Postoperative tetanus after gangrenous ileus

Tetanus has become an uncommon disease in developed countries. Tetanus is caused by exotoxins from the bacteria Clostridium tetani. This microbe, which is obligate anaerobe, is present in soil, and animal and human faeces. The condition usually appears after contamination of wounds. However, reports have been published of tetanus occurring after both acute and selective gastrointestinal surgery. We present a case of severe postoperative tetanus in a 57 year-old woman who underwent bowel resection after strangulation of the ileum. The patient was treated on an intensive care unit and was artificially ventilated for 64 days. Seven months later she had fully recovered. Clinical presentation, diagnosis, treatment, and complications are discussed in the report. The diagnosis of tetanus is made by clinical observation. Nowadays, lack of suspicion of this condition may cause delay in administering proper treatment. Women and older men are often inadequately immunized. Doctors should therefore examine the immunization status of these groups of patients regularly.     

Bovine IgG2a antibodies to Haemophilus somnus and allotype expression

AIMS/BACKGROUND: To characterise clinically a large kindred segregating retinitis pigmentosa and sensorineural hearing impairment in an autosomal dominant pattern and perform genetic linkage studies in this family. Extensive linkage analysis in this family had previously excluded the majority of loci shown to be involved in the aetiologies of RP, some other forms of inherited retinal degeneration, and inherited deafness. METHODS: Members of the family were subjected to detailed ophthalmic and audiological assessment. In addition, some family members underwent skeletal muscle biopsy, electromyography, and electrocardiography. Linkage analysis using anonymous microsatellite markers was performed on DNA samples from all living members of the pedigree. RESULTS: Patients in this kindred have a retinopathy typical of retinitis pigmentosa in addition to a hearing impairment. Those members of the pedigree examined demonstrated a subclinical myopathy, as evidence by abnormal skeletal muscle histology, electromyography, and electrocardiography. LOD scores of Zmax = 3.75 (theta = 0.10), Zmax = 3.41 (theta = 0.10), and Zmax = 3.25 (theta = 0.15) respectively were obtained with the markers D9S118, D9S121, and ASS, located on chromosome 9q34-qter, suggesting that the causative gene in this family may lie on the long arm (q) of chromosome 9. CONCLUSIONS: These data indicate that the gene responsible for the phenotype in this kindred is located on chromosome 9 q. These data, together with evidence that a murine deafness gene is located in a syntenic area of the mouse genome, should direct the research community to consider this area as a candidate region for retinopathy and/or deafness genes.     

Concurrent primary carcinoma of the gallbladder and acute cholecystitis

BACKGROUND/AIMS: Primary carcinoma of the gallbladder is rare and associated with a late diagnosis and poor prognosis. Concurrent acute cholecystitis frequently obscures the presence of carcinoma. The information regarding gallbladder carcinoma with acute cholecystitis is limited. In order to better understand the presentation of gallbladder carcinoma with acute cholecystitis, we retrospectively reviewed the data of patients with primary carcinoma of the gallbladder. METHODOLOGY: The data of 86 patients with primary carcinoma of the gallbladder treated between 1979 and 1994 were compiled and reviewed. The patients were divided into 2 groups: Group 1 (with acute cholecystitis, 21 patients) and Group 2 (without cholecystitis, 65 patients). Clinicopathological comparisons were made and evaluated between these two groups RESULTS: The average age of Group 1 patients was older than that of Group 2 patients (75+/-2 years vs. 63+/-2 years; p<0.05). Three Group 1 patients presented with sepsis. The interval between the onset of symptoms and hospital admission in Group 2 patients was significantly (p<0.05) longer than that in Group 1 patients (243+/-95 days vs. 20+/-11 days). Leukocytosis (>11,000/mm3) was more common in Group 1 patients than in Group 2 patients (47.6% vs. 15.4%). Jaundice was more common in Group 2, and fever was common in Group 1. The majority of Group 2 gallbladder cancers were stage V (75.4%). In contrast, 52.4% of Group 1 gallbladder cancers were stage III and 38.1% were stage V. The 30-day postoperative mortality rate in Group 1 and Group 2 patients was 9.5% and 7.7%, respectively. The cumulative survival of Group 1 patients was not different from that of Group 2 patients (log-rank test, p>0.05). CONCLUSIONS: Age, the interval of symptoms prior to admission, the location of abdominal pain, fever, leukocytosis, and the absence of jaundice suggested the presence of acute cholecystitis in gallbladder carcinoma. A high index of suspicion of the disease, intraoperative examination of gallbladder specimens, and more aggressive surgical treatment may improve patient survival.     

