Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary type V hyperlipoproteinemia was identified in two preadolescent children. The propositus (kindred N) was a 10-year-old girl with severely creamy plasma, lipemia retinalis, hypertriglyceridemia (triglyceridelevel, 6,800 mg/100 ml), and ypercholesterolemia (cholesterol level, 490 mg/100 ml). Her parents and an 8-year-old sister all had endogenous hypertriglyceridemia (type IV hyperlipoproteinemia). In kindred A, an 11-year-old boy had triglyceride levels as high as 1,100 mg/100 ml and recurrent abdominal pain. His father had type V hyperlipoproteinemia; his mother was normal. All three of his older teenage siblings had type IV hyperlipoproteinemia. The enzymatic activities of lipoprotein lipase (LPL), hepatic triglyceride lipase (HTL), and histaminase (H) were studied in postheparin plasma. The LPL level was low in the children and both parents in kindred N. LPL level in kindred A was normal, except for one child with type IV hyperlipoproteinemia. HTL level was normal to above normal in both kindreds. Most patients had a normal H level, but one parent (kindred N) had no preheparin H and very low levels of postheparin H. There was a strong correlation (r = 0.58, significant at less than 1% level) between release of LPL and H but not between HTL and H (r= 0.22). The mean (+/- 1 S.D.) levels of the enzymes were as follows: LPL, 2.8 +/- 0.7 micronmol/ml/hr in kindred N and 5.4 +/- 2.2 micronmol/ml/hr in kindred A; H, 13.4 +/- 6.8 units/ml in kindred N and 22.0 +/- 11.9 units/ml in kindred A; and HTL, 18.0 +/- 7.1 micronmol/ml/hr in kindred N and 14.9 +/- 6.3 micronmol/ml/hr in kindred A. The enzymatic activities of kindreds N and A were significantly different for LPL (P less than .001) and H (.025 less than P less than .05) but not for HTL. All but one child had at least one high insulin level, which was accompanied by hyperglycemia in two children. The hypertriglyceridemia in all but one child was ameliorated on therapeutic diets. These data suggest that the genetic basis of the hypertriglyceridemia in these two families is different and that hyperchylomicronemia in childhood is not confined to the rara type I hyperliporproteinemia.
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PMID:The clinical, biochemical, and familial presentation of type V hyperlipoproteinemia in childhood. 19 90

A 58 year old Chinese male, one week after arriving in Canada from Hong Kong, presented with acute abdominal pain and diarrhoea which was rapidly followed by Escherichia coli infection causing septicaemia and meningitis. His past history revealed bronchial asthma for 15 years treated with steroids. At laparotomy, 7 days after the onset of symptoms, he was found to have extensive haemorrhagic infarction of the small bowel and right colon. Examination of the fibrosed mesenteric vessels revealed numerous filariform larvae of Strongyloides stercoralis, within the walls, and in all layers of bowel wall. The role of the parasite in the production of obliterative arteritis in this fatal case of haemorrhagic enteropathy is discussed. Clinical strongyloidiasis, in uncomplicated cases, varies from mild to severe with gastroenteritis, nausea, colicky abdominal pain, electrolyte imbalance and symptoms of malabsorption syndrome (MARCIAL-ROJAS, 1971). In malnourished individuals and patients with debilitating infections, either newly acquired or asymptomatic latent infection with S. stercoralis can assume severe dimensions (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). Similarly, in patients on steroid (CRUZ et al., 1966; WILLIS and MWOKOLO, 1966; NEEFE et al., 1973) and immunosuppressive therapy for lymphomatous diseases or deficient in immune response (ROGERS and NELSON, 1966; RIVERA et al., 1970), systemic strongyloidiasis is often fatal. The increased frequency of auto-infection in such patients with a breached immune barrier is, however, unclear. Further complications of this infection due to severe enterocolitis result in sepsis, bacteraemia and meningitis (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). This paper presents a fatal case of S. stercoralis infection which illustrates an uncommon if not unique, mechanism in its production of haemorrhagic enteropathy leading to sepsis and death.
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PMID:Fatal bowel infarction and sepsis: an unusual complication of systemic strongyloidiasis. 122 84

