From: zero dockus <[email protected]>
Subject: Re: Ketone
Date: Thu, 24 Feb 2000 11:23:30 -0800
Message-ID: <[email protected]>
On Thu, 24 Feb 2000 19:19:30 +0100, [email protected] (Tilman
>>Research on a substance known as ketone, which people produce when they
>>are dehydrated, starving or even fasting, according to Rinder and Marty
>>Rathbun, another church official. Tests of McPherson's bodily fluids
>>showed no ketone, they said.
>I thought ketone is produced when the body tries to survive on body fat.
>Can anyone confirm that ketone is produced when people are dehydrated?
The answer is "yes" especially if the patient is hyperglycemic.
I wonder of Lisa McPherson has any record of diabetes in her health
TITL: [The hyperglycemic dehydration syndrome (see comments)]. Het
AUTH: Melief PH; de Meijer PH; Meinders AE
ORGA: Leids Universitair Medisch Centrum, afd. Algemene Interne
Geneeskunde, RC, Leiden.
CITE: Ned Tijdschr Geneeskd 1998 Jul 11; 142 (28): 1585-8
LANG: DUT; Dutch (1401-)
ABST: Two patients, men aged 47 and 64 years, were found in a comatose
condition in their homes, after a period of fatigue, polyuria and
polydipsia. They had not been known to suffer from diabetes mellitus,
but now displayed a hyperglycaemic hyperosmolar non-ketoacidotic
disorder as the first manifestation of diabetes mellitus type 2. In
that condition, just sufficient insulin is present to counteract
ketone production, but not enough to prevent hyperglycaemia.
Neurological and thromboembolic manifestations, possibly fatal, may
result from severe dehydration brought about by a vicious circle in
which osmotic diuresis reduces the effective circulating volume,
causing renal function to decrease and hyperglycaemia to increase even
more. Both patients recovered fully after adequate treatment with
solutions of NaCl and glucose. (AUTHOR)
MJTR: Diabetes Mellitus, Non-Insulin-Dependent CO. Diabetes
Mellitus, Non-Insulin-Dependent DI. Hyperglycemic Hyperosmolar
Nonketotic Coma ET.
MNTR: Case Report. Dehydration ET. English Abstract. Fluid
Therapy. Human. Hyperglycemic Hyperosmolar Nonketotic Coma TH.
Male. Middle Age. JOURNAL ARTICLE
IDEN: ISSN: 0028-2162. JOURNAL-CODE: NUK. ENTRY-DATE: 981217.
TITL: Assessment of dehydration in adults using hematologic and
biochemical tests [letter].
AUTH: Ooi SB; Koh-Tai BC; Aw TC; Lau TC; Chan ST
CITE: Acad Emerg Med 1997 Aug; 4 (8): 840-4
LANG: ENG; English
MJTR: Dehydration DI. Ketones BL. Ketones UR.
MNTR: Adolescence. Adult. Aged. Aged, 80 and over. Blood
Chemical Analysis. Human. Middle Age. Reagent Kits,
Diagnostic. Urinalysis. LETTER
RNUM: 0 (Ketones); 0 (Reagent Kits, Diagnostic)
GEOT: UNITED STATES
IDEN: ISSN: 1069-6563. JOURNAL-CODE: CE1. ENTRY-DATE: 971002.
JOURNAL-SUBSET: M. IM-DATE: 9712.
TITL: Serum electrolytes, ketone bodies, pyruvic and lactic acid in
infants with moderate and severe diarrhoeal dehydration.
AUTH: Ghazal A; Zeitoun MM; Hassanein EA; Selim MM
CITE: Trop Geogr Med 1970 Jun; 22 (2): 149-54
LANG: ENG; English
MJTR: Diarrhea, Infantile BL. Ketone Bodies BL. Lactates BL.
Potassium BL. Pyruvates BL. Sodium BL.
MNTR: Blood Glucose AN. Dehydration ET. Human. Hyponatremia
ME. Infant. Infant Nutrition Disorders CO. Water-Electrolyte
Balance. JOURNAL ARTICLE
IDEN: ISSN: 0041-3232. JOURNAL-CODE: WGJ. ENTRY-DATE: 700906.
JOURNAL-SUBSET: M. IM-DATE: 7010.
TITL: Ketoacidosis. 17 REFS
AUTH: Felts PW
CITE: Med Clin North Am 1983 Jul; 67 (4): 831-43
LANG: ENG; English
MJTR: Diabetic Ketoacidosis.
MNTR: Dehydration CO. Diabetic Ketoacidosis ET. Diabetic
Ketoacidosis PP. Diabetic Ketoacidosis TH. Fluid Therapy.
