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)

A case of acute Mast-cell leukemia was studied. A 39 years old female presenting with a brief history of abdominal pain and attacks of flushing; peripheral blood and bone marrow contained up to 60% of poorly differentiated blasts with clumping of deep purpule granules. Peroxydase reaction stains were negative, chloroacetate esterase were strongly positive. Toluidine blue revealed metachromatic stain. Histamine content of the cells was highly greater than normal but nos heparinoid activity could be demonstrated. These abnormal mast-cells have been investigated with the electron microscope; only the dense particular type of granule substructure was found, without any lamellae component. The cells were temptatively classified as "immature" mast-cell. The disease was interpretated as an acute leukemic variety of systemic mastocytosis.
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PMID:[Acute mast-cell leukemia. Cytochemical and ultrastructural study, about a particular case (author's transl)]. 5

A female patient, currently aged 40, has attended our Lupus Clinic for 8 years with a clinical picture of urticarial vasculitis, joint pains, severe myalgias and abdominal pain which has occurred in bouts at irregular intervals. She has been found to have consistently reduced C4 levels, C1-esterase inhibitor deficiency and a persistent monoclonal band in the gamma region on electrophoresis. Her serum IgA level has been continuously low. Her symptoms have failed to respond to antihistamines and a variety of other measures but have been partially alleviated by immunosuppressive therapy ('pulsed' cyclophosphamide). We believe that this is the first patient described showing this combination of clinical and laboratory features.
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PMID:Urticarial vasculitis, IgA deficiency and C1 esterase inhibitor deficiency in the presence of an IgG monoclonal gammopathy--a case report. 151 41

We report an extremely high serum CA125 value of 1243 units/mL in a 21-year-old-patient with Crohn's disease who developed endometriosis. Such a high CA125 value has not been reported to date in endometriosis or other pathologies except ovarian carcinoma. The pelvic mass of unknown nature in the above patient was discovered by ultrasound during a sudden onset of severe abdominal pain which subsided within two days. The high CA125 value six days after the onset of pain and at the end of menses declined spontaneously to 100 units/mL in 15 to 30 days, and stabilized over the three months prior to colectomy and removal of the left ovarian endometrioma, after which it gradually declined to 7 to 11 units/mL as found a year earlier. Although primary cells from endometrioma produced 113 units/mL of CA125 in the culture medium, the cell line established from it gave a value of less than 7 units/mL even after treatment with interferons. The adherent cells were moderately positive for CA125, cytokeratin and non-specific esterase, were strongly positive for periodic acid Schiff's (PAS) and acid phosphatase, and had epithelioid morphology. In addition to the extremely high CA125 level in our endometriosis patient and the establishment of the cell line, the case illustrates the usefulness of CA125 estimation in helping to determine the nature of abdominal masses in female inflammatory bowel disease patients.
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PMID:An extremely elevated serum CA125 level in a Crohn's patient developing endometriosis and the establishment of a cell line (MD-E) from the endometrioma. 177 Mar 21

Sixteen years old girl was admitted because of for the past ten years' frequent edema attack and abdominal pain. Laboratory examination revealed hypocomplementemia, marked depletion of the fourth component of complement and low level of C1-inactivator. Familial studies revealed that her mother was also hypocomplementemic and in low level of C1-inactivator. Serial studies performed on the alterlation of components of complement, C1-inactivator, alpha 1-antitrypsin, antithrombin III, and alpha 2-macroglobulin during edema attack. The fourth component of complement and C1-inactivator were markedly depleted in remission and attack. Remarkable depletion was found in antithrombin III and esterase inhibition activity of C1-inactivator during attack. In contrast, alpha 1-antitrypsin and alpha 2-macroglobulin did not change. The present study may explain that Hageman factor fragments, activated by C1s, promotes kinin generation via kalikrein activation. And the condition that complete functional deficiency of C1-inactivator was main role in this circuit. Fibrynolysis and late components of complement was less influence on edema attack.
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PMID:[A case report of hereditary angioedema and studies on the serum components of complement, C1-inactivator and proteinase inhibitors during edema attack]. 361 41

Two patients with hereditary angioneurotic oedema, a condition characterized by repeated episodes of abdominal pain and oedema, and by an absence of complement-1 esterase inhibitor activity in the plasma are presented in detail. Both underwent multiple surgical procedures before the diagnosis was established. Abdominal pain is often the presenting complaint, and although a complete history will usually lead to the proper diagnosis, cases in which the family history is not clear can present a diagnostic dilemma. Characteristic radiological demonstration of localized intestinal oedema will only be obtained if studies are performed early during the acute attack.
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PMID:Hereditary angioneurotic oedema: an unusual cause of recurring abdominal pain. 551 19