Vascular invasion is not a prominent feature of cholangiocarcinoma (CCC), in contrast to hepatocellular carcinoma (HCC), which frequently shows extensive vascular tumor thrombi. We report an autopsy case of CCC with extensive portal tumor thrombi and portal hypertension. A 57-yr-old man presented with abdominal pain. Liver imaging revealed no tumors, but showed intrahepatic portal venous obstruction. HCC with portal tumor thrombi was suspected clinically. His clinical course was rapid; he died of hepatic failure 50 days after admission. At autopsy, the liver (2,700 g) was studded with diffuse whitish yellow granular areas with flecks of coalescent granules. Intrahepatic portal veins were diffusely occluded by tumor thrombi. Microscopically, the tumor was poorly differentiated adenocarcinoma with mucin; tumor cells were immunohistochemically positive for carcinoembryonic antigen, CA 19-9, DU-PAN-2, and biliary type cytokeratins, but negative for alpha-fetoprotein. Tumor cells were diffuse in the liver, and there were numerous tumor thrombi in the small portal veins. Hepatic veins and small arteries were occasionally occluded by tumor thrombi. There was ascites, splenomegaly and tumor thrombi in the gastric and esophageal veins, suggesting that portal hypertension had been present. This tumor seemed to have marked affinity to invade portal veins. It must be stressed that there are CCCs with extensive portal tumor thrombi and resultant portal hypertension.
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PMID:Extensive portal tumor thrombi with portal hypertension in an autopsy case of intrahepatic cholangiocarcinoma. 132 98

A case of obstructive colitis associated with rectal carcinoma in a 56 year old Japanese man is reported herein. He presented to Shinkokura Hospital with severe abdominal pain following a one month history of anal bleeding and mild abdominal pain. On palpation, muscle guarding was observed in the left lower quadrant and the white blood cell count was 14,200/mm3. An exploratory laparotomy was performed under the provisional diagnosis of acute abdomen, which revealed localized peritonitis 8 cm oral to an area of rectal carcinoma. An anterior resection of the lesion was therefore performed together with a descendo-proctostomy. The histopathologic diagnosis revealed adenocarcinoma and obstructive colitis involving the entire thickness of the sigmoid colon and resultant fibrino-purulent peritonitis. His post-operative course was uneventful and he was continuing to do well on the 30th postoperative day, at the time of writing. The clinical significance of this combination of obstructive colitis with rectal carcinoma is briefly discussed following the presentation of this case.
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PMID:A case of localized peritonitis caused by obstructive colitis proximal to rectal carcinoma: a rare manifestation of obstructive colitis. 139 36

A 23-year-old Finnish man was examined because of an 8-year history of recurrent bouts of fever and abdominal pain. His father had been repeatedly investigated because of similar episodes since he was 24 years old, and one of the father's sisters was reported to have had recurrent periods of fever. The clinical features closely resembled those of familial Mediterranean fever (FMF), a syndrome rarely described in families of European descent. Unlike typical FMF, which is inherited as an autosomal recessive trait, the mode of inheritance of the syndrome in our family may be regarded as dominant. During a recent attack, serum concentrations of interleukin-1-beta, interleukin-6 and acute phase reactants, including serum amyloid A protein, were high. No signs of amyloidosis were detected in our patients.
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PMID:Autosomal dominant 'Mediterranean fever' in a Finnish family. 140 41

We reported clinical and neuropathological observations of a 41-year-old man with Degos disease. He first noted painless skin lesions over the upper extremities in January, 1982. Three years later he was diagnosed as Degos disease by skin biopsy, and treatment with aspirin was started. In September, 1985, he complained of paresthesia on his right arm, followed by a series of new neurological manifestations suggesting multifocal spinal cord lesions. On October 28, examination of admission showed papules with central umblication over the whole body except the head, face, palms, soles and scrotum. Neurological examination revealed no weakness, diminished right biceps reflex, exaggerated patellar reflexes and Achilles reflexes, left extensor plantar reflex, hypesthesia and hypalgesia to the level of Th8, mild left spastic gait, and retention of urine. In November, he had paraparesis, loss of vibration sense of lower extremities, hypesthesia and hypalgesia to the level of TH4, and weakness of right upper extremity. In December, he showed tetraplegia, left-sided facial palsy, and hypesthesia and hypalgesia to the level of C5. In January, 1986, he showed right facial palsy, left facial hypesthesia, pseudobulbar palsy. In February, he had bilateral abducens nerve palsy and hiccups. On February 18, he died of intracranial hemorrhages. He had episodic abdominal pain several times during admission. His condition deteriorated progressively in four months after the first manifestation of neurological symptoms, despite the therapy with heparin, urokinase, ticlopidine, dipyridamole, and prednisolone. Laboratory studies showed gradual increase of CSF proteins (from 156 mg/dl to 602 mg/dl) and extremely increased platelet aggregation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of Degos disease with neurological symptoms--neuropathological observations and increased platelet aggregation]. 162 33

Hepatic microabscesses have been described in immunosuppressed patients. However, there has been no previous report concerning hepatic microabscesses caused by Escherichia coli (E. coli). Recently, we experienced a 75-year-old male patient who had suffered from fever and upper abdominal pain for 4 days. His laboratory tests revealed an increased erythrocyte sedimentation rate (55 mm/hr), the white cell count was 7500/cumm with 82% segmented leukocytes, minimally elevated serum alkaline phosphatase and serum glutamic-pyruvic transaminase. Ultrasonography (US) showed multiple tiny hypo- or nearly anechoic lesions (3-8mm) diffusely scattered in both hepatic lobes. Some lesions were too small to be demonstrated and only distal acoustic enhancement posterior to the lesions could be noted. Contrast-enhanced computed tomography (CT) scan subsequently demonstrated the tiny hypodense and cystic lesions and confirmed the US diagnosis of microabscesses. Cultures of blood and liver aspirates showed E. coli. Although US and CT appearance of hepatic microabscesses caused by E. coli may be characteristic, it is not specific. Differential diagnosis should include multiple biliary hamartomas, and definite diagnosis should be made by needle aspiration.
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PMID:Hepatic microabscesses caused by Escherichia coli--US and CT appearance. 164 78

