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PubMed1976

Evaluation of mithramycin in the treatment of anaplastic gliomas.

A controlled, prospective, randomized study evaluated the use of mithramycin in the treatment of anaplastic glioma compared to a similar group of patients receiving best conventional care. From a total of 116 patients in the study, 96 were within the valid study group. All patients were operated on, had histological confirmation of anaplastic glioma, and received radiotherapy at the discretion of the principal investigator. Fifty-two patients received mithramycin at a dose of 25 mug/kg/day for 21 days, while 44 patients were in the control group. There was no significant difference in the median survival from time of randomization in those receiving mithramycin (21 weeks) as compared to those not receiving mithramycin (26 weeks). There was no significant difference between the two groups in relation to age distribution, sex, location, diagnosis, tumor characteristics, signs or symptoms, or radiotherapy received. Duration of symptoms correlates positively with survival and was also significantly longer in the control group than in the treated group. This, however, did not account for the failure of mithramycin to be found an effective agent. Although the study was not designed to evaluate the efficacy of radiotherapy, patients who were so treated had a significant improvement in survival. The toxic complications of mithramycin included gastrointestinal symptoms, dermatological involvement, anemia, and liver dysfunction, indicating the need for close supervision.

Adult↗

PubMed1992

[Amyloidosis associated with rheumatoid arthritis after total joint replacement].

Rheumatoid arthritis patients who had secondary amyloidosis have been studied retrospectively. There were eight patients out of 105 rheumatoid arthritis patients who had total joint replacement surgery from 1979 to 1990 in our institute. The grade of inflammation, renal and hepatic function have been compared with the RA patients without amyloidosis pre- and post- operatively. All of eight patients was female, and their average age at the diagnosis of amyloidosis was 57.8 year-old (range 4-76 year-old). The average preoperative period was 14.4 years (range 4-27 years), and the secondary amyloidosis had been diagnosed at the time of 3.8 years (range 1-9 years) after operation. The major clinical features leading to the diagnosis were gastrointestinal disturbance in six cases and renal dysfunction in two cases. The data of the renal function of amyloidosis patients showed slightly lower than that of the RA patients without amyloidosis, and showed significantly decrease postoperatively. The white blood cell (WBC) count was higher at the time of operation in the amyloidosis patients and showed continuous increase postoperatively. Lansbury index, alpha 2-globulin and WBC count did not improve in the amyloidosis patients during three years after operation. On the contrary, the patients without amyloidosis improved in these clinical data during the same period. Three amyloidosis patients died of renal failure and one died of bronchopneumonia. The average survival period was 1.8 years (range 1-5 years) after diagnosis of amyloidosis, and was 6.3 years (range 2-10 years) after operation in these four patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

[Two sibling patients with late-onset familial amyloidotic polyneuropathy and atypical clinical manifestations].

Brothers (case 1 and case 2) had familial amyloidotic polyneuropathy type 1 (FAP type 1) confirmed with sural nerve biopsy and DNA analysis. Both patients were unique in that their ages at onset were 56 and 52, and that their only manifestation was sensori-motor polyneuropathy, without clinically apparent autonomic involvements such as orthostatic hypotension, sweat dysfunction and sphincter dysfunction, or severe organ involvement such as gastrointestinal features and myocardial involvement after the onset. They are also unique in that their parents were healthy. The initial manifestation was sensori-motor polyneuropathy starting in the lower extremities. These atypical manifestations made the diagnosis of FAP type 1 difficult in the present cases. Based on reports in the literature and the present cases, there might be a tendency that in patients with late-onset FAP type 1 the clinical manifestations are generally mild and autonomic involvement and organ disturbance are absent or mild. In the etiological diagnosis of polyneuropathy, FAP type 1 should be considered especially in steadily progressive patients.

Age Factors↗

PubMed1990

Serious chemical sclerosing cholangitis associated with hepatic arterial 5FU and MMC chemotherapy.

A case of iatrogenic sclerosing cholangitis secondary to hepatic intra-arterial 5-fluorouracil (5FU) and Mitomycin C (MMC) chemotherapy is described. When any unexplained elevation of liver function results in alkaline phosphatase and bilirubin level, chemotherapy should be discontinued, and further examination carried out using ultrasonography, transhepatic cholangiography and endoscopic retrograde cholangio-pancreatography (ERCP). Although percutaneous transhepatic biliary drainage has been effective in some cases, in our case, the clinical course was irreversible and the patient died of hepatic failure and gastrointestinal bleeding. When clinical signs of hepatic dysfunction occur in the absence of tumor progression, iatrogenic sclerosing cholangitis must be suspected.

