[Diagnostic image (84). A woman with persisting perianal fissures]. / Diagnose in beeld (84). Een vrouw met persisterende anusfissuren.

A 63-year-old woman had perianal fissures, which were caused by an amelanotic melanoma of the anus.

Transanal endoscopic microsurgery for rectal cancer.

If curation is intended for rectal cancer, total mesorectal excision with autonomic nerve preservation (TME) is the gold standard. Transanal resection is tempting because of low mortality and morbidity rates. However, inferior tumour control, provoked by the limitations of the technique, resulted in its cautious application and use mainly for palliation. Transanal endoscopic microsurgery (TEM) is a minimal invasive technique for the local resection of rectal tumours. It is a one-port system, introduced transanally. An optical system with a 3D-view, 6-fold magnification and resolution as the human eye, together with the creation of a stabile pneumorectum, and specially designed instruments allow full-thickness excision under excellent view and a proper histological examination. The technique can also be applied for larger and more proximal tumours. Mortality, morbidity as well as incomplete excision rates are minimal. Local recurrence and survival rates seem comparable to TME in early rectal cancer. TEM is the method of choice when local resection of rectal cancer is indicated. Results justify a re-evaluation of the indications for the local excision of rectal cancer with a curative intent.

[Rubberband ligation of hemorrhoids: symptoms almost gone after 6 weeks, but many patients need retreatment in the long run]. / Rubberbandligering van hemorroïden: klachten na 6 weken veelal verdwenen, maar nieuwe behandeling op langere termijn bij veel patiënten noodzakelijk.

OBJECTIVE: To assess the short and middle-long term results of outpatient treatment of internal haemorrhoids by rubber band ligation. DESIGN: Prospective. METHODS: The results and the complications of rubber band ligation were assessed in a group of consecutive patients treated for internal haemorrhoids by one surgeon in March 1995-September 1997 in the Laurentius Hospital Roermond, the Netherlands. Middle-long term results were assessed by an independent examiner who questioned the patients by phone. RESULTS: Ninety-four patients were treated: 43 women and 51 men, with a mean age of 51 years (range: 23-80). After 6-18 weeks 80 out of 90 accessible patients (89%) were symptom-free, 71 (79%) of them after one treatment. Serious complications were not reported. However, the days after treatment mild complaints of anal urgency and pain were present in 16 patients (20%). Twenty-three patients underwent sigmoidoscopy. In 10 patients (43%) adenomatous polyps (in 9 patients) or diverticulosis (in 1 patient) were found. After a mean of 18 months (range: 6-31) 32 patients (41%) (still) had anal complaints compatible with haemorrhoids. CONCLUSION: Rubber band ligation is an easy and safe outpatient treatment of internal haemorrhoids. Most patients become symptom-free, often after one treatment. However, about 40% of the patients have recurrent symptoms within a few years after initial treatment.

Dysmenorrhea related to gallstone spilling after laparoscopic cholecystectomy.

A 28-year-old woman is presented with severe dysmenorrhea since a previous laparoscopic cholecystectomy for cholelithiasis. Spilled gallstones were embedded in the Douglas cavity and the visceral peritoneum of the genitalia interna. Dysmenorrhea was treated successfully by laparotomic hysterectomy and removal of all gallstones.

A rare complication of implanted central-venous access devices: catheter fracture and embolization.

Totally implanted central-venous access devices are frequently used for the administration of chemotherapy or parenteral nutrition. Catheter fracture is a rare complication of these devices, with an estimated rate of 0.1%. We have lately seen three cases of catheter fracture with embolization of a catheter fragment to the heart and pulmonary vessels. These cases are described in this article. Catheter fracture is caused by intermittent compression of the catheter between the clavicula and the first rib, which can occur when the catheter has been inserted too far medially. When, on an X-ray of the chest, the catheter is shown to be compressed at the point where the clavicula crosses the first rib, or when infusion through the device suddenly becomes difficult, the chance of catheter fracture is high and the device should be removed.

Parotidectomy for parotid tumours: 19-year experience from The Netherlands.

