- Email: [email protected]
OUTPATIENT PREPARATION FOR COLONOSCOPY
695 blood cultures taken during gentamicin therapy were positive for B. cereus, even after removal of the venous catheter. All rotates were sensitive to gentamicin. We conclude that even the seldom pathogenic Bacillus species present a threat to the compromised patient under gnotobiotic care. G. G. D. COLPIN
Academisch Ziekenhuis, 2333AA Leiden, Netherlands
H. F. L. GUIOT R. F. A. SIMONIS F. E. ZWAAN
BONE FORMATION AND RESORPTION IN POSTMENOPAUSAL OSTEOPOROSIS
Necropsy showed increased marrow fibrosis and infiltration of liver, spleen, lymph node, and lung by megakaryocytes and blast cells.
Despite the previously held belief that no specific form of leukaemia is related to Down syndrome,l a review of the literature2-10 reveals a further eleven cases of Down syndrome associated with a leukaemic process identifiable as representing the megakaryoblastic leukaemia/acute myelofibrosis syndrome first described by Lewis and Szur. 11In contrast, myelofibrosis is very 2 rare in chromosomally normal children. I suggest that trisomy 21 is the first chromosomal anomaly to be linked with megakaryoblastic leukaemia. Department of Haematology, Hospital, Harrow, Middlesex
Northwick Park
SIR,-Dr Darby (Sept. 5, p. 536) seems to misunderstand the fundamental concept behind our paper of Aug. 8. There is nothing invalid in principle in expressing formation rates in absolute terms and destruction rates in fractional terms. This is common practice in biology; for example, androstenedione production is normally expressed in ng (or nmol)/day whereas its removal from the plasma is always expressed as a metabolic clearance rate in litres of plasma or whole blood. The latter is a fractional removal rate since whatever the concentration of androstenedione in the plasma, the fraction removed in any given unit of time is a constant for that individual. The plasma androstenedione concentration in the steady state is the level at which the fractional removal multiplied by the plasma concentration is equal to the absolute production rate. What our paper suggests is that the regulation of trabecular bone volume can be treated in much the same way. Taking the total forming surface as an indicator of bone formation rate and the percent resorbing surface as a measure of the rate at which bone is being destroyed, we have shown that the differences in trabecular bone volume between young and old women and between old women and osteoporotic women can be quantitatively explained by the relation between absolute forming surface on the one hand and percent resorbing surface on the other. Darby’s comments in his second paragraph are reasonable and have been raised many times before. However, the fact remains that our analysis turns out to be entirely compatible with our model-and that is the best that one can hope for in testing any hypothesis. Confirmation of the model does not prove that it is correct but the analysis so far has failed to show that it is incorrect. Endocrine Unit,
Royal Adelaide Hospital, Adelaide, South Australia 5000
B. E. C. NORDIN
ASSOCIATION BETWEEN MEGAKARYOBLASTIC LEUKAEMIA AND DOWN SYNDROME
SIR,-I have studied a child with Down syndrome and megakaryoblastic leukaemia at Northwick Park Hospital. At birth, cytogenetic analysis (Dr E. Hudson) revealed trisomy 21. Aged 20 months he was admitted under the care of Dr M. Liberman. He had hepatomegaly and purpura. Hb 10-22 g/dl ; WBC 9 - 3 x 109/1 (neutrophils 2-1, lymphocytes 5 - 3, monocytes 0 - 7, and blasts 1 2 x 109/1); platelets 18x10/1. The blood film was leucoerythroblastic and displayed giant platelets. Circulating megakaryocytes were noted. Platelet function was abnormal. Bone marrow contained giant, bizarre megakaryocytes, some with hypogranular cytoplasm and 25% blasts. Some blasts exhibited the cytoplasmic budding characteristic of the megakaryoblast. Blasts stained negatively with periodic-acid/Schiff and sudan-black but showed strong granular positivity with non-specific esterase. These reactions are consistent with a megakaryoblast origin, and surface marker analysis (Dr M. Greaves and Dr G. Janossy) confirmed a megakaryoblastic identity. Cytogenetic analysis demonstrated the acquisition of a marker chromosome. Although the patient was given no treatment the platelet count returned to normal and blasts disappeared from the peripheral blood. He died 10 months later with a high peripheral blood blast count and hepatosplenomegaly. Bone marrow, aspirated with great difficulty, contained 40% blasts. Serum uric acid was 566 mol/1.
*Present address: St
Mary’s Hospital.