Gluconeogenesis. Human. Insulin TU. Ketone Bodies ME.
Kidney ME. Liver ME. Models, Biological. Muscles ME. JOURNAL
RNUM: 0 (Ketone Bodies); 11061-68-0 (Insulin)
GEOT: UNITED STATES
IDEN: ISSN: 0025-7125. JOURNAL-CODE: LU6. ENTRY-DATE: 830920.
JOURNAL-SUBSET: A M. IM-DATE: 8311.
TITL: [New etiologic approach to periodic ketoacidosis in children].
Nouvelle approache etiologique des etats d'acidocetose periodigue e
l'enfant. 26 REFS
AUTH: Boisse J
CITE: Can Med Assoc J 1971 Aug 7; 105 (3): 295-300
LANG: FRE; French (1600-)
MJTR: Diabetic Ketoacidosis ET.
MNTR: Alanine BL. Amino Acid Metabolism, Inborn Errors CO.
Butyrates ME. Carbohydrate Metabolism, Inborn Errors CO. Child.
Child, Preschool. Dehydration ET. Diabetic Ketoacidosis BL.
Diabetic Ketoacidosis CO. Diabetic Ketoacidosis GE. Diabetic
Ketoacidosis ME. English Abstract. Female. Glycogen Storage
Disease CO. Hexoses ME. Human. Hydrogen-Ion Concentration.
Hypoglycemia CO. Infant. Infant, Newborn. Ketone Bodies ME.
Lactation Disorders CO. Lipid Metabolism, Inborn Errors CO.
Maple Syrup Urine Disease CO. Methionine ME. Periodicity.
Pregnancy. Propionates ME. Pyruvates BL. Vomiting ET. JOURNAL
IDEN: ISSN: 0008-4409. JOURNAL-CODE: CKW. ENTRY-DATE: 720210.
JOURNAL-SUBSET: A M. IM-DATE: 7203.
Post Graduate Medicine
SECTION: Vol. 101, No. 4; Pg. 193
LENGTH: 4024 words
HEADLINE: Diabetic ketoacidosis
BYLINE: David S. H. Bell, MB Jimmy Alele, MD; David S. H. Bell, MBDr
Bell is professor of medicine and director of the endocrinology
clinic, department of medicine, University of Alabama School of
Medicine, Birmingham. Correspondence: David S. H. Bell, MB, 2000 6th
Ave S, Birmingham, AL 35233.; Jimmy Alele, MDDr Alele is an endocrine
fellow, department of medicine, University of Alabama School of
With severe dehydration, there is an anion gap acidosis. However, with
lesser degrees of dehydration or with rehydration, ketones (and thus
potential bicarbonate) are lost in the urine, and hyperchloremic
In spite of severe dehydration and hemoconcentration, patients with
diabetic ketoacidosis do not experience renal shutdown or gangrene of
the extremities. Vasodilation and peripheral circulation are adequate,
and the patients are warm.11 (Reference) These effects are mediated
through the vasodilating prostaglandins, prostacyclin (PGI2) and
dinoprostone (PGE2), which are overproduced by fat cells when there is
not enough insulin on board.12 (Reference)
With insulin administration, the levels of vasodilating prostaglandins
decrease rapidly, and administration of nonsteroidal anti-inflammatory
drugs is not necessary. Unfortunately, prostaglandins are also
responsible for the nausea, vomiting, and abdominal pain that occur
with ketosis and exacerbate dehydration.
Clinical features Patients with diabetic ketoacidosis usually have a
l2- to 24-hour history of polyuria, polydipsia, abdominal pain,
nausea, and vomiting. Those with known diabetes have had high blood
glucose levels, and they may have taken extra insulin. Most patients
have not checked their urine for ketones because they lack testing
The situation usually becomes worse with the onset of nausea and
vomiting, which exacerbate the already hypovolemic state. Insulin
administration is ineffective because of the dehydration and poor
In addition to the obvious dehydration with dry mucous membranes and
loss of skin turgor, patients may have tachycardia with low blood
pressure that drops significantly on sitting up. Acidosis causes
tachypnea, a fruity odor on the breath, and altered mental status.
