised ESR and hypoalbuminaemia. Florid histiocytic inflammation of the small bowel was identified at endoscopy and a barium swallow showed narrowing of the distal duodenum and proximal jejunum without obstruction. Gut biopsies and skin samples confirmed the diagnosis of LCH. Results Dual therapy consisting of vinblastine and prednisolone was commenced with quick regression of her bone and skin disease. The addition of mercaptopurine and methotrexate was eventually required to control her GI disease. Almost three years post diagnosis she remains on this quadruple regimen as maintenance therapy. Her current disease status is that of regressing disease although her symptoms return towards the end of treatment intervals. Discussion The prevalence of GI involvement may be underestimated given its presentation; mild cases could be overlooked without endoscopic examination and biopsies. We may see a rise in recorded cases with increased availability of endoscopy. From our experience of this case we recommend that combination therapy is considered for cases of LCH with GI involvement.

Die Versorgung der dorsalen Endphalanxbasisfraktur der Langfinger mittels Hakenplatte

Anatomical reposition and stabilization of dorsal distal phalanx fractures with a hook plate. Dislocated mallet fractures type Doyle IVb with dislocation of the fragment by more than 2 mm and/or tilting of the fragment as well as dislocation of the dorsal distal phalanx fractures type Doyle IVc. Florid inflammation of and injuries to the soft tissues in the operation area. Dorsal approach to the distal interphalangeal joint (Y-, S-, H-shaped). Preparation of the fragment, cleaning the fracture gap, repositioning of the fragment, mounting of the plate, placing the screw. Controlling by image converter. Suture of the skin; tape. Stack splint for 4 weeks. After week 3, start with exercising of the distal interphalangeal joint within the splint. Physiotherapy is usually not required. Full exertion after 6-8 weeks is possible. The period of inability to work is dependent on the patient's occupation. Due to the danger of perforation and infection, it is recommended that the plate be removed after 3-6 months. From February 2002 to September 2009, 77 mallet fractures type Doyle IVb and IVc were operatively stabilized with a hook plate. In a retrospective study, 59 patients were followed up at a mean interval of 38.3 (3-69) months after the operation. Wound healing problems or inflammation were not observed. Visible disturbances of nail growth were macroscopically seen in 11.9%. Results were very good in 35 patients (59.3%), good in 16 patients (27.1%), sufficient in 5 patients (8.5%), satisfying in 1 patient (1.7%), and insufficient in 2 patients (3.4%).

Characterization of Retrokeratoprosthetic Membranes in the Boston Type 1 Keratoprosthesis

To evaluate retroprosthetic membranes that can occur in 25% to 65% of patients with the Boston type 1 keratoprosthesis (KPro). Two patients with Peter anomaly and 2 with neurotrophic scarred corneas underwent revisions of their type 1 KPros because of visually compromising retroprosthetic membranes. The excised membranes were studied by light microscopy with hematoxylin-eosin, periodic acid-Schiff, and toluidine blue stains. Immunohistochemical and transmission electron microscopic examination were also used. Light microscopic examination revealed that the retro-KPro fibrous membranes originated from the host's corneal stroma. These mildly to moderately vascularized membranes grew through gaps in the Descemet membrane to reach behind the KPro back plate and adhere to the anterior iris surface, which had undergone partial lysis. In 2 cases, the fibrous membranes merged at the pupil with matrical portions of metaplastic lens epithelium, forming a bilayered structure that crossed the optical axis. Retro-KPro membranes stained positively for α-smooth muscle actin but negatively for pancytokeratin. Electron microscopy confirmed the presence of actin filaments within myofibroblasts and small surviving clusters of metaplastic lens epithelial cells. Stromal downgrowth, rather than epithelial downgrowth, was the major element of the retro-KPro membranes in this series. Metaplastic lens epithelium also contributed to opacification of the visual axis. Florid membranous inflammation was not a prominent finding and thus probably not a requisite stimulus for membrane development. Further advances in prosthetic design and newer antifibroproliferative agents may reduce membrane formation.

Immune Activation and Gut Microbes in Irritable Bowel Syndrome

Irritable bowel syndrome (IBS) is a highly prevalent disorder that is characterized by chronic abdominal pain and altered bowel habit. The diagnosis of IBS has traditionally been made by matching the complaints of the patient with established clinical criteria, since the underlying pathophysiology was not known. Various new findings have recently been reported in IBS patients that challenge our concept of IBS as a syndrome with no explanation. While the florid inflammation characteristic of inflammatory bowel disease is absent in IBS, changes suggesting immune activation are present in nearly all IBS patients. Is IBS an autoimmune disease, or is the immune activation responding to a trigger? In this review we present evidence that points to a state of immune activation in IBS and show data that suggest that small intestinal bacterial overgrowth triggers immune activation in IBS.

Fatal unmasking tuberculosis immune reconstitution disease with bronchiolitis obliterans organizing pneumonia: the role of macrophages

Fatal unmasking tuberculosis immune reconstitution disease with bronchiolitis obliterans organizing pneumonia: the role of macrophages