Adult↗

PubMed1990

Pure red cell aplasia associated with essential thrombocythemia (a case report).

A rare case of erythroblastopenia associated with essential thrombocythemia (ET) is described. The patient had markedly elevated platelet count (5200 x 10(9)/1) and significant platelet dysfunction leading to extensive soft tissue and gastrointestinal hemorrhage. There was paucity of erythroid precursors in the bone marrow - a feature hitherto undescribed in ET. The thrombocytosis responded to well busulphan therapy but patient succumbed to fulminant infection consequent upon drug induced neutropenia.

Female↗

PubMed1990

[Acute toxicity of trichloroethylene. Description of a case series at the Autonomous Service of Toxicology of Florence during the 1977-1988 period].

The authors report the number of acute trichloroethylene intoxications admitted to the Toxicological Unit of Florence University from January 1977 to December 1988. The identification of the solvent metabolic pathway allowed to clarify the pathogenesis of hepatorenal dysfunction observed during acute intoxications. Together with gastrointestinal decontamination and cardiac arrhythmia control we have studied the effect of drugs supposed to act as blockers of trichloroethylene metabolism or as inactivators of the hepatotoxic free radical metabolite 2-2(1)-3 trichloroxirane. The prognostic modification related to new therapeutic protocols is reported and discussed.

Acute Disease↗

PubMed1990

[Gallstone and Parkinson's disease--ultrasound echography study].

Gastrointestinal symptoms caused by autonomic nervous system dysfunction has been well known in Parkinson's disease. This time we had a chance to see a patient with Parkinson's disease associated with acute abdominal pain because of gallstones. This study extended to examine abdominal findings in 79 cases of Parkinson's disease using abdominal ultrasound echography and also studied relationships between echographic findings and age, Hoen-Yahr stage and duration of the illness. Results were as follows: Echographic abnormalities were found 53.2% of the cases. Among them, gallstone was the most frequent findings and the incidence was 29.1% which showed significantly higher than that of the gallstone holding ratio (16.6%) in a age matched Japanese autopsy study. Subsequent findings were renal cyst (16.5%), renal stone (8.9%), liver cyst, portal dilatation and so on. No remarkable relationship was found between Hoen-Yahr stage and gallstone, however good correlation was found between duration of the illness and gallstone. It was concluded that gallstone holding ratio in Parkinson's disease is considerably high compared to that of a age matched Japanese autopsy study, which might be of great use in our daily clinics.

Age Factors↗

PubMed1989

[Combination therapy with medroxyprogesterone acetate and tegafur in tamoxifen- and adriamycin-resistant advanced breast cancers].

Medroxyprogesterone acetate (MPA) plus Tegafur (TGF) therapy was performed to evaluate the efficacy in a treatment for Tamoxifen- and Adriamycin-resistant advanced breast cancers. The patients were medicated in different doses on 800 mg or 1,200 mg daily po for MPA and TGF. Sixteen patients were evaluable in this trial. According to criteria of the Japan Mammary Cancer Society, one was regarded as CR and five as PR. The response rate was 37.5%. There was no difference in response rates between premenopausal and postmenopausal patients or ER positive and negative patients. No difference was noted either in response rates and incidence of side effects between two different doses of MPA. This means that an 800 mg daily dose of MPA lower than the recommended 1,200 mg might be better in the treatment for Japanese patients with advanced breast cancers. Gastrointestinal disorders, bone marrow suppression and liver dysfunction which could be found in high-dose TGF therapy, were not frequently observed in this trial. Patients could expect good quality of life during the treatment because of fewer side effects. This combination therapy with MPA and TGF was regarded as a good modality for the treatment of Tamoxifen- and Adriamycin-resistant advanced breast cancers.

Adult↗

PubMed1989

[Vasoactive polypeptides in rosacea].

Plasma kininogenesis components were studied in 110 patients with rosacea and in 3 groups of subjects at risk of developing this condition because of chronic gastrointestinal diseases, nervous system stress, or endocrine dysfunctions, conducive to rosacea. Changes in kininogenesis parameters similar to those detected in all rosacea patients were detected in all the 3 risk groups. Vasoactive polypeptide hyperproduction is a common component of rosacea pathogenesis. Vasoactive trend of the kinin action in kinin hyperproduction in rosacea induces vascular changes in the face and general vascular disorders, characteristic of this condition.

