Cutaneous lupus erythematosus: Diagnosis and treatment

Cutaneous lupus erythematosus (CLE) encompasses a wide range of dermatologic manifestations, which may or may not be associated with the development of systemic disease. Cutaneous lupus is divided into several sub-types, including acute CLE (ACLE), sub-acute CLE (SCLE) and chronic CLE (CCLE). CCLE includes discoid lupus erythematosus (DLE), LE profundus (LEP), chilblain cutaneous lupus and lupus tumidus. The diagnosis of these diseases requires proper classification of the sub-type, through a combination of physical examination, laboratory studies, histology, antibody serology and occasionally direct immunofluorescence, while ensuring to exclude systemic disease. The treatment of cutaneous lupus consists of patient education on proper sun protection along with appropriate topical and systemic agents. Systemic agents are indicated in cases of widespread, scarring or treatment-refractory disease. In this chapter, we discuss issues in classification and diagnosis of the various sub-types of CLE, as well as provide an update on therapeutic management.     

Hyperbaric oxygen: a novel modality to ameliorate experimental colitis

Background—Hyperbaric oxygen (HBO) has beensuggested to be beneficial in inflammatory bowel disease but themechanisms responsible for its therapeutic effects have not been elucidated.
Aim—To assess the effect of HBO treatment oncolonic damage in two models of experimental colitis, and to examinewhether this effect is mediated by modulation of NO synthesis.
Methods—Colitis was induced by either flushing thecolon with 2 ml 5% acetic acid or intracolonic administration of 30 mg trinitrobenzenesulphonic acid (TNB) dissolved in 0.25 ml 50% ethanol. Rats were exposed to HBO (100% oxygen at 2.4 atmosphere absolute) forone hour twice on the day of colitis induction and once daily thereafter. Control rats were treated only with acetic acid or TNB.Rats were killed 24 hours after acetic acid administration or one andseven days after TNB treatment. The colon was isolated, washed, andweighed, the lesion area was measured, and mucosal scrapings wereprocessed for determination of myeloperoxidase (MPO) and NO synthase(NOS) activities, prostaglandin E₂ (PGE₂) andleukotriene B₄ (LTB₄) generation.
Results—In control rats exposed for seven days toHBO, colonic NOS activity was significantly decreased by 61%, comparedwith its activity in untreated rats (2.93 (0.17) nmol/g/min). HBOsignificantly reduced by 51 and 62% the extent of injury induced byacetic acid and TNB respectively. The protection provided by HBO wasaccompanied by a significant decrease in colonic weight,PGE₂ generation, MPO, and NOS activities. In acetic acidcolitis, LTB₄ generation was also significantly decreased.
Conclusions—(1) HBO effectively decreases colitisinduced by acetic acid and TNB. (2) The decreased NOS activity inducedby HBO suggests that reduction in NO generation may be among the mechanisms responsible for the anti-inflammatory effect of HBO. (3) HBOmay be considered in the treatment of patients with refractory inflammatory bowel disease.

Keywords:hyperbaric oxygen; acetic acid colitis; trinitrobenzenesulphonic acid colitis; inflammatory bowel disease

     

Pouch Ileitis—Recurrence of the Inflammatory Bowel Disease in the Heal Reservoir

"Pouchitis" is an inflammation of the ileal pouch that has been described as occurring after Kock's procedure--the continent ileal pouch. The case presented herein demonstrates clinical and histological features that resemble ulcerative colitis, implying that this disorder may be a recurrence of the patient's original inflammatory bowel disease and not merely a local and nonspecific process as previously suggested.     

Esophageal Involvement in Pemphigus Vulgaris

Eight patients with pemphigus vulgaris were examined endoscopically for esophageal involvement. Most of them (seven of eight) had gastrointestinal symptoms of various types. Four of the patients had microscopical evidence of pemphigus vulgaris involving the esophagus. Three patients were found to have other diseases in their upper gastrointestinal tract accounting for their symptoms. There was no correlation between patients symptoms and macroscopic and microscopic findings. In patients with pemphigus vulgaris, endoscopy should be performed whenever gastrointestinal complaints appear, because the approaches to therapy could differ, according to the endoscopic findings.     

The use of carcinoembryonic antigen for identification of human tumor cells in malignant effusions

A specific anti-carcinoembryonic antigen (CEA) antiserum was used to identify CEA-positive tumor cells in peritoneal and pleural effusions obtained from patients with various malignant neoplasia. In 7 out of 10 fluids in which tumor cells were detected by cytological examinations, cytoplasmic CEA-positive cells were also detected by an indirect immunofluorescence test. In addition, out of 11 fluid samples cytologically negative for tumor cells, CEA-positive cells were found in 8 cases. When both staining for cytoplasmic CEA and soluble fluid CEA levels were considered in combination, 81% of the samples were found to be positive by either one or both of these markers, whereas only 54% were positive by using cytological criteria. The data suggest that CEA marker may be used to identify tumor cells and to assess malignancy in pleural and peritoneal effusions in patients with certain types of cancer. The CEA marker was also used for identifying tumor cells grown in tissue cultures and for separating viable CEA-positive and CEA-negative cells from a mixed cell population using the fluorescence-activated cell sorter.     