D. S. LEWIS* London W2 1NY
OUTPATIENT PREPARATION FOR COLONOSCOPY
SIR,-When day facilities are not available, preparation of patients for colonoscopy becomes a major problem. In Oxford, colonic wash-outs can only be obtained for inpatients, so all patients have to be admitted for the night before colonoscopy, which is expensive in terms of beds and nursing time. We have recently compared our standard preparation (liquid diet, 45 ml castor oil, and colonic wash-outs) with a new oral form of preparation, sodium picosulphate (’Picolax’; Nordic Pharmaceuticals). One sachet of sodium picosulphate is taken before breakfast on the day before colonoscopy and is followed by a low residue diet and a large fluid intake. During the afternoon a second sachet is taken, and only clear fluids are then allowed until the examination the following morning. During May and June, 1981, twenty-five patients were prepared as outpatients in this way and twenty patients received the standard inpatient preparation. Preparation was judged to have been poor in only two of the outpatients, while eight of the twenty patients prepared in the standard way were deemed to have been poorly prepared. Patients prepared with sodium picosulphate often had a moderate amount of liquid contents in the caecum which could be readily aspirated. Even in the two with poor preparation, the right side of the colon could be aspirated. This was in contrast to the standard preparation where a poor preparation usually meant that the examination had to be abandoned. All patients tolerated sodium picosulphate well and experienced no discomfort. The new preparation had previously been found effective for barium enema examinations. Our results indicate that it can be used’ successfully for outpatients scheduled for colonoscopy. It is cheap, saves nursing time by avoiding colonic wash-outs, and it is safe when diathermy is being used.
Gastroenterology Unit,
J. J. BROWN D. P. JEWELL
John Radcliffe Hospital, Oxford OX3 9DU
1. Rosner F, Lee SL. Down’s syndrome and acute leukaemia. Lancet 1973; i: 110. 2. Evans DIK. Acute myelofibrosis in children with Down’s syndrome. Arch Dis Child 3.
1975; 59: 458-62. Rosenberg HS, Taylor
FM. The
myeloproliferative syndrome
in children.
J Pediat
1958; 52: 407. 4 Hillman F, Forrester RM.
Myelofibrosis simulating acute leukaemia in a female infant syndrome. Irish J Med Sci 1968; 1: 167 Fujinami T, Sugiyama T, Tankawa H, et al A case of megakaryocitic myelosis in a child. Ann Paediat Jap 1961, 7: 226. Okada H, et al. Down’s syndrome associated with a myeloproliferative disorder. AmJ with Down’s
5. 6.
Dis Child 1972; 124: 107-10. et al. A case of mongolism associated with congenital leukaemia. Jap J Paediat 1965, 18: 1032-41 8 Nordan U, Humbert JR. Myelofibrosis and acute lymphoblastic leukaemia in a child with Down’s syndrome J Pediat 1979; 94: 253-55. 9. Cosson A, Despnes C, Gazenger J, Breton-Gorius M, et al. Unusual leukaemic syndrome in newborn trisomy 21. Nouv Revue Fr Hématol 1974, 14: 182-98 10 Boisseau M, le Menn R Ultrastructure ofblood platelets in two new-born with trisomy 21, thrombocythaemia and leukaemic syndrome. Nouv Revue Fr Hématol 1974; 14: 7.
Tsujino G,
371-82. 11 Lewis SM, Szur L.
Malignant myelosclerosis
Br. MedJ
1963, ii:
472.
Academisch Ziekenhuis, 2333AA Leiden, Netherlands
H. F. L. GUIOT R. F. A. SIMONIS F. E. ZWAAN
BONE FORMATION AND RESORPTION IN POSTMENOPAUSAL OSTEOPOROSIS
Necropsy showed increased marrow fibrosis and infiltration of liver, spleen, lymph node, and lung by megakaryocytes and blast cells.
Despite the previously held belief that no specific form of leukaemia is related to Down syndrome,l a review of the literature2-10 reveals a further eleven cases of Down syndrome associated with a leukaemic process identifiable as representing the megakaryoblastic leukaemia/acute myelofibrosis syndrome first described by Lewis and Szur. 11In contrast, myelofibrosis is very 2 rare in chromosomally normal children. I suggest that trisomy 21 is the first chromosomal anomaly to be linked with megakaryoblastic leukaemia. Department of Haematology, Hospital, Harrow, Middlesex
Northwick Park
SIR,-Dr Darby (Sept. 5, p. 536) seems to misunderstand the fundamental concept behind our paper of Aug. 8. There is nothing invalid in principle in expressing formation rates in absolute terms and destruction rates in fractional terms. This is common practice in biology; for example, androstenedione production is normally expressed in ng (or nmol)/day whereas its removal from the plasma is always expressed as a metabolic clearance rate in litres of plasma or whole blood. The latter is a fractional removal rate since whatever the concentration of androstenedione in the plasma, the fraction removed in any given unit of time is a constant for that individual. The plasma androstenedione concentration in the steady state is the level at which the fractional removal multiplied by the plasma concentration is equal to the absolute production rate. What our paper suggests is that the regulation of trabecular bone volume can be treated in much the same way. Taking the total forming surface as an indicator of bone formation rate and the percent resorbing surface as a measure of the rate at which bone is being destroyed, we have shown that the differences in trabecular bone volume between young and old women and between old women and osteoporotic women can be quantitatively explained by the relation between absolute forming surface on the one hand and percent resorbing surface on the other. Darby’s comments in his second paragraph are reasonable and have been raised many times before. However, the fact remains that our analysis turns out to be entirely compatible with our model-and that is the best that one can hope for in testing any hypothesis. Confirmation of the model does not prove that it is correct but the analysis so far has failed to show that it is incorrect. Endocrine Unit,
