Non-familial juvenile polyposis with histological evidence of adenomatous transformation.

A 14-year-old male presented with abdominal pain, diarrhoea and a sensation of something prolapsing through the anus during defecation, and was found to have diffuse colonic polyposis. There was no evidence of mucocutaneous hyperpigmentation and family history was negative, suggesting a diagnosis of non-familial juvenile polyposis. Histological analysis of multiple endoscopic biopsies showed features typical of juvenile or retention type (hamartomatous) lesions: dilated cystic glands lined by mucocus-secreting epithelium and prominent, inflamed and congested lamina propria. However, admixed with these features, focal areas of atypical adenomatous changes were recognized. Even the intervening normal-looking colonic mucosa showed some dysplastic changes. These findings indicate that hamartomatous and atypical adenomatous epithelial changes can co exist in non-familial juvenile polyposis and the latter may confer a risk of malignant transformation in this otherwise non-neoplastic disease.     

True epiphrenic diverticulum of esophagus secondary to tubercular adenitis.

Ephiphrenic esophageal diverticulum is rare and usually is a pulsion-type pseudodiverticulum that occurs in association with motility disorders of the esophagus. We report a 35-year-old man with tubercular lymphadenitis causing true traction type of epiphrenic diverticulum. Esophageal diverticulectomy and esophagomyotomy was done; he is doing well on antitubercular drugs.     

External duodenal fistula following closure of duodenal perforation.

AIM: Retrospective analysis of experience with management of external duodenal fistula (EDF) without using total parenteral nutrition (TPN). METHOD: Medical records of 31 patients with EDF following closure of duodenal ulcer perforation, treated over a 7-year period (1994-2001), were studied. Twenty-one patients (68%) had evidence of sepsis at presentation or during the course of treatment. None could afford TPN for optimum time. All patients received hospital-based enteral nutrition through nasojejunal tube, besides supportive medical treatment and/or surgery. Peritonitis or failure to insert nasojejunal tube for enteric alimentation led to early surgery. RESULTS: Two patients died of septicemia and multi-organ failure within 48 hours of admission. Fourteen patients (48.3%) initially received conservative treatment (Group I); six of them later required surgery. Fifteen patients (51.7%) underwent early surgery due to peritonitis (n=9) or failure to establish enteral feeding (n=6) (Group II); wound infection, intra-abdominal abscess and septicemia were more common in these patients than those in Group I. Survival rate was higher in Group I than in Group II (86% versus 40%; p< 0.05). Septicemia and gastrectomy were the independent factors associated with high mortality. CONCLUSIONS: EDF can be satisfactorily managed without TPN. Successful placement of enteral feeding line, supportive treatment and delayed surgery can achieve survival in 85% of patients. Minimum intervention is recommended when early surgery is performed in peritonitis or to establish enteral feeding line.     

Scleromyxoedema with features of systemic sclerosis.

The case is described of a patient with scleromyxoedema with features typical of systemic sclerosis. The features were so characteristic that the disease was misdiagnosed as systemic sclerosis. A brief review of the association of the two diseases is given.     

Modification of apomorphine-induced behaviour following chronic swim exercise in rats.

Four week swim exercise schedule (45 min day-1, 6 days each week) in rats led to a significant adaptive change in functional responsiveness of dopamine receptors (auto-receptors) in the nigrostriatal and mesolimbic system that was evident from the modification of behavioural responses elicited by a low dose of apomorphine, a direct acting dopamine receptor agonist. Thus, a remarkable increase in yawning response, development of full blown stereotypy, as well as profound attenuation of locomotory and hypothermic response was observed in exercise-trained rats as compared with the non-exercise group (control), following intraperitoneal administration of 0.3 mg kg-1 of apomorphine.     

Antagonists that demonstrate species differences in neurokinin-1 receptors.