A total of 150 patients were treated for parotid tumours over a period of 19 years. In 94 per cent superficial or total parotidectomy was performed. Histological diagnosis of the resected specimen revealed pleomorphic adenoma in 92 patients (61 per cent), Whartin's tumour in 30 (20 per cent), various benign neoplasms in 11 (7 per cent) and malignant tumour in 17 (11 per cent). After a mean follow-up of 7.7 years, no recurrence of a benign tumour was seen. Malignant tumours recurred in five patients. Permanent partial facial paralysis was seen in 4 per cent of patients after surgery for benign lesions. Frey's syndrome was observed in 43 per cent of patients, and was not prevented by resection of the auriculotemporal nerve.

Cross-linking of both Fc gamma RI and Fc gamma RII induces secretion of tumor necrosis factor by human monocytes, requiring high affinity Fc-Fc gamma R interactions. Functional activation of Fc gamma RII by treatment with proteases or neuraminidase.

Cross-linking of Fc gamma R on human monocytes with human IgG has been shown to induce secretion of the inflammatory and immunoregulatory cytokine TNF. In the present study we examined the role of both constitutively expressed monocyte Fc gamma R, the 72-kDa high affinity Fc gamma R (Fc gamma RI), and the 40-kDa low affinity receptor (Fc gamma RII), in the induction of TNF secretion. On the basis of preferential binding of the Fc moiety of murine mAb of different isotype, Fc gamma RI and Fc gamma RII were selectively cross-linked by using either solid-phase murine (m)IgG2a, or solid-phase mIgG1, respectively. On freshly isolated, untreated monocytes only cross-linking of Fc gamma RI with solid-phase mIgG2a induced TNF secretion. The interaction between Fc gamma RII and mIgG1 could be enhanced by treatment of monocytes with proteases or with the desialylating enzyme neuraminidase. After treatment of monocytes with these enzymes, TNF secretion was effectively induced by solid-phase mIgG1, apparently through cross-linking of Fc gamma RII. However, mIgG1-induced TNF secretion differed between protease-treated monocytes from high responder individuals and monocytes from low responder individuals, TNF secretion being considerably less in the latter population. Protease-treated monocytes and mononuclear cells from individuals with an inherited defect in cell membrane expression of Fc gamma RI were induced to secrete TNF by solid-phase human IgG, confirming the capacity of Fc gamma RII to induce TNF secretion. It was not possible to induce TNF secretion by cross-linking Fc gamma RI or Fc gamma RII with anti-Fc gamma R mAb and soluble or solid-phase anti-mIgG, indicating that high affinity Fc-Fc gamma R interactions are necessary to induce release of this cytokine.

Inhibitory effect of corticosteroids on the secretion of tumour necrosis factor (TNF) by monocytes is dependent on the stimulus inducing TNF synthesis.

The cytokine tumour necrosis factor (TNF) is believed to be involved in the pathophysiology of several human disease states, both septic and non-septic. Different pathways of induction are involved in the generation ofTNF in these disease states. We therefore used four different stimulatory agents, lipopolysaccharide, phorbol myristate acetate, silica quartz, and anti-human IgG antibody to study the influence of the corticosteroids prednisolone and budesonide on the secretion of TNF by human monocytes. Both prednisolone and budesonide inhibited TNF secretion induced by these four stimulating agents in a different degree. Inhibition was strong when TNF secretion was induced by lipopolysaccharide or anti-human IgG antibody. A weaker inhibitory effect was observed when TNF secretion was induced by silica quartz. Only minimal inhibition of phorbol myristate acetate induced TNF secretion was observed. Furthermore, it is shown that inhibition is dependent on the dose of corticosteroid, but not or only minimally on the dose of stimulating agent, indicating that inhibition cannot be overcome by increasing the cell-activating stimulus. Finally, optimal inhibition of TNF secretion by corticosteroids is shown to be dependent on the presence of corticosteroids during the phase of cell stimulation.

Plasma tumor necrosis factor and mortality in critically ill septic patients.