Development of Curricular Milestones for Hospice and Palliative Medicine Fellowship Training in the U.S.

Context

A physician workgroup of the American Academy of Hospice and Palliative Medicine sought to define curricular milestones (CMs) for hospice and palliative medicine (HPM) Fellowship Programs. The developed list of CMs would serve as components upon which to organize curriculum and standardize what to teach during training. These would complement entrustable professional activities previously developed by this group and new specialty-specific reporting milestones (RMs) for HPM developed through the Accreditation Council for Graduate Medical Education.

Role of vasoactive intestinal peptide (VIP) in pathogenesis of ethanol-induced gastric mucosal damage in rats

To elucidate the possible role of vasoactive intestinal peptide (VIP) in the pathogenesis of acute gastric mucosal damage, rats were treated intragastrically with 1.0 ml 96% ethanol with or without intravenous or intraperitoneal coadministration of VIP (1 nmol/liter to 1 mol/liter/100 g). VIP was found to double the mean lesion area when compared with that induced by ethanol alone (P<0.05), an effect that was prevented by VIP antagonist (1 mol/liter/100 g). A substance P antagonist (1 mol/liter/100 g) also reduced the extent of gastric damage induced by coadministration of VIP and ethanol. VIP antagonist or substance P antagonist significantly reduced ethanol-induced gastric mucosal damage. Gastric mucosal levels of LTB₄, LTC₄, VIP, and substance P were significantly increased in ethanol-treated rats as compared with saline-treated animals (P<0.05). The augmentation of ethanol-induced damage by VIP was associated with increased gastric mucosal levels of LTB₄. In VIP-treated rats, gastric mucosal levels of substance P were found to be significantly increased compared with control rats (P<0.05). Administration of VIP to pyloric-ligated rats significantly increased gastric acid output and blood pepsinogen A levels as compared with saline treated rats (P<0.05). Ketotifen, a mast cell stabilizer (100 g/100 g), administered orally 30 min before damage induction by ethanol, with or without VIP, totally abolished the damage of the surface epithelium of the entire gastric mucosa and significantly reduced the mucosal levels of LTC₄ and LTB₄ (P<0.05). It is suggested that VIP is involved in the pathogenesis of acute ethanol-induced gastric mucosal damage. The effective mucosal protection by ketotifen suggests a role for mast cells and their mediators in the pathogenesis of acute gastric mucosal damage.     

Ketotifen effectively prevents mucosal damage in experimental colitis.

The effects of ketotifen, a 'mast cell stabiliser,' on two models of experimental colitis were examined. The inflammatory response elicited by either trinitrobenzene sulphonic acid or acetic acid resulted in increased colonic synthesis of platelet activating factor, prostaglandin E2, thromboxane B2, leukotrienes B4 and C4, and myeloperoxidase activity. Intragastric administration of ketotifen 100 micrograms/100 grams twice daily significantly decreased mucosal damage when given prophylactically 48 hours before the induction of colitis and then throughout the experiment. This effect was consistent in both models and was accompanied by a significant reduction in mucosal generation of platelet activating factor, prostaglandin E2, thromboxane B2, and leukotrienes C4 and B4. Myeloperoxidase activity was reduced as well, reaching significance only in the acetic acid model. This study shows that both trinitrobenzene sulphonic acid and acetic acid colitis can be pharmacologically manipulated by ketotifen. The mechanism of action of ketotifen has not yet been determined. Ketotifen's potential in the treatment of active inflammatory bowel disease or in the prevention of exacertations, or both, remains to be elucidated.     

Octreotide effectively decreases mucosal damage in experimental colitis.

The effect of octreotide, a synthetic analogue of somatostatin, on the modulation of the acetic acid model of experimental colitis was examined. Colitis was induced by intracolonic administration of 2 ml of 5% acetic acid. The inflammatory response elicited by the acetic acid resulted in increased colonic synthesis of platelet activating factor, leukotriene B4 and decreased mucosal somatostatin levels. Subcutaneous administration of octreotide (10 micrograms/rat) 1 hour before or immediately after damage induction, as well as 1 and 23 hours after acetic acid application, resulted in a significant reduction in mucosal damage. The protective effect was accompanied by a significant reduction in platelet activating factor activity, leukotriene B4, and vasoactive intestinal peptide concentrations. There were no significant changes in mucosal leukotriene C4 and calcitonin gene related peptide levels. This study shows that acetic acid induced colitis is pharmacologically manipulated by octreotide. The mechanism of action of octreotide has not yet been fully determined. The potential use of octreotide in treating active inflammatory bowel disease remains to be evaluated.