Copyright © 1992 American Academy of Pediatrics
Pediatrics 1992; 89: 330-332
SECTION: EXPERIENCE AND REASON - BRIEFLY RECORDED
LENGTH: 1161 words
TITLE: Not All Severe Hyperglycemia Is Diabetes
AUTHOR: SUSAN D. BOULWARE, MD, WILLIAM V. TAMBORLANE, MD, Department
of Pediatrics (Endocrinology), The Children's Clinical Research
Center, Yale University School of Medicine, New Haven, Connecticut
Severe hyperglycemia without ketosis at the clinical onset of
insulin-dependent diabetes mellitus (IDDM) has been reported in
children and adolescents. [n1] Nondiabetic children can develop modest
hyperglycemia (usually in the range of 11 to 14 mmol/L (200 to 250
mg/dL)) without ketosis in response to physiologic stress such as
trauma, burns, or sepsis, [n2,n3] but severe hyperglycemia is seen
rarely in this setting. We recently encountered the case of a
22-month-old infant with severe nonketotic hyperglycemic hyperosmolar
syndrome due to gastroenteritis and dehydration who rapidly recovered
and has had no subsequent evidence of diabetes mellitus.
A 22-month-old Hispanic male infant was brought to the Yale-New Haven
Hospital Pediatric Emergency Room with a 48-hour history of fever,
diarrhea (8 to 10 stools/day), and vomiting (approximately hourly for
the previous 24 hours). Intake for the 48 hours of illness was limited
to carbonated beverages and fruit juices. The child previously had
been healthy with no antecedent polydipsia or polyuria. Family history
was remarkable for IDDM in the maternal great-grandmother and for
hypothyroidism in the mother.
Physical examination revealed temperature 105 degrees F rectally,
pulse 180 beats per minute, and respiratory rate 40 breaths per
minute. The infant appeared lethargic and markedly dehydrated with
sunken eyes, dry mucous membranes, and tenting of the skin without
"doughiness." His breath did not smell of acetone. Initial laboratory
studies obtained before intravenous rehydration were remarkable for
serum glucose 34.1 mmol/L (614 mg/dL), venous pH 7.12, serum
bicarbonate 6.7 mmol/L, sodium 139 mmol/L, and chloride 113 mmol/L.
The blood urea nitrogen level was 13.9 mmol/L (39 mg/dL) and
creatinine concentration was 180 mu mol/L (2.4 mg/dL). The potassium
level obtained 1 hour after initiation of therapy was 3.6 mmol/L.
Urinalysis showed 4+ glucose and negative ketones.
With hydration alone (normal saline 20 mL/kg, no exogenous insulin)
plasma glucose level decreased to 24.6 mmol/L (443 mg/dL) at 1 hour,
7.7 mmol/L (138 mg/dL) at 3 hours, and 5.1 mmol/dL (92 mg/dL) at 6
hours (Table). Similarly, blood pH, blood urea nitrogen, and
creatinine values normalized with hydration alone. Serum sodium
increased slightly to 150 mmol/L at 3 hours after rehydration and
normalized by 10 hours after initial examination. Plasma glucose
levels remained normal, and the urine was free of ketones throughout
the subsequent 2 days of hospitalization.
Hormone concentrations determined from plasma samples obtained prior
to the start of treatment were markedly elevated: plasma insulin 650
pmol/L (91 mu U/mL), cortisol 2810 nmol/L (102 mu g/dL), and growth
hormone 28 mu g/L. In addition, glycosylated hemoglobin was normal at
5.3% (normal 4% to 8%), islet cell antibodies were negative, and HLA
typing for DR antigens revealed DR-2 and 7. One month later, fasting
and 2-hour postprandial plasma glucose and insulin levels were normal.
The child has remained asymptomatic for the 12 months since his
TABLE. Flowsheet of Glucose and Electrolytes for First 6 Hours
[SEE ORIGINAL SOURCE]
This child was brought to our emergency department like the usual
toddler with new-onset IDDM: severe dehydration, lethargy, and marked
hyperglycemia. The absence of ketones, however, was unexpected and
atypical for diabetes, indicating that the profound acidosis resulted
from poor tissue perfusion and tissue hypoxia. Although the serum
glucose level seemed inappropriately elevated for stress
hyperglycemia, 3 hours after treatment the glucose had decreased to
7.7 mmol/L (138 mg/dL) without exogenous insulin, and a diagnosis of
IDDM was deemed highly unlikely. An initial insulin level of 650
pmol/L (91 mu U/mL) is higher than values usually found in new-onset
IDDM. [n4] Furthermore, the normal glycosylated hemoglobin, markedly
elevated growth hormone and cortisol levels at examination, and the
subsequent course are consistent with stress-induced hyperglycemia.
