Cases reported "Thrombocytopenia"

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1/6. Portosystemic myelopathy: spastic paraparesis after portosystemic shunting.

    Portosystemic encephalopathy (PSE) is a well-known, common complication of portal hypertension. It is thought to be caused by nitrogenous substances such as ammonia, which are normally cleared from the blood stream by the liver. In cirrhosis and other hepatic disorders with portosystemic shunting (PSS)-- either surgical portosystemic anastomoses (PSA) or spontaneous PSS-- the collateral vessels bypass the liver allowing the accumulation of toxic, ammoniacal substances in the blood and tissues. PSE is characterized by encephalopathy; portosystemic myelopathy (PSM) is characterized by paresis of the extremities, Babinski signs and muscle spasticity in patients with cirrhosis and/or PSS. Usually only the lower extremities are involved. This report presents the first case of this syndrome observed 5 years after a transjugular intrahepatic portosystemic shunt. The 31 year old man with chronic hepatitis b developed complete spastic paraparesis within 4 weeks after onset of clinical/neurological symptoms, accompanied by an episode of severe hepatic encephalopathy. The transcortical magnetic stimulation showed normal motoric stimulation times to the abductor digiti minimi muscles but no stimulation to the tibialis muscles was seen. Lumbar stimulation to the tibialis muscles, however, was normal. This indicates loss of motor neurons in the spinal cord, a characteristic finding in patients with portosystemic myelopathy. We performed a search of the literature for all reported cases of cirrhosis and/or PSS that developed PSM. However, the intervals between the construction of a shunt and the diagnosis of portosystemic myelopathy were shorter in total portacaval shunts (median 16 months) than in partial, non-portacaval shunts (median 60 months, p < 0.01). This suggests that not only the shunt itself but also the shunted volume contributes to the development of the syndrome Sixty-one patients with PSM have been reported in the literature since 1944. PSE had developed before PSM in almost all cases. PSM occurred from 1 month to 10 years after the creation of portacaval anastomoses (PCA) or splenorenal shunts (SRS) or in cirrhotic patients without shunts. No one type of liver disease or type of shunt appears to predispose to PSM. The mechanisms of PSE and PSM are thought to be similar and of nitrogenous origin, but their pathogenesis remains unknown. lathyrism, a toxic syndrome with similar symptoms and signs, is caused by the ingestion of a legume, lathyrus sativa, which contains beta-N-oxalo-L amino-L-alanine (BOAA). This animal model with or without BOAA appears to offer a reliable way of studying PSM experimentally.
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2/6. digitoxin intoxication with severe thrombocytopenia: reversal by digoxin-specific antibodies.

    As a result of overdosage a 77-year-old patient with heart disease developed digitoxin intoxication, associated with arrhythmias, extracardiac symptoms of intoxication and severe thrombocytopenia. Treatment with digoxin-specific antibody fragments relieved the signs and symptoms of intoxication within a few hours. The rise in platelet count from the pretreatment value of 26 000/mm3 to 47 000 within 12 h and to over 60 000/mm3 within 16 h of starting the antibody infusion may also be attributed to the treatment with antibodies. Such a rapid recovery from digitoxin-induced thrombocytopenia has not hitherto been described. digoxin-specific antibodies, obtained by immunization of sheep with a digoxin-albumin conjugate, were used to treat intoxication with digitoxin, since cross-reaction had been demonstrated in vitro and in animal experiments. The present paper briefly discusses the mode of action and the general problems relating to the antibody therapy of digitalis poisoning.
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3/6. Recurrent thrombocytopenia, erythroid hypoplasia and sideroblastic anaemia associated with hypothermia.

    A distinct and previously undescribed haematological picture was noted in three patients with hypothermia. During hypothermia there was anaemia with reduced normoblastic erythropoiesis, marked sideroblastic change and thrombocytopenia in the presence of a normal number of megakaryocytes. In two patients as the body temperature returned to normal these changes were slowly reversed. Evidence both from observations in patients and from animal experiments is given why the haematological changes are due to the hypothermia.
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4/6. Meniscal ossification. I. Human.

    Ossicles appearing in the medial menisci of three patients appeared to be post-traumatic in two and developmental in one. The histologic analysis in the two post-traumatic patients showed relatively normal bone and cartilage, but without the specific structural cartilaginous adaptations found in a naturally occurring large animal model. The third patient, with tibia vara and TAR (thrombocytopenia--absent radius) syndrome, developed the ossicle spontaneously. He is the youngest reported patient, to date, to develop this anatomic variation.
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5/6. Direct cultivation of the causative agent of human granulocytic ehrlichiosis.

    BACKGROUND. Human granulocytic ehrlichiosis is a potentially fatal tick-borne infection that has recently been described. This acute febrile illness is characterized by myalgias, headache, thrombocytopenia, and elevated serum aminotransferase levels. The disease is difficult to diagnose because the symptoms are non-specific, intraleukocytic inclusions (morulae) may not be seen, and the serologic results are often initially negative. Little is known about the causative agent because it has never been cultivated. methods. We studied three patients with symptoms and laboratory findings suggestive of human granulocytic ehrlichiosis, including unexplained fever after probable exposure to ticks, granulocytopenia, and thrombocytopenia. Peripheral blood was examined for ehrlichia microscopically and with use of the polymerase chain reaction (PCR). blood was inoculated into cultures of HL60 cells (a line of human promyelocytic leukemia cells), and the cultures were monitored for infection by Giemsa staining and PCR. RESULTS. blood from the three patients, only one of whom had inclusions suggestive of ehrlichia in neutrophils, was positive for human granulocytic ehrlichiosis on PCR. blood from all three patients was inoculated into HL60 cell cultures and caused infection, with intracellular organisms visualized as early as 5 days after inoculation and cell lysis occurring within 12 to 14 days. The identity of the cultured organisms was confirmed by immunofluorescence microscopy, PCR analysis, and dna sequencing. dna from the infected cells was sequenced in regions of the 16S ribosomal gene reported to differ between the agent of human granulocytic ehrlichiosis and closely related species, including ehrlichia equi and E. phagocytophila which cause infection in animals. The sequences from all three human isolates were identical and differed from the strain of E. equi studied in having guanine rather than adenine at nucleotide 84. CONCLUSIONS. We describe the cultivation of the agent of human granulocytic ehrlichiosis in cell culture. The ability to isolate this organism should lead to a better understanding of the biology, treatment, and epidemiology of this emerging infection.
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6/6. A cluster of airport malaria in belgium in 1995.

    In europe 64 cases of airport malaria have been registered between 1969 and 1996, most of them in france, switzerland and belgium. In the summer of 1995 six cases of airport malaria occurred at the International airport of Brussels, belgium. Of the six patients three were airport employees, three were occasional visitors. One patient died, the diagnosis was made by PCR amplification and dna sequencing after exhumation. Two different species of plasmodium were detected, and infections occurred on at least two different floors of the airport. An inquiry revealed that the cabin of airplanes is correctly sprayed, according to WHO recommendations, but that the inside of the hand luggage, the cargo hold, the animal compartment, the wheel bays and container flights remain possible shelters for infected mosquitoes. In a case of fever of unknown origin, airport malaria should be considered in the differential diagnosis, especially during hot summers, and when thrombocytopenia is present. Additional antimosquito measures should be generalised, encompassing highly exposed personnel, container content and handling buildings, animal cages, wheel bays, and the boundary between the sorting and the reception of luggage.
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