A 57-year-old white man who had abdominal pain and distension, died after a short hospitalization for increasing ascites, anorexia, and deteriorating mental status. At autopsy, the principal gross finding was a dilated, hyperemic, thickened proximal jejunum that by light microscopy consisted of a transmural infiltrate of large mononuclear cells. Intense naphthol AS-D chloroacetate esterase (NASD) positivity was observed within most of the cells, suggesting granulocytic sarcoma. However, bacterial strains and electron-microscopic examination revealed that the massive jejunal infiltrate was composed of macrophages containing numerous phagocytosed bacteria. Although occasional cells had primary and secondary granules characteristic of myeloid precursors present within their cytoplasm, most cells lacked specific granules. Attempts to reproduce this markedly enhanced NASD result experimentally in peritoneal macrophages of mice were unsuccessful. This case shows that intense NASD cytoplasmic staining may occasionally occur macrophages that have phagocytosed large numbers of bacteria.
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PMID:Bacterial infection stimulating granulocytic sarcoma of the small bowel. 694 27

Although angiotensin-converting enzyme inhibitors (ACEIs) are well-known causes of orofacial angioedema, angioedema from these agents involving the bowel is not often considered. We report a case of simultaneous onset of small bowel and orofacial angioedema due to captopril. A 61-year-old black man with hypertension, coronary artery disease, and congestive heart failure had been treated with captopril for 5 years. He had sudden swelling of the lips, face, and tongue, followed by nausea, emesis, abdominal pain, and diarrhea. Other medications included aspirin, indomethacin, allopurinol, colchicine, and nifedipine. Examination showed swelling of the tongue, buccal mucosa, and neck; he also had midabdominal tenderness but no respiratory distress. Laboratory data were normal. A C1-esterase inhibitor level was normal. An ileus pattern was present on abdominal x-ray film. Angioedema was diagnosed, and all signs and symptoms resolved in 24 hours after captopril was discontinued. Clinicians need to be vigilant for bowel involvement from ACEI angioedema.
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PMID:Simultaneous mucosal and small bowel angioedema due to captopril. 982 92

A 29-year-old man with Crohn's disease involving the ileum and cecum was seen. He had angioneurotic edema with C1' esterase inhibitor deficiency. Later, his 50-year-old mother was evaluated because of abdominal pain. She had recurrent urticaria, C1' esterase inhibitor deficiency and radiographic studies showed Crohn's disease of the ileum. A maternal family history revealed other members affected with either Crohn's disease or angioneurotic edema. The clinical observations in this family suggest that angioneurotic edema associated with C1' esterase inhibitor deficiency may be closely linked genetically with a familial form of Crohn's disease.
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PMID:Hereditary angioneurotic edema and familial Crohn's disease. 1079 78

Hereditary angioedema (HAE) is a rare disease resulting from deficiency of complement 1 esterase inhibitor (C1-INH). The clinical manifestations of this disease include recurrent attacks of self-limiting edema affecting face, extremities, gastrointestinal system and upper airways. In this report, we present eleven members of a family with HAE. Edema of the extremities was the most common symptom, occurring in ten patients. Three patients experienced severe laryngeal edema that required tracheotomy. Three patients developed facial and scrotal edema. Three patients experienced severe abdominal pain. The mean age at onset of symptoms was 11 years. C1-INH levels were undetectable in two patients and low in nine patients. CH50 was undetectable in all of the patients. C4 level for all patients was low. HAE in our first case, a 10-year-old boy, was diagnosed on the basis of low C1-INH, CH50 and C4, in addition to his familial history. Eleven members of this family, for whom laboratory studies could not be done, had similar symptoms and course. Two patients died as a result of laryngeal edema before establishment of diagnosis. This case report indicates the importance of recognition and early treatment of HAE to prevent a potentially fatal outcome.
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PMID:Hereditary angioedema: case report of a family. 1110 24

Hereditary angioedema (HAE) is the autosomal dominant deficiency of C1-esterase inhibitor. There have hitherto been no reports on the US appearances of HAE. The unique case of a 12-year-old girl with recurrent abdominal pain is reported, in whom HAE was diagnosed by US and family history of paroxysmal dyspnoea, cutaneous swelling and attacks of abdominal pain. Pertinent US features were intestinal oedema and ascites. Sonographic evidence of intestinal swelling was only seen on the initial day of an episode of abdominal pain. Oedema, as demonstrated by MRI the following day, regressed rapidly, whereas ascites persisted for at least 3 days. It is therefore important to perform imaging in the acute phase to demonstrate the massive intestinal oedema, which is characteristic for the disease.
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PMID:Sonographic appearances of the abdominal manifestations of hereditary angioedema. 1132 52


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