125I-Bolton-Hunter-substance P (125I-BH-SP) binding properties of three novel classes of neurokinin-1 (NK-1) receptor antagonists were investigated in tissues derived from humans, guinea pigs, and rats. 125I-BH-SP was shown to bind to a single class of binding sites, with similar dissociation constants, Kd, in human astrocytoma cells (U-373 MG), human urinary bladder, guinea pig forebrain, guinea pig ileum longitudinal smooth muscle, rat forebrain, and rat duodenum. In each tissue preparation, known peptide agonists and peptide antagonists yielded potencies typical for a NK-1 receptor profile, with little difference in binding properties between the various tissues. However, when the three classes of compounds, heterosteroids, cyanines, and modified peptides, were tested for their ability to displace 125I-BH-SP binding from the NK-1 receptor, very different binding profiles were observed. The heterosteroids were shown to be as much as 3 orders of magnitude more potent in tissues derived from rats than from humans or guinea pigs. A distinct species-dependent structure-activity relationship (SAR) was also observed for this class of compounds. Like the heterosteroids, the cyanines displaced 125I-BH-SP with 10-30-fold higher affinity in rat tissues than in human and guinea pig tissues. However, the SAR generated by the cyanines was comparable in all tissues studied. The modified peptides, on the other hand, were up to 10-100-fold more potent in human and guinea pig than rat tissues, producing a SAR that differed between the various species. No differences in binding properties between central nervous system and peripheral tissues from the same species were seen with these compounds. These results provide evidence for species differences in NK-1 receptors in humans, guinea pigs, and rats. Because it is known that there exists great sequence identity between rat and human NK-1 receptors, it is hypothesized that key amino acid changes or different lipid environments within the transmembrane binding region of the receptor may account for the observed species difference. Furthermore, this study emphasizes that caution is necessary in the choice of species to be used in development programs targeted towards therapeutic entities in the NK-1 receptor antagonist area.     

Neurogenic bladder in acquired immune deficiency syndrome (AIDS).

This is the first report of incidence of neurogenic bladder in patients with acquired immune deficiency syndrome (AIDS) and emphasizes that it is a significant cause of various voiding dysfunctions in these patients. Neurologic disease occurs in about one third of patients with AIDS. Both central and peripheral nervous systems may be involved. Urodynamic evaluation is necessary for assessment and management of neurogenic voiding disorders in this group of patients.     

Acute polymyositis associated with W. bancrofti

Two cases of acute polymyosotis associated with W. bancrofti , presented with generalised painful swelling and weakness of the muscles. These patients had elevated muscle enzymes, a myopathic EMG pattern, inflammatory myopathy on biopsy and W. bancrofti in the peripheral blood smear. The clinical, improvement of the disorder and total clearance of microfilariae was obtained with the combination therapy of steroid and diethyl-carbamazine in comparison with steroid alone.     

Acute hypercalcemia, pancreatic duct permeability, and pancreatitis in cats

We investigated the effects of hypercalcemia on pancreatic duct permeability and pancreatitis in cats. Acute hypercalcemia was maintained by an infusion of calcium gluconate; controls received saline solution. Chronic hypercalcemia was maintained by diet and by vitamin D and dihydrotachysterol injections. Portal venous blood was analyzed for large dextran molecules that had been perfused through the pancreatic duct. In a separate group of hypercalcemic animals, we perfused the duct with activated pancreatic enzymes to induce acute pancreatitis. After 24 hours of hypercalcemia, dextrans were detected in the portal venous blood of 6 of 11 hypercalcemic and none of the 6 control animals (p less than 0.05). After 12 hours of hypercalcemia, dextrans were detected in all 7 hypercalcemic and 1 of 7 control animals (p less than 0.001). The degree of pancreatic inflammation was greater in the 12-hour animals than in the controls (p less than 0.001). After 14 days of hypercalcemia, however, there were no differences in dextran permeability or pancreatitis in experimental or control animals. Our results indicate that acute hypercalcemia increases the permeability of the pancreatic duct to molecules the size of pancreatic enzymes. This could be important in the pathogenesis of acute pancreatitis associated with hypercalcemic states.