Although our patient had normal serum sodium values, hyperglycemia has
been associated most commonly with hypernatremic dehydration. [n5-n8]
After fluid resuscitation (normal saline 20 mL/kg), the sodium
increased to above-normal levels (peak 150 mmol/L) as the plasma
glucose fell. Regardless of the serum sodium level, hyperglycemia
associated with severe dehydration most likely is due to the elevation
of stress hormones which stimulate gluconeogenesis and inhibit insulin
secretion and action. [n9] In our patient, cortisol (102 mu g/dL) and
growth hormone (28 mu g/L) were elevated markedly. Moreover, as the
dehydration worsens, the volume depletion leads to renal hypoperfusion
which compounds the hyperglycemia by limiting urinary glucose
excretion. Markedly impaired renal function in this baby was
illustrated by sharply elevated blood urea nitrogen and creatinine on
The most striking aspect of this case was the degree of hyperglycemia.
Although there are isolated reports of stress-induced hyperglycemia of
similar magnitude to that seen in this case, the vast majority of
cases have had much more moderate elevations. Because this level of
hyperglycemia is seen so rarely in the absence of IDDM, we were
concerned about the possibility of a "prediabetes" state in this
child. The absence of islet cell antibodies appears to be a good
prognostic sign. Schatz et al [n10] have demonstrated recently that 4
of 29 children with incidental hyperglycemia or glucosuria were
positive for islet cell antibodies. After 1 to 8 years of follow up,
two of the islet cell antibody-positive children developed IDDM,
whereas none of those who were islet cell antibody-negative did so.
Similarly, in a recent report by Vardi et al [n11] of 12 children in
whom stress hyperglycemia had been diagnosed and followed up for 1 to
12 months, 3 of 4 children with positive islet cell antibodies
developed IDDM compared with 1 of 8 islet cell antibody-negative
patients who went on to develop IDDM. [n11] Genetic studies indicate
that the presence of HLA-DR2 antigen, as seen in this child, may be
protective against the development of IDDM. [n12]
This case serves as a reminder that blood glucose levels, even in
excess of 33 mmol/L (600 mg/dL) are not necessarily diagnostic of
diabetes, particularly in the nonketotic patient with severe
dehydration. Correction of hyperglycemia with hydration alone, without
the addition of insulin, allowed an appropriate diagnosis. This
approach saved the child from inappropriate insulin treatment that
resulted in severe hypoglycemia and seizures in other youngsters with
stress hyperglycemia who were misdiagnosed as having IDDM. [n5,n6]
Dr Boulware is the recipient of a Fellowship grant from the Juvenile
Diabetes Foundation International.
SUPPLEMENTARY INFORMATION: Received for publication Jan 11, 1991;
accepted Feb 21, 1991.
Reprint requests to (S.D.B.) PO Box 3333, 333 Cedar St, New Haven, CT
[n1.] Ehrlich RM, Bain HW. Hyperglycemia and hyperosmolarity in an
eighteen-month-old child. N Engl J Med. 1967;276:683-684
[n2.] Parish RA, Webb KS. Hyperglycemia is not a poor prognostic sign
in head-injured children. J Trauma. 1988;28:17-519
[n3.] Taylor FHL, Levenson SM, Adams MA. Abnormal carbohydrate
metabolism in human thermal burns. N Engl J Med. 1944;231:439-445
[n4.] Theodoridis CG, Chance GW, Brown GA, Williams JW. Plasma insulin
and growth hormone levels in untreated diabetic children. Arch Dis
[n5.] Stevenson RE, Bowyer FP. Hyperglycemia with hyperosmolal
dehydration in nondiabetic infants. J Pediatr. 1970;77:818-823
[n6.] Heggarty H, Trindade P, Bryan EM. Hyperglycaemia in hyperosmolar
dehydration. Arch Dis Child. 1973;48:740-741
[n7.] Mandell F, Fellers FX. Hyperglycemia in hypernatremic
dehydration. Clin Pediatr. 1974;13:367-369
[n8.] Rabinowitz L, Joffe BI, Abkiewicz C, Shires R, Greef MC, Seftel
HC. Hyperglycaemia in infantile gastroenteritis. Arch Dis Child.
[n9.] Gelfand RA, DeFronzo RA, Gusberg R. Metabolic alterations
associated with major injury and infection. In: Kleinberger G, Deutsch
E, eds. Proceedings of the Fourth Congress of the European Society of
Parenteral-Enteral Nutrution: new aspects of clinical nutrition.
Basel: Karger; 1983:211-239
[n10.] Schatz DA, Kowa H, Winter WE, Riley WJ. Natural history of
incidental hyperglycemia and glycosuria of childhood. J. Pediatr.
[n11.] Vardi P, Shehade N, Etzioni A, et al. Stress hyperglycemia in
childhood: a very high risk group for the development of type I
diabetes. J Pediatr. 1990;117:75-77.
[n12.] Eisenbarth GS. Type I diabetes mellitus. N Engl J Med.