Antibodies to orthopoxvirus in domestic cats in Norway

Hemangiomata is the more frequent pediatric tumor, absent at birth and usually growing, sometimes very quickly, during the first week of life. It potentially represents a serious problem because of his unforeseeable evolution during the time: is it more useful to use a corticosteroid therapy or to wait for the involution of the tumor? Here we have the results of the treatment on 51 babies who presented with hemangiomas of various sites: 52.6% of the lesions were on the face and head, 13.4% on chest wall, 10% on upper limbs, 4% on abdominal wall, 10% on pelvis region and 10% multiple. Therapy was compression in 10% of patients, corticosteroid injection in 66%, oral administered corticosteroid in 12%, surgery post corticosteroid therapy in 11.5%, others in 2.5%. Best results were obtained on the lesion of the head and face (good in 96%), worst in those of the abdomen (any modification in 100%).     

Local removal of phagocytic synovial lining cells by clodronate-liposomes decreases cartilage destruction during collagen type II arthritis

OBJECTIVE: To investigate whether local removal of phagocytic synovial lining cells (SLCs) from the knee joint before onset of collagen type II arthritis has an effect on development of cartilage destruction. METHODS: Phagocytic SLCs were selectively depleted by a single injection of clodronate laden liposomes in the knee joint seven days before induction of collagen type II arthritis (CIA). Clodronate laden liposomes were given in one knee joint either alone or in combination with a short-term oral treatment of dexamethasone. Cartilage damage including proteoglycan depletion and chondrocyte death was measured in total knee joints sections stained with safranin-o or haematoxylin. RESULTS: Local removal of phagocytic SLCs, seven days before arthritis onset, prevented cell influx for the larger part. Chondrocyte death was significantly decreased in the SLC depleted arthritic joint both at an early (6 days) and late (12 days) time point after CIA induction. However, depletion of proteoglycans from femoral and patellar cartilage layers was not prevented. If the mild acute inflammation caused by a single clodronate laden liposome injection in the left knee joint, was blocked by a short-term (on consecutive days 9, 8, 7, 6, 5 before CIA onset) oral treatment with dexamethasone, cell influx, but also proteoglycan depletion was almost completely blocked. In the contralateral control right knee joint prominent cell influx and severe cartilage damage was observed, indicating that there was no effect of dexamethasone anymore at the onset of CIA. CONCLUSIONS: This study shows that removal of phagocytic lining cells before CIA induction, particularly in the presence of a short-term treatment with dexamethasone, decreases cartilage destruction.     

A glycosylated Bence Jones protein and its autologous amyloid light chain containing potentially amyloidogenic residues

Amyloidosis is characterized by deposition of protein fibrils in various tissues. The wide variety of sequences of both amyloidogenic and non-amyloidogenic immunoglobulin light chains makes them a unique tool for addressing the importance of primary structure in the formation of insoluble fibrils. In this study, we have determined the primary structure of the kappa I immunoglobulin light chain from both the urinary Bence Jones protein and the deposited amyloid fibrils of a patient (MH) with primary amyloidosis. The sequence identity of urinary-excreted and tissue-deposited light chains excluded biclonality and somatic mutations and confirmed that the light chain existed in both a soluble and an insoluble form. Several residues have been previously reported to be significantly associated with amyloidogenic kappa chains. Many of these were found in the MH sequence, including Asp31, Asn45, Phe49, Gln55, His70, Asn/Gly93 and ProN/Val96, thereby supporting their potential role in fibrillogenesis. In addition, Asn20 and Pro60 of protein MH replaced the normally conserved Thr20 and Ser60. Asn20 was glycosylated in both the Bence Jones and the amyloid fibril protein MH. Cumulative effects of amyloid-associated residues and glycosylation might have rendered the immunoglobulin light chain MH prone to fibril formation.     

Genetic risk of neuropsychological impairment in schizophrenia: a study of monozygotic twins discordant and concordant for the disorder

We investigated the effect of the adenosine receptor agonist 5'-(N-ethylcarboxamido)adenosine (NECA) in catecholamine secretion from adrenal chromaffin cells that exhibit only the A2b subtype adenosine receptor. NECA reduced catecholamine release evoked by the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP) in a time-dependent manner. Inhibition reached 25% after 30-40-min exposure to NECA. This effect on DMPP-evoked catecholamine secretion was mirrored by a similar (27.7 +/- 3.3%), slowly developing inhibition of [Ca2+]i transients induced by DMPP that peaked at 30-min preincubation with NECA. The capacity of the chromaffin cells to buffer Ca2+ load was not affected by the treatment with NECA. Short-term treatment with NECA failed both to modify [Ca2+]i levels and to increase endogenous diacylglycerol production, showing that NECA does not activate the intracellular Ca2+/protein kinase C signaling pathway. The inhibitory effects of NECA were accompanied by a 30% increase of protein phosphatase activity in chromaffin cell cytosol. We suggest that dephosphorylation of a protein involved in DMPP-evoked Ca2+ influx pathway (e.g., L-type Ca2+ channels) could be the mechanism of the inhibitory action of adenosine receptor stimulation on catecholamine secretion from adrenal chromaffin cells.     

Malignant melanoma in the small intestine

A case story of malignant melanoma is presented. The tumour was localised to the jejunum. The symptoms, diagnosis and treatment are described and the pathogenesis is discussed.