We report a case of benign multicystic mesothelial proliferation (the so-called multicystic peritoneal mesothelioma) arising multifocally in the abdomen of a 46-year-old white man. His anamnesis showed an 8-year history of intermittent pain in the right lower abdominal quadrant. Mucin stains, immunohistochemistry, and electron microscopy confirmed the mesothelial origin of the lesion. Review of the available literature allowed us to find another 85 reported cases of benign multicystic mesothelial proliferations of the peritoneum. Out of these cases, eighteen only occurred in men, the majority being reported in middle-aged women mostly with complaints of abdominal pain. Electron microscopy or immunohistochemistry are needed to make a differential diagnosis towards other multicystic lesions, such as peritoneal cystic lymphangioma. Although multicystic mesothelial proliferations of the peritoneum have often been regarded as benign neoplasms, the true nature--neoplastic or hyperplastic--of these lesions still remains greatly elusive. Therefore, we believe that the unbinding term benign multicystic mesothelial proliferation (first used with regard to the unique hitherto reported case arisen in the pleural cavity) should be considered at present more appropriate to indicate even these peritoneal lesions.
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PMID:Benign multicystic mesothelial proliferation of the peritoneum: immunohistochemical and electron microscopical study of a case and review of the literature. 172 39

On first admission on June 5, 1989, pulmonary adenocarcinoma of left S3b in a 62-year-old male had already metastasized to the brain and the clinical stage was T2N2M1. Radiation therapy for the metastatic brain lesion was very successful but chemotherapy for the primary lesion was not effective. He was discharged on August 24, 1989. He was readmitted to our hospital on Jan. 5, 1990 because of severe abdominal pain. His chest roentgenogram showed free air under the diaphragm. An emergency laparotomy was performed, because perforation of gastrointestinal tract was suspected. At operation, two localized tumors were found, one located in the jejunum approximately 20 cm distal to the ligament of Treitz, accompanied by perforation and another approximately 20 cm distal to the above lesion in the mesentery. The resected specimen of the perforated lesion demonstrated a deep and large ulcer, compared to the tumor size, similar to a submucosal tumor, accompanied by bridging folds. The pathologic interpretation was adenocarcinoma of the lung metastatic to the jejunum and mesentery. Primary lung cancer metastasizes to a wide variety of organs, but metastasis to the small intestine is uncommon, even on postmortem examination. Furthermore, it is rare that the metastatic lesion causes abdominal symptom leading to laparotomy.
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PMID:[A case of jejunal metastasis from pulmonary adenocarcinoma occurring as perforative peritonitis]. 188 9

A 23-year-old man was admitted with progressively disturbed vision and easy fatigability. CT scans demonstrated an enhanced mass in the sellar region. Physical and endocrinological examinations revealed atrophy of both optic nerves, temporal field cuts in both eyes, and panhypopituitarism. Concentrations of human chorionic gonadotropin (HCG) in the serum and cerebrospinal fluid were 12 and 33IU/L, respectively. On November 11, 1987, the tumor was partially removed using the transsphenoidal approach. The histological diagnosis was germinoma with syncytiotrophoblastic giant cells. Following postoperative craniospinal irradiation (whole brain, 30Gy; local, 18Gy; spinal canal 28Gy), CT scans showed no residual tumor and the HCG levels decreased until they were undetectable. Eighteen months later, the patient complained of abdominal pain. His serum HCG level had increased to 2,554 IU/L. CT scans of the abdomen revealed multiple low density areas in the liver. Chest X-ray was negative. A Ga scintigram disclosed only liver metastasis. Administration of a chemotherapy was started on June 26, 1989. Cisplatin and etoposide in doses of 20mg and 40mg respectively were given for 5 consecutive days in one course. Following four courses of the combined chemotherapy, the tumor entirely disappeared on CT scans and the HCG level returned to normal. The patient is now able to work well without evidence of recurrence. Multiple liver metastases of an intracranial germ cell tumor had been fatal in previous reports. This may be the first case with liver metastases in which the victim is still alive. The present case indicates that combined chemotherapy with cisplatin and etoposide is effective for extraneural metastases of an intracranial germ cell tumor.
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PMID:[Multiple liver metastases of a suprasellar germ cell tumor treated with combined chemotherapy of cisplatin and etoposide]. 189 Oct 59


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