[Indirect hyperbilirubinemia secondary to Epstein-Barr viral hepatitis].
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Biomedical subjects
Publications and source records attributed to A Cosme.
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Primary melanoma of the esophagus is rare. Until 1990, eight cases had been reported in Spain. We report two patients, 50 and 61-year-old men. Melanomas were located in the distal esophagus and were polypoid (5-6 cm), pediculated and pigmented. Endoscopic biopsy was diagnostic in both cases. Fontana staining technique and monoclonal HMB-45 and S-100 antibodies were used. A revision of clinical characteristics, treatment and survival of the patients with primary melanoma of the esophagus in our country is made.
The Peutz-Jeghers syndrome is characterized by gastrointestinal polyposis and mucocutaneous melanin pigmentation. Between the complications are the appearance of gastrointestinal neoplasms. There is an increasing evidence suggesting the hamartoma-adenoma-carcinoma sequence in Peutz-Jeghers syndrome. We present a 32-years-old man with Peutz-Jeghers syndrome who developed an adenocarcinoma arising in a gastric hamartomatous polyp. We discuss the risk to develop gastrointestinal neoplasms and the necessity for periodic surveillance.
We report a case of a woman who showed hepatic and renal AA amyloidosis with a liver adenoma associated with the use of oral contraceptives. A nephrotic syndrome secondary to the renal amyloidosis underwent complete remission 7 years after the withdrawal of oral contraceptive therapy. Twenty-nine months after the initial presentation, the patient was admitted with acute upper abdominal pain and abdominal tenderness. The abdominal ultrasound revealed a subphrenic fluid collection, and a presumptive diagnosis of a ruptured hepatic adenoma was made. The liver adenoma diminished from 8 cm to 1 cm over a 13-year follow up after the discontinuance of oral contraceptive therapy.
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Jejunal diverticulosis is an unusual finding. We present the case of 70-year-old man with bacterial overgrowth secondary to multiple diverticula of the small intestine. The diagnosis was based on clinical events, x-ray films and mainly on the optimal answer to antibiotic treatment.
The involvement of the esophagus in amyloidosis secondary to rheumatoid arthritis is rare. The case of a female patient with rheumatoid arthritis and secondary esophageal amyloidosis (type AA) with a radiologic and endoscopic clinical picture compatible with achalasia is presented. In the manometry carried out after two cardiomyotomies, abundant non propulsant tertiary waves were seen, as were two primary waves, intraesophageal pressure higher than that of the gastric fundus and lower hypertensive esophageal sphincter which was completely relaxed on one occasion, resulting in a manometric pattern which was different to that of the other two cases published with the same disease. Endoscopic cardiomyotomies and dilatations were performed. The patient died after 2 years due to post dilatation esophageal perforation. The manometric findings are compared with those of the two previous similar cases with emphasis being made in that the anarchic arrangement of the amyloid in the esophagus produces different unforeseen and uncharacteristic motility patterns. The authors only found in the literature two cases of esophageal amyloidosis secondary to rheumatoid arthritis simulating achalasia.
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Twenty patients with one or several primary hepatic vascular tumours were studied. Three of them had an angiosarcoma and the other seventeen had twenty nine hepatic haemangiomas. From these seventeen patients, six corresponded to a giant cavernomatous haemangioma. Symptoms, diagnostic methods and treatment of patients with angiosarcoma (3 cases), giant cavernomatous haemangioma (6 cases) and haemangiomas with size less than 4 cm (11 cases) are separately analyzed. We report our series and a critical revision of diagnosis and treatment of these tumours is made.
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Three patients, two male and one female, 42, 64 and 20 years old respectively, with a Dubin-Johnson syndrome are reported. Both men referred jaundice since several years and in the woman's case, the onset of the illness took place during the last term of her second pregnancy. In two patients, liver aspect and it's biopsy were diagnostic. In the other, who was hospitalized because of a myocardial infarction, a hepatic gammagraphy with Tc 99 HIDA was made. No case was associated with biliary lithiasis and only one patient had other members in his family with the illness.