Female↗

PubMed1995

[A long-term clinical analysis of the rheumatoid patients treated by a combination of GST and CCA].

It has been well known that DMARDs are very effective for rheumatoid arthritis but lose their effect after long term administration. The authors would expect that Lobenzarit disodium (CCA) could slow the reduction of effectiveness of the DMARDs. The aim of this paper is to clarify the effects of Lobenzarit disodium (CCA) for the rheumatoid patients maintained by sodium aurothiomalate and D-penicillamine. The classical and definite rheumatoid patients were divided into two groups. One (group-A) was the rheumatoid patients who were treated in combination with CCA (79 patients). Another (group-B) was rheumatoid patients who were treated by sodium aurothiomalate or D-penicillamine (78 patients). All of them were followed for four years. In group-A, Lansbury index didn't improve in comparison with group-B. However, in the parameters of Lansbury index, improvement of the swelling joints was clearly higher in group-A than in group-B. Furthermore, this effect started in three months after administration of CCA and continued until the end of this study. On the other hand, according to roentogenographic examination utilizing MD's method, density of the metacarpal bones decreased more in group-B than in group-A. The sid-effects were few. They were five cases of gastrointestinal disorders and three cases of renal dysfunction. However, the renal dysfunction seems unlikely to be causally related to CCA. The authors could confirm the certain and expected results of combination therapy with CCA and sodium aurothiomalate and D-penicillamine for the rheumatoid patients.

Activities of Daily Living↗

PubMed1997

[Megakaryocytic thrombopenic purpura associated with enamel hypoplasia].

Patients with platelet disorders usually bleed into superficial sites such as the skin, mucous membranes, genitourinary tract and gastrointestinal tract caused by thrombocytopenia or thrombocyte dysfunction. Thrombocytopenia is caused by one of three mechanisms-decreased marrow production, increased splenic sequestration, or accelerated destruction of platelets. We report a 9-year-old male patient with thrombocytopenic purpura, dyserythropoetic anaemia, freckles on the skin and nanosomia, resembling Fanconi's (constitutional) anaemia. Although many patients with constitutional anaemia own other bony abnormalities, it was not found in this case. On the other hand, the patient showed enamel hypoplasia. To our knowledge, this association has never been reported before. Laboratory diagnosis, clinical findings, dental abnormalities and treatment are presented in details.

Abnormalities, Multiple↗

PubMedDate not supplied

Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management.

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1999

Anorexia nervosa with severe liver dysfunction and subsequent critical complications.

A twenty-year-old woman with anorexia nervosa (body mass index=11) suffered from severe liver dysfunction (aspartate aminotransferase 5,000 IU/l, alanine aminotransferase 3,980 IU/l, prothrombin time 32%), hypoglycemia (serum glucose 27 mg/dl), and pancreatic dysfunction (amylase 820 IU/l, lipase 558 IU/l). She fell into a depressive state with irritability, which was not improved by intravenous glucose. Despite treatment with plasmapheresis for the liver dysfunction, she subsequently developed pulmonary edema, acute renal failure, gastrointestinal bleeding, and disseminated intravascular coagulation. Hemodialysis, mechanical ventilation and drug therapy including prednisolone, prostaglandin E1, and branched-chain amino acid, improved her critical condition. In this case, malnutrition may have been the cause for the liver dysfunction and subsequent complications.

Acute Kidney Injury↗

PubMed1998

Association of autonomic nervous dysfunction and esophageal dysmotility in systemic sclerosis.

OBJECTIVE: The primary event in the pathogenesis of gastrointestinal involvement in systemic sclerosis (SSc) has been hypothesized to be an early neural lesion. We investigated the association of autonomic nervous dysfunction and esophageal involvement in SSc. METHODS: Thirty-six consecutive patients with SSc were investigated by esophageal manometry and autonomic nervous function tests for cardiovascular and pupillary autonomic dysfunction. RESULTS: In 27 of 36 patients, esophageal manometry showed esophageal dysfunction. Twelve patients had either pupillary (n = 6) or cardiovascular (n = 5) dysfunction or both (n = 1). All patients with autonomic dysfunction had esophageal dysfunction. Patients with autonomic dysfunction had significantly reduced mean distal esophageal contraction amplitudes compared to patients without autonomic nervous dysfunction (p < 0.05). The association of autonomic dysfunction and esophageal dysfunction was significant (p = 0.02). CONCLUSION: Our results support the concept of a role for neurogenic defects in the development of esophageal dysfunction in SSc.

