Cutaneous leishmaniasis: Clinical report of two cases and review of the recent literature

With 1–1.5 million cases reported every year cutaneous leishmaniasis represents an increasing health problem. The course of cutaneous leishmaniasis varies from a single self‐healing ulcer to a persistent ulcer or progressive mucosal disease with nasopharyngeal destruction. An enormous array of topical and systemic treatment modalities has been endorsed. The response to treatment depends on the species of parasite as well as the host's immunological and genetic status. Species‐specific treatment guidelines based on evidence from controlled studies are highly desirable. We present two cases of cutaneous leishmaniasis, one in a child and one during pregnancy, reviewing various diagnostic and therapeutic measures with special attention to problems in young and pregnant patients.     

Incretin mimetics as a novel therapeutic option for hepatic steatosis.

BACKGROUND: Fat accumulation in the liver or non-alcoholic fatty liver disease (NAFLD) is regarded as a key pathogenic factor and component of the metabolic syndrome. It was reported that administration of the incretin mimetic exenatide reversed hepatic steatosis in an obese mouse model. We had the opportunity to study the effect of additional exenatide administration on liver fat content in a patient with type 2 diabetes. CASE REPORT: A 59-year-old male with poorly controlled type 2 diabetes was treated with exenatide in addition to metformin monotherapy. Following 44 weeks of exenatide therapy, mean the liver fat measured by liver spectroscopy declined from 15.8% to 4.3%. This dramatic decrease in liver fat was accompanied by significant beneficial changes in several cardiovascular disease risk factors and improvement of all liver enzymes, in particular alanine aminotransferase, the most important marker of liver steatosis. CONCLUSION: This case report suggests that the incretin mimetic exenatide decreases hepatic fat accumulation and may play a role in the future treatment of NAFLD, and the associated insulin resistance and cardiovascular risk factors in an ever-growing high-risk population.     

Interleukin-6 and tumour necrosis factor alpha are expressed by keratinocytes but not by Langerhans cells.

The presence of human cytokines was examined in parallel skin biopsies and epidermal single cell preparations obtained from normal individuals. Using biotin-avidin-peroxidase and immunofluorescence techniques and antibodies against recombinant cytokines, a granular intercellular/membrane-associated staining for interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF alpha), but not IL-1 alpha or beta, was observed. An epidermal cytoplasmic staining pattern was also detected, which was most pronounced using the anti-rIL-6 antiserum. In the epidermal single cell preparations, membrane-associated staining was detected for both IL-6 and TNF alpha. Double staining revealed that CD1-positive Langerhans cells (LC) failed to express any of the examined cytokines. In vitro binding of rIL-6 or rTNF alpha to skin sections and epidermal single cell preparations indicated that the cell surface-associated IL-6 and TNF alpha originally demonstrated on keratinocytes were truly membrane-bound. Finally, co-cultivation of epidermal cells with an IL-6 responsive cell line, B9, and testing of epidermal cell supernatants in this assay, indicated that the in vivo membrane-bound IL-6 had biological activity.     

Elastolytic activity of human monocytes from synovial fluid and blood of patients with arthritis. Relations to levels of interleukin 6 and soluble interleukin 2 receptor

Synovial fluid (SF) and blood from 24 patients with non-traumatic, sterile hydarthron were examined for monocyte elastolysis (M?E) and for levels of interleukin 6 (IL-6) and of soluble interleukin 2 receptor (sIL-2R). Six patients had osteoarthrosis (OA) and 18 patients had inflammatory hydarthron (IH), 10 of whom had rheumatoid arthritis (RA). Blood M?E was lower in OA than in IH, both measured as basal M?E activity and after in vitro stimulation with immune complexes and phorbol myristate acetate (PMA). SF M?E was higher than M?E in blood (p less than 0.01). This increase in SF M?E could be mimicked in vitro by prestimulation of blood M? with low levels of IC. SF IL-6 and sIL-2R were also elevated (p less than 0.01). All three parameters correlated to the degree of joint inflammation evaluated by SF leucocyte level, complement activation, blood C Reactive Protein, and to the clinical evaluation of the joint. The increase in SF M?E, IL-6 and sIL-2R in patients with IH, points to a stimulation of M? and lymphocytes in the joint.     

Emotional abuse, self-blame, and self-silencing in women with irritable bowel syndrome

OBJECTIVE: The purpose of this study was to investigate the presence of emotional abuse and two psychosocial constructs (self-blame and self-silencing) in a sample of women diagnosed with irritable bowel syndrome (IBS) relative to a comparison sample of women diagnosed with inflammatory bowel disease (IBD). METHODS: Women diagnosed with IBS (N = 25) were compared with women diagnosed with IBD (N = 25) on measures of history of abuse, self-blame, and self-silencing. RESULTS: It was found that women in the IBS sample scored significantly higher on emotional abuse, self-blame, and self-silencing than did women in the IBD sample. These three variables were also found to be significantly intercorrelated in both the IBS and IBD samples. Finally, emotional abuse was significantly higher in IBS patients than in IBD patients beyond the differences accounted for by physical and/or sexual abuse history. CONCLUSIONS: These findings empirically demonstrate an association between IBS and emotional abuse, as well as a possible connection with psychosocial variables, that may mediate the connection between emotional abuse and functional bowel symptoms. We suggest that these variables be further evaluated in the context of clinically relevant research on IBS.     

Evaluation of the significance of binding of calcium-45 to isolated rat mast cells during histamine release

Conclusions The present study of binding of Ca-45 during histamine release could not distinguish between specific uptake of calcium and non-specific equilibration of calcium secondarily to morphological changes in connection with secretion. The results do not exclude a possible role of calcium to trigger secretion, but studies on Ca-45 binding do not seem to give conclusive information as to the functional significance of calcium in the release process.     

The mechanism of histamine release induced by the ionophore X537A from isolated rat mast cells. II. The relationship between increase of cell volume and histamine release

The ionophore X537A induced swelling of isolated rat mast cells parallel to histamine release. Both actions were depressed by extracellular calcium and BSA, temperatures below 37°C, NEM, PMSF, and TTX, and were enhanced by high potassium and pretreatment of the cells with ATP. DSCG, theophylline, and DFP enhanced the histamine release noted after 10 min of incubation without influencing the swelling action of X537A. The swelling action could not be separated from histamine release and it is suggested that it right be inherent in the mechanism of secretion induced by X537A. The present results further distinguish histamine release induced by the two ionophores X537A and A23187.     

The influence of phosphatidyl serine on the release of histamine from isolated rat mast cells induced by different agents

The influence of phosphatidyl serine (PS) on histamine release from isolated rat mast cells induced by antigen, compound 48/80, adenosine-5′-triphosphate (ATP), the ionophore A23187, and decylamine was studied. PS enhanced antigen-induced release but inhibited the release caused by compound 48/80, A23187, and decylamine. PS did not influence the release induced by ATP. The different effects of PS on the action of the various histamine releasing agents do not conform to a unifying model for the action of PS on the release process. Possible interactions between PS and the agents in the incubation medium as well as at specific reactive sites on the plasma membrane might explain some of the effects of PS. Consequently, the results cannot be used as evidence for the existence of basic differences in the release process induced by various calcium-and energy-dependent releasing agents.