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Rare causes of hypoglycemia

Rare causes of hypoglycemia


Hypoglycemia in the Non-Diabetic Patient

Neonatal hypoglycemia

Insulinomas

Postprandial hypoglycemia

Endocrine causes of hypoglycemia

Hepatic and renal causes of hypoglycemia

Drug-induced hypoglycemia

Alcohol-induced hypoglycemia

Factitious hypoglycemia


Hypoglycemia develops when hepatic glucose output falls below the rate of glucose uptake
by peripheral tissues. Hepatic glucose output may be reduced by:

 inhibition of hepatic glycogenolysis and gluconeogenesis by insulin depletion of hepatic glycogen reserves by malnutrition, fasting, exercise, or advanced liver disease.impaired gluconeogenesis (e.g. following alcohol ingestion).

Neonatal hypoglycmia 

defined as a plasma glucose level of less than 30 mg/dL (1.65 mmol/L) in the first 24 hours of life and less than 45 mg/dL (2.5 mmol/L) there after .new born baby`s mother may be diabetic.

usually, corrected by 10% dextrose.

Insulinomas

Insulinomas are pancreatic islet cell tumors that secrete insulin. Most are sporadic but some
patients have multiple tumors arising from neural crest tissue (multiple endocrine neoplasias).
Some 95% of these tumors are benign
The classic presentation is with fasting hypoglycemia, but early symptoms may also develop in the late morning or afternoon. 

Recurrent hypoglycemia is often present for months or years before the diagnosis is made, and
the symptoms may be atypical or even bizarre; 
in elderly people, epilepsy, and cerebrovascular disease. Whipple's triad remains the basis of
clinical diagnosis.
 This is satisfied when:
• symptoms are associated with fasting or exercise
• hypoglycemia is confirmed during these episodes
• glucose relieves the symptoms.

Presenting feature s of insulinoma
• Diplopia
• Sweating, palpitations, weakness
• Confusion or abnormal behavior
• Loss of consciousness
• Grand mal seizures
A fourth criterion – demonstration of inappropriately high insulin levels during
hypoglycemia – may usefully be added.
The diagnosis is confirmed by the demonstration of hypoglycemia in association with
inappropriate and excessive insulin secretion. Hypoglycemia is demonstrated by:

• Measurement of overnight fasting (16 h) glucose and insulin levels on three occasions. About
90% of patients with insulinomas will have low glucose and non-suppressed (normal or
elevated) insulin levels.

• A prolonged 72-h supervised fast if overnight testing is inconclusive and symptoms persist.
Autonomous insulin secretion is demonstrated by a lack of normal feedback suppression
during hypoglycemia. This may be shown by measuring insulin, C-peptide, or proinsulin
during a spontaneous episode of hypoglycemia.
Management
The most effective therapy is surgical excision of the tumor but insulinomas are often very
small and difficult to localize. 

Postprandial hypoglycemia

If frequent venous blood glucose samples are taken following a prolonged glucose tolerance
test, about 1 in 4 subjects will have at least one value below 3 mmol/L. The arteriovenous
glucose difference is quite marked during this phase, so that very few are truly hypoglycaemic
in terms of arterial (or capillary) blood glucose content. Failure to appreciate this simple fact
led some authorities to believe that postprandial (or reactive) hypoglycemia was a potential
‘organic’ explanation for a variety of complaints that might otherwise have been considered
psychosomatic. 
.
True postprandial hypoglycemia may develop in the presence of alcohol, which ‘primes’
the cells to produce an exaggerated insulin response to carbohydrates. The person who
substitutes alcoholic beverages for lunch is, particularly at risk. Postprandial hypoglycemia
sometimes occurs after gastric surgery, owing to rapid gastric emptying and mismatching of
nutrient absorption and insulin secretion. This is referred to as ‘dumping’ but it is now rarely
encountered.

Hepatic and renal causes of hypoglycemia

The liver can maintain a normal glucose output despite extensive damage, and hepatic
hypoglycemia is uncommon. It is, however, a particular problem with acute hepatic failure.
The kidney has a subsidiary role in glucose production (via gluconeogenesis in the renal
cortex), and hypoglycemia is sometimes a problem in terminal renal failure.

Endocrine causes of hypoglycemia

Deficiencies of hormones antagonistic to insulin are rare but well-recognized causes of
hypoglycemia. These include 
hypopituitarism
 isolated adrenocorticotrophic hormone
(ACTH) deficiency and 
Addison's disease.

Drug-induced hypoglycemia

Many drugs have been reported to produce isolated cases of hypoglycemia, but usually only
when other predisposing factors are present:
 Sulphonylureas 
 Quinine 
 Salicylates 
 Propranolol 
 Pentamidine

Alcohol-induced hypoglycemia

Alcohol inhibits gluconeogenesis. Alcohol-induced hypoglycemia occurs in poorly nourished
chronic alcohol users, binge drinkers, and children who have taken relatively small amounts of
alcohol, since they have a diminished hepatic glycogen reserve. They present with coma and
hypothermia (hypothermia is a feature of hypoglycemia, due to the suppression of central
thermoregulation, particularly the shivering response; children manifest hypothermia more
frequently due to their high ratio of surface area to body mass).

Factitious hypoglycemia

This is a relatively common variant of self-induced disease and is more common than an
insulinoma. Hypoglycemia is produced by surreptitious self-administration of insulin or
sulphonylureas. Many patients in this category have been extensively investigated for an
insulinoma. Measurement of C-peptide levels during hypoglycemia should identify patients
who are injecting insulin; sulphonylurea abuse can be detected by chromatography of plasma or urine.

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