Adolescent↗

PubMed2000

[Diabetes and urination disorders].

Diabetic neuropathy of can induce multi-organ dysfunction. The diabetes simultaneously has profound repercussions on gastrointestinal, sexual and erectile functions. One of the main sequelae of diabetic neuropathy is autonomic neuropathy affecting the vesicosphincteric control. The objective of this study was to review the epidemiological, clinical, laboratory and therapeutic data concerning voiding disorders observed in diabetes. Although the therapeutic management of an isolated voiding disorder in diabetics still remains symptomatic, it raises aetiological problems due to the comorbidity, particularly prostatic obstructive syndromes in men, pelvic dysfunction in women and ageing. Diabetic patients in renal failure also present specific vesicosphincteric disorders which are reviewed. Diabetic patients should be more systematically screened for the development of diabetic bladder disease, especially for associated factors which participate in its clinical expression. This implies extreme caution in the management of benign prostatic hyperplasia in the case of comorbidity, to avoid deteriorating a sometimes fragile detrusor-sphincter equilibrium. Diabetic detrusor hyperactivity must be better known in order to be more effectively detected. Pharmacological treatment of this condition raises problems related to detrusor hypocontractility also related to diabetic bladder disease. Clinical examination should be able to select those patients requiring further urodynamic studies in order to assess the individual detrusor-sphincter equilibrium. These investigations are required when surgical treatment of an associated urological or gynaecological disorder is considered.

Diabetes Complications↗

PubMed2002

Autistic disorder and gastrointestinal disease.

Autistic disorder is a pervasive developmental disorder manifested in the first 3 years of life by dysfunction in social interaction and communication. Many efforts have been made to explore the biologic basis of this disorder, but the etiology remains unknown. Recent publications describing upper gastrointestinal abnormalities and ileocolitis have focused attention on gastrointestinal function and morphology in these children. High prevalence of histologic abnormalities in the esophagus, stomach, small intestine and colon, and dysfunction of liver conjugation capacity and intestinal permeability were reported. Three surveys conducted in the United States described high prevalence of gastrointestinal symptoms in children with autistic disorder. Treatment of the digestive problems may have positive effects on their behavior.

Age Factors↗

PubMed1992

Idiopathic inflammatory bowel disease in dogs and cats: 84 cases (1987-1990).

Idiopathic inflammatory bowel disease was the diagnosis for 58 dogs and 26 cats, with signs of persistent gastroenteritis, failed responses to dietary trials, and histologic evidence of cellular infiltrates unrelated to other causes of gastrointestinal tract inflammation. Clinical signs of large intestinal dysfunction, watery diarrhea, vomiting, and anorexia with weight loss were common. Nonspecific hematologic, biochemical, and radiographic abnormalities frequently were observed. Mucosal biopsy specimens, obtained endoscopically, were histologically evaluated for severity of mucosal epithelial damage. Mucosal erythema, friability, enhanced granularity, and ulceration or erosion were the predominant endoscopic lesions. Inflammatory bowel disease lesions of moderate severity predominated in the stomach, duodenum, and colon. Lymphocytic/plasmacytic infiltrates were limited to the lamina propria in biopsy specimens from all regions of the gastrointestinal tract. Inflammatory bowel disease commonly is associated with chronic gastroenteritis in dogs and cats.

Animals↗

PubMed2002

Gastrointestinal perception: pathophysiological implications.

Physiological gut stimuli during the digestive process are not normally perceived. However, gut stimuli activate a variety of afferent pathways and in some circumstances may induce conscious sensations. Experimental evidence gathered during the past decade suggests that patients with functional gut disorders and unexplained abdominal symptoms may have a sensory dysfunction of the gut, so that physiological stimuli would induce symptoms. Assessment of visceral sensitivity is still poorly developed, but in analogy to somatosensory testing, differential stimulation of visceral afferents may be achieved by a combination of stimulation techniques, which may help to characterize sensory dysfunctions. Visceral afferent input is modulated by a series of mechanisms at different levels of the brain gut axis, and conceivably, a dysfunction of these regulatory mechanisms could cause hyperalgesia. The sensory dysfunction in functional patients seems associated to altered reflex activity, and both mechanisms may interact to produce the symptoms. Evidence of a gut sensory-reflex dysfunction as a common pathophysiological mechanism in different functional gastrointestinal disorders, would suggest that they are different forms of the same process, and that the clinical manifestations depend on the specific pathways affected.

Digestive System↗