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close this bookScurvy and its Prevention and Control in Major Emergencies (WHO; 1999; 70 pages)
View the documentAcknowledgements
View the documentScurvy: definition
open this folder and view contentsIntroduction
close this folderScurvy
open this folder and view contentsSigns and symptoms
View the documentDiagnosis of scurvy
open this folder and view contentsHistory of scurvy
open this folder and view contentsVitamin C
open this folder and view contentsRecommended Daily Allowance (RDA)
open this folder and view contentsSources of vitamin C
open this folder and view contentsStrategies to prevent scurvy in large refugee populations
View the documentCosts
open this folder and view contentsConclusions and recommendations
View the documentReferences
View the documentAnnex 1
View the documentAnnex 2
View the documentAnnex 3
View the documentBack Cover
 

Diagnosis of scurvy

The main criteria for diagnosing scurvy are:

• A history of dietary inadequacy of vitamin C.

• Clinical manifestations characteristic of a scorbutic state (Tables 3 and 4).

• Biochemical indices, i.e. low levels of vitamin C in the blood (serum, white blood cells and whole blood) and a low urinary excretion rate.

The clinical picture of scurvy in children is quite different from that seen in adults, the impact on growing bones being one of its earliest and most prominent distinguishing features. In contrast to adult scurvy, haemorrhaging is less common among children during the early stages of the disease.

Biochemical evaluation of vitamin C status in humans is usually conducted through a determination of serum (plasma) ascorbic acid levels. Serum levels of ascorbic acid show a linear relationship with vitamin C intake. When deprived of vitamin C, a subject's concentration of plasma ascorbic acid decreases rapidly while, with a given intake of the vitamin, the plasma ascorbic acid concentration will plateau at a given level (Sauberlich et al., 1974). The maximum plasma ascorbic acid level appears to be about 1.4 mg/100 ml, at which point renal clearance of the vitamin rises abruptly. Although low plasma ascorbic acid levels do not necessarily indicate scurvy, clinical cases of scurvy always have low or no plasma ascorbic acid. However, continued low levels of plasma ascorbic acid of less than 0.1 mg/100 ml would probably eventually lead to scurvy (Hodges et al., 1971).

There is also a well-defined relationship between whole blood ascorbic acid values and the body reserves of the vitamin, with signs of scurvy appearing when the whole blood ascorbate level falls below 0.3 mg/100 ml (Hodges et al., 1969). Whole blood ascorbic acid levels are probably a less sensitive indicator of vitamin C nutriture than serum levels of the vitamin since the ascorbic acid levels in red blood cells never fall to the low levels encountered in serum or plasma (Sauberlich et al., 1974).

Table 3. Clinical manifestations of scurvy in adults

Body system

Typical lesion

Skin:

• Diffuse petechial haemorrhages*

• Hyperkeratotic follicular papules** on the calves and buttocks with spiral unerupted hairs

Mouth:

• Bleeding gums
• Loosening of teeth
• Petechial haemorrhages*

Eye:

Intra-ocular haemorrhages

Blood:

Moderately severe anaemia

Bones:

• Irregular masses of calcified cartilage in fibrous tissue
• Marrow spaces become filled with a loose connective tissue
• Bone shafts become less dense

* Small purplish red spots due to intradermal or submucous bleeding.
** Thickening of the corneal layer or small elevations of the skin.

Table 4. Clinical manifestations of scurvy in infants and young children

Most frequent symptoms
• General irritability
• Tenderness of the limbs, especially of the legs
• Pseudo paralysis, usually involving the lower extremities
• Involvement of costochondral junctions: changes such as beading of ribs
• Haemorrhage around erupting teeth (in infants without teeth gums appear normal)
• Anaemia

Possible symptoms
• Anorexia
• Low-grade fever
• Mild diarrhoea, sometimes bloody
• Petechial haemorrhages in the skin

White blood cell ascorbic acid concentrations are more closely related to tissue stores of the vitamin than are serum levels. With vitamin C deprivation, white blood cell ascorbic acid levels fall more slowly than plasma ascorbic acid levels and are most pronounced in association with the onset of signs of scurvy (Sauberlich et al., 1974). However, because determination of ascorbic acid in white blood cells is technically difficult and requires relatively large blood samples, it is impractical for routine use in nutrition surveys.

Table 5 proposes cutoff points for mild, moderate and severe vitamin C deficiency based on ascorbic acid levels in whole blood, plasma and white blood cells. Table 6 suggests guidelines for differentiating among levels of risk for vitamin C deficiency in a population.

Table 5. Cutoff points for interpreting vitamin C biochemical data (all age groups)

 