Tumor necrosis factor (TNF) cachectin has been implicated as an important host mediator responsible for shock and multiple organ failure (MOF) observed during sepsis. Using a sensitive enzyme-linked immunosorbent assay, we measured plasma TNF levels in 43 septic patients suffering from a broad range of diseases. Measurements were taken on the day that sepsis was diagnosed. Eleven patients had detectable TNF plasma levels ranging from 10 to 100 pg/ml (TNF-positive group); in 32 patients circulating TNF could not be detected (TNF-negative group). The groups did not differ significantly as to age, underlying disease, percentage positive bacteremia and bacteriologic profile, sepsis score, and extent of MOF. Eight (73%) of 11 TNF-positive patients died from sepsis during ICU stay, vs. 11 (34%) of 32 TNF-negative patients (p less than .05). This study demonstrates that sepsis is accompanied by detectable circulating TNF in 25% of the cases, and for these patients mortality is twice that for comparable TNF-negative patients.

Evidence of involvement of tumor necrosis factor in adverse reactions during treatment of kidney allograft rejection with antithymocyte globulin.

Serial plasma concentrations of the pyrogenic cytokines tumor necrosis factor and interleukin-1 beta were measured during treatment of acute renal allograft rejection with antithymocyte globulin in 7 consecutive kidney transplant recipients. TNF and IL-1 beta were measured with specific enzyme-linked immunosorbent assays. In 6 of 7 patients TNF could not be detected in the plasma before the start of the ATG infusion. During the first ATG infusion, which was accompanied by fever and other side effects in all patients, plasma TNF levels were shown to be elevated, ranging between 100 and 700 pg/ml. During the second ATG infusion, when side effects were minimal or absent, plasma TNF levels were only slightly raised. Circulating IL-1 beta could not be detected in any of the patients before or during ATG infusion. Additional experiments showed that TNF is rapidly secreted in cultures of peripheral blood mononuclear cells incubated with both ATG and the monoclonal antibody OKT3. These findings suggest that side effects, including fever and chills, during antilymphocyte antibody infusion are related to increased plasma levels of the pyrogenic cytokine TNF.

Fc-receptor cross-linking induces rapid secretion of tumor necrosis factor (cachectin) by human peripheral blood monocytes.

In this study it was demonstrated that cross-linking of FcR on human monocytes induces the secretion of the cytotoxic and immunoregulatory cytokine TNF. Both soluble and insoluble immune complexes, solid-phase antibody and antibody-coated phagocytizable particles were used to cross-link FcR on monocytes. It was observed that monocytes secreted large amounts of TNF in each of these instances. Kinetic studies performed with soluble immune complexes showed that TNF was secreted very rapidly, e.g., within 2 h after addition of immune complexes to monocytes. These findings are relevant for the understanding of FcR-mediated immune responses by monocytes and macrophages, for example antibody-dependent cellular cytotoxicity and phagocytosis, and for disease states associated with circulating or tissue-fixed immune complexes.

T cell-mediated production of tumour necrosis factor-alpha by monocytes.

The aim of this study was to examine the tumour necrosis factor (TNF)-alpha production by peripheral blood mononuclear cells activated by mitogens. Considerable amounts of TNF-alpha, ranging from 1.0 to 5.0 ng/ml, were present in the supernatants of cultures of human peripheral blood mononuclear cells (PBMC), stimulated with either the anti-CD3 monoclonal antibody OKT3 or the lectin phytohaemagglutinin (PHA). The amount of TNF-alpha secreted in the supernatant was closely correlated to the degree of T cell proliferation in such cultures, as measured by [3H]TdR incorporation. In the absence of proliferating T cells the mitogens did not induce secretion of TNF-alpha by monocytes. Supernatants of proliferating T cells were shown to induce TNF-alpha production by monocytes. The macrophage-activating factor gamma interferon (IFN-gamma) was also shown to induce, in the absence of endotoxin, TNF-alpha secretion by monocytes in a dose-dependent manner. The induction of TNF-alpha production by supernatants of proliferating T cells could largely be abrogated by passaging the supernatants on an anti-IFN-gamma column before adding them to the monocytes. It is therefore concluded from this study that the production of TNF-alpha by monocytes can be induced by proliferating T cells and that this induction can largely be attributed to the T cell lymphokine IFN-gamma.