The differential diagnosis between intra- and extrahepatic causes of jaundice was studied. At the "20 Noviembre" ISSSTE Hospital in Mexico City, between January 1977 and May 1984, data were collected in 1,263 jaundiced patients. To the clinical data for 1,000 of these 1,263 patients and a new set of 105 jaundiced patients, the COMIC study group algorithm was applied. The differential diagnosis between medical and surgical causes of jaundice was correct in 90% of the cases. In 85% the algorithm could also differentiate between acute and chronic disease, or between benign and malignant causes of jaundice. The COMIC algorithm was then modified and applied to the same 1,000 cases examined previously, with 96% accuracy in distinguishing medical and surgical causes of jaundice and 94% accuracy in discriminating between acute and chronic, or benign and malignant, disease. In a new set of 105 cases of jaundiced patients the modified COMIC algorithm made the correct diagnosis between intra- and extrahepatic causes for 98% of the patients, and for 93% it was also capable of distinguishing benign from malignant and acute from chronic causes of jaundice.
Clinical data were collected in 194 cases of jaundiced patients treated at the "Adolfo Lopez Mateos" ISSSTE Hospital in Mexico City from July 1985 to July 1986. A copy of the clinical history of each patient was given to each of four physicians--one recently graduated from medical school, another in his first year of gastroenterology, and two others who were experienced gastroenterologists. The same clinical data were processed by a computer set up to use a modified Danish COMIC algorithm. All physicians and the computer technician were blinded to the "gold standard" pathologic diagnoses, with which their diagnoses were compared. Accuracy rates of the physicians in distinguishing intrahepatic (medical) from extrahepatic (surgical) jaundice were 78%, 86%, 86%, and 91%, and the accuracy of computer-assisted diagnoses was 96%. Chi-squared analysis of the diagnoses of three of the physicians and those of the computer showed significant differences (p between 0.1 and 0.01). For the diagnoses of the remaining physician, however, no significant difference was found after chi-squared continuity correction.
Hereditary thrombocytopenia is a rare disorder. The inheritance pattern may be autosomal dominant or X-linked recessive. In the classical description of this disorder, there is a heterogeneous group of hereditary thrombocytopenias with a predominantly autosomal dominant mode of inheritance and with a normal mean platelet volume (MPV), aggregation, and bone marrow megakaryocytes, closely resembling idiopathic thrombocytopenic purpura (ITP) [ I d ] . In this disorder, splenectomy has been described as ineffective [ 1-31.We studied a family with mild thrombocytopenia affecting the mother and her three children (two males and one female). The platelet counts ranged between 33 X 109/L and 64 X 109/L. The MPV (performed by the Coulter Counter S Plus) were in the upper normal limit. The Ivy bleeding time was normal or less than 2 min prolonged. Platelet and granulocyte morphology were normal on light microscopic examination. Antinuclear antibodies (ANA) were negative. Platelet aggregation with ADP, ristocetin, collagen, and epinephrine were normal when counted for the platelet count. Plateletassociated immunoglobulins (IgG and IgA), performed by immunofluorescent technique, were undetectable. The bone marrow megakaryocytes were normal in number and morphology.Three years before the family study, the mother was diagnosed as having idiopathic thrombocytopenic purpura (ITP) and was splenectomized with a normalization of the platelet number. For this reason, the older child was also splenectomized, and her platelet count rose from 33 X 109/L to 130 X lO'/L. In both patients the platelet count remained stable for 6 and 1% years, respectively.The spleen has been suspected to contribute to the production of small platelets and to the rapid elimination of these platelets in Wiscott-Aldrich syndrome [ 5 ] . We could not study the platelet life span in our patients, and we do not know whether this study is a good indication for splenectomy. The role of the spleen in this family seems most probably to be the cause of enhanced destruction of the platelets, but whether the anomaly is in the apparently normally functional platelets or in the spleen remains unanswered. A guide for further studies of this syndrome should be based on the search for some element in the miscellaneous group of familial isolated thrombocytopenias resembling ITP, which would permit us to distinguish between those patients who will benefit from a splenectomy and those who will not obtain improvement. REFERENCES
Bone metastasis infrequently appears as the first manifestation of hepatocellular calcinoma (HCC), and in any case in most patients the primary tumour is detected a few months after its development. We report the case of a patient with alcoholic liver disease, increased levels of alpha-fetoprotein, and no evidence of hepatic lesion in the different imaging modalities, in whom metastasis of HCC was detected in the ribs, whereas the primary tumour was not diagnosed until 15 months later. We believe that all patients with increased levels of alpha-fetoprotein should be tested in an intensified search for HCC and possible metastases, given that hepatic lesions may not be detected until many months alter the diagnosis of metastatic disease.
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