Familial Myeloproliferative Disease

Dl, Randall; Cw, Reiquam; Jh, Githens; Robinson, Arthur

doi:10.1001/archpedi.1965.02090030503001

Cited by 43 publications

(6 citation statements)

References 28 publications

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“…In all these models the genetic background is of some importance. The present results and the familial occurrence of myeloproliferative diseases resembling juvenile myelomonocytic leukaemia (Randall et al, 1965;Holton and Johnson 1968) suggest that it may also play a part in these conditions.…”

Section: Discussionsupporting

confidence: 58%

Immunological Abnormalities in Juvenile Myelomonocytic Leukaemia

Cannat¹,

Séligmann²

1973

BMJ

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to collisions of cars and lorries. Among 296 deaths of car occupants within 12 hours of injury, Ruffel Smith (1970) found that more than half were due to collisions with lorries. In our present series of 564 car occupant deaths 40% were from such collisions. It is difficult to apply appropriate weightings for different traffic conditions, but if 40% is a fair estimate it implies that in Great Britain car/lorry collisions cause about 1,000 deaths annually. This is as many as all the deaths due to accidents at work as studied by the recent Robens inquiry (Secretary of State for Employment, 1972).At first sight it is surprising that these collisions should be so common since lorries are outnumbered by cars by 7-1. The explanation seems to be an incompatability between the two types of vehicle. The lorry is heavy and strongly built to carry heavy loads. Rising gradients slow it down, falling gradients may cause it to go out of control. The car by contrast is light and built to maintain high speeds with light loads. Grime (1971) studied the theoretical mechanics of impacts between vehicles of different sizes. Of the lorries in our survey of which we know the weights, more than half were over 5 tons unladen. Most of the collisions, therefore, had a "mass-ratio" of at least 5. In Grime's analysis this implies a 95% or more risk of serious injury to car occupants with virtually no risk to the lorry occupants. This is consistent with our finding of 224 deaths of car occupants with five deaths of those in lorries.The unfavourable terms of this conflict has important implications for methods of protection. Whereas several studies show that seat belts will prevent 50% of injuries to car occupants, in our car/lorry collisions we estimate this could be only about 20%. The figure falls to about 10% for collisions of cars into the rear of lorries where so often the rear overhang or protruding load penetrates the windscreen area and so eliminates the protection normally afforded by the front of the car.Collisions into the rear of lorries are several times more frequent in dark than in light conditions in spite of there being less traffic of all kinds at night. This suggests there is room for improvement in making lorries more conspicuous. The current experiment with extra coloured markings may yield some benefit and there could well be other ways to warn motorists of impending danger. Elimination of the rear overhang of lorries and improved lighting might prevent some of the worst collisions but the underlying incompatibility of light and heavy vehicles remains. A more fundamental solution is the segregation of the two types of traffic on separate roads as on some highways in the United States. Another solution, perhaps more appropriate to this country, is to take account of the impending world shortage of oil supplies and save both fuel and human lives by using rail rather than road transport.We wish to thank Miss B. Roberts, for her help in this analysis, and the coroners and police of the areas studied, for their kind co-o...

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Section: Discussionsupporting

confidence: 58%

Immunological Abnormalities in Juvenile Myelomonocytic Leukaemia

Cannat¹,

Séligmann²

1973

BMJ

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“…The findings reported here show that very high Hb-F levels are not unique to juvenile CGL but may be found in other types of leukaemia as well. Randall, Reiquam, Githens and Robinson (1965) Many patients with chronic myeloproliferative syndromes develop leukaemia, particularly acute myeloblastic leukaemia. The preleukaemic state (Block, Jacobson and Bethard, 1953) in patients with atypical myeloproliferative syndromes is well recognized, and Hb-F measurements in these atypical syndromes may have diagnostic and prognostic significance.…”

Section: Discussionmentioning

confidence: 99%

Raised Foetal Haemoglobin in Childhood Leukaemia

Miller

1969

Br J Haematol

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Summary. Very high (13–50 per cent) concentrations of foetal haemoglobin (Hb F), usually found in the juvenile type of chronic granulocytic leukaemia or erythroleukaemia, were detected in three leukaemic children. One with acute myeloblastic and another with histiomonocytic leukaemia died 2 and 5 years respectively after the onset of an atypical syndrome characterized by frequent infections, lymph‐adenopathy, pulmonary infiltrations, hepatosplenomegaly, skin rash and monocytosis. A third child had acute monomyeloblastic leukaemia. Hb F was increased in 18 (55 per cent) of 32 other children with leukaemia; the levels were far below those found in the patients presented, but significantly greater than control values. The occurrence of such high Hb‐F concentrations in acute myeloblastic, monomyeloblastic and histiomonocytic leukaemia has not been reported previously. A raised Hb F in atypical myelo‐ or reticuloproliferative syndromes may have diagnostic and prognostic significance.

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“…Randall et al [13] have recently described a new syndrome, "familial myeloproliferative disease". The present case resembles this condition in many ways, especially in the early onset of splenomegaly, anaemia and thrombocytopenia, and in the myeloid leukaemic picture a t autopsy.…”

Section: Discussionmentioning

confidence: 99%

Myelofibrosis and Myeloid Leukaemia

Krasilnikoff¹

1967

Acta Paediatrica

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Familial Myeloproliferative Disease

Cited by 43 publications

References 28 publications

Immunological Abnormalities in Juvenile Myelomonocytic Leukaemia

Immunological Abnormalities in Juvenile Myelomonocytic Leukaemia

Raised Foetal Haemoglobin in Childhood Leukaemia

Myelofibrosis and Myeloid Leukaemia

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