Royal Adelaide Hospital, Adelaide, South Australia 5000
B. E. C. NORDIN
ASSOCIATION BETWEEN MEGAKARYOBLASTIC LEUKAEMIA AND DOWN SYNDROME
SIR,-I have studied a child with Down syndrome and megakaryoblastic leukaemia at Northwick Park Hospital. At birth, cytogenetic analysis (Dr E. Hudson) revealed trisomy 21. Aged 20 months he was admitted under the care of Dr M. Liberman. He had hepatomegaly and purpura. Hb 10-22 g/dl ; WBC 9 - 3 x 109/1 (neutrophils 2-1, lymphocytes 5 - 3, monocytes 0 - 7, and blasts 1 2 x 109/1); platelets 18x10/1. The blood film was leucoerythroblastic and displayed giant platelets. Circulating megakaryocytes were noted. Platelet function was abnormal. Bone marrow contained giant, bizarre megakaryocytes, some with hypogranular cytoplasm and 25% blasts. Some blasts exhibited the cytoplasmic budding characteristic of the megakaryoblast. Blasts stained negatively with periodic-acid/Schiff and sudan-black but showed strong granular positivity with non-specific esterase. These reactions are consistent with a megakaryoblast origin, and surface marker analysis (Dr M. Greaves and Dr G. Janossy) confirmed a megakaryoblastic identity. Cytogenetic analysis demonstrated the acquisition of a marker chromosome. Although the patient was given no treatment the platelet count returned to normal and blasts disappeared from the peripheral blood. He died 10 months later with a high peripheral blood blast count and hepatosplenomegaly. Bone marrow, aspirated with great difficulty, contained 40% blasts. Serum uric acid was 566 mol/1.
*Present address: St
Mary’s Hospital.
D. S. LEWIS* London W2 1NY
OUTPATIENT PREPARATION FOR COLONOSCOPY
SIR,-When day facilities are not available, preparation of patients for colonoscopy becomes a major problem. In Oxford, colonic wash-outs can only be obtained for inpatients, so all patients have to be admitted for the night before colonoscopy, which is expensive in terms of beds and nursing time. We have recently compared our standard preparation (liquid diet, 45 ml castor oil, and colonic wash-outs) with a new oral form of preparation, sodium picosulphate (’Picolax’; Nordic Pharmaceuticals). One sachet of sodium picosulphate is taken before breakfast on the day before colonoscopy and is followed by a low residue diet and a large fluid intake. During the afternoon a second sachet is taken, and only clear fluids are then allowed until the examination the following morning. During May and June, 1981, twenty-five patients were prepared as outpatients in this way and twenty patients received the standard inpatient preparation. Preparation was judged to have been poor in only two of the outpatients, while eight of the twenty patients prepared in the standard way were deemed to have been poorly prepared. Patients prepared with sodium picosulphate often had a moderate amount of liquid contents in the caecum which could be readily aspirated. Even in the two with poor preparation, the right side of the colon could be aspirated. This was in contrast to the standard preparation where a poor preparation usually meant that the examination had to be abandoned. All patients tolerated sodium picosulphate well and experienced no discomfort. The new preparation had previously been found effective for barium enema examinations. Our results indicate that it can be used’ successfully for outpatients scheduled for colonoscopy. It is cheap, saves nursing time by avoiding colonic wash-outs, and it is safe when diathermy is being used.
Gastroenterology Unit,
J. J. BROWN D. P. JEWELL
John Radcliffe Hospital, Oxford OX3 9DU
1. Rosner F, Lee SL. Down’s syndrome and acute leukaemia. Lancet 1973; i: 110. 2. Evans DIK. Acute myelofibrosis in children with Down’s syndrome. Arch Dis Child 3.
1975; 59: 458-62. Rosenberg HS, Taylor
FM. The
myeloproliferative syndrome
in children.
J Pediat
1958; 52: 407. 4 Hillman F, Forrester RM.
Myelofibrosis simulating acute leukaemia in a female infant syndrome. Irish J Med Sci 1968; 1: 167 Fujinami T, Sugiyama T, Tankawa H, et al A case of megakaryocitic myelosis in a child. Ann Paediat Jap 1961, 7: 226. Okada H, et al. Down’s syndrome associated with a myeloproliferative disorder. AmJ with Down’s
5. 6.
Dis Child 1972; 124: 107-10. et al. A case of mongolism associated with congenital leukaemia. Jap J Paediat 1965, 18: 1032-41 8 Nordan U, Humbert JR. Myelofibrosis and acute lymphoblastic leukaemia in a child with Down’s syndrome J Pediat 1979; 94: 253-55. 9. Cosson A, Despnes C, Gazenger J, Breton-Gorius M, et al. Unusual leukaemic syndrome in newborn trisomy 21. Nouv Revue Fr Hématol 1974, 14: 182-98 10 Boisseau M, le Menn R Ultrastructure ofblood platelets in two new-born with trisomy 21, thrombocythaemia and leukaemic syndrome. Nouv Revue Fr Hématol 1974; 14: 7.
Tsujino G,
371-82. 11 Lewis SM, Szur L.
Malignant myelosclerosis
Br. MedJ
1963, ii:
472.