The surface epithelium of normal gastric mucosa from patients with gastric adenocarcinoma expressed the type 1 blood group precursor only in Lewis (Le) non-secretor individuals, Le a+b- (se/se, Le/-) and Le a-b- (se/se, le/le). In secretors, the superficial mucosa was negative. Deep areas of the mucosa showed no type 1 precursor regardless of secretor status. Expression of type 1 precursor was anomalously found in neoplastic cells in 14 of 16 Le a-b+ (secretors) patients and in 4 of 5 Le a-b- (secretors) patients. The 1 Le a-b- non-secretor carcinoma expressed type 1 precursor strongly. 6 of 8 Le a+b- non-secretor carcinomas showed positivity for the monoclonal antibody K-21. Thus the type 1 precursor reacted with the non-neoplastic gastric surface of non-secretors but not with those of secretors, and also with most gastric adenocarcinoma regardless of secretor status and Lewis phenotype.
Alterations in the expression of type 1 blood group-related antigens (Lewis a and b) were examined immunohistochemically in 371 consecutives gastric biopsy and 80 surgical specimens from patients of gastric carcinoma. The ABH and Lewis phenotype and secretor status of the patients were correlated with histologic findings. An anomalous expression of Lewis a antigen was found in 88 of 249 gastric biopsy specimens of Lewis (a-b+) phenotype patients. The prevalence of this anomaly increased with the evolution of the premalignant process, in agreement with the commonly accepted model of gastric carcinogenesis. Thus, anomalous Lewis a antigen appeared in 66.6% of gastric dysplasia cases, in 64.6% of intestinal metaplasia, in 15.4% of atrophic gastritis, and in 7.4% of superficial gastritis. No alterations were found in subjects with normal gastric mucosa. Forty-seven of the 49 Lewis (a-b+) phenotype gastric carcinoma patients showed antigenic alterations in tumor cells (anomalous Lewis a antigen in 36 and loss of Lewis antigens in 11). In 26 of these gastric specimens an anomalous Lewis a antigen was present in areas of intestinal metaplasia and/or dysplasia away from the area of neoplastic transformation. The expression of Lewis a antigen in Lewis (a-b+) phenotype patients is a frequent phenomenon in gastric neoplastic cells and could result from the blocked synthesis of Lewis b antigen with accumulation of its precursors. These findings suggest that, during gastric carcinogenesis, antigenic alterations may precede neoplastic transformation. An anomalous Lewis a antigen could constitute a significant index of severity of the histologic lesion and contribute to identifying high-risk individuals.
The laparoscopic findings in 13 patients with liver fasciolasis are described. Diagnosis was made in three cases in base of the presence of ova Fasciola Hepatica in the patient's faeces and in 10 cases, because they fulfilled the following conditions: ingestion of fresh watercress, eosinophilic count exceeding 30%, positive serologic tests, eosinophilic granulomas with Charcot-Leyden crystals in liver biopsy and good response to treatment with dihidroemetine or bithionol. Nine cases (68.2%) showed hepatomegaly. In 12 of 13 (92.3%) lesions suggestive of hepatic distomatosis were found. Hepatic nodules of different sizes and shapes could be seen in 10 patients (76.9%), Glisson capsule was involved in five cases (38.4%) and peritoneum in three (23%). The latter was always affected with the liver but, on the other hand, liver capsule was found affected alone in two cases. In our experience, laparoscopy with liver biopsy is an important method for diagnosis of abdominal fasciolasis.
The distribution of the blood group-related antigens type 1 (Lewis(a) [Le(a)], Lewis(b) [Le(b)]) and type 2 (H type 2, Y) has been examined in histologically normal and malignant mucosa of 40 surgical specimens of patients with adenocarcinoma of the stomach, with the use of a panel of monoclonal antibodies. Patients' Lewis phenotype and secretor status are correlated to the authors' findings. The surface epithelium of normal pyloric and fundic mucosa expressed the Lewis isoantigen (Le(a) in Le[a+b-] phenotype and Le(b) in Le[a-b+] phenotype), whereas the deep areas of this mucosa no showed the Le(a), Le(b) antigens and expressed the Y and H type 2 antigens whatever the secretor status of patients. Nineteen of 24 patients with Le(a-b+) phenotype showed anomalous expression of Lea antigen in neoplastic cells. In three of them, this alteration was found in tumor adjacent mucosa. No expression of Le(a) or Le(b) antigens was found in tumors or normal mucosa from Le(a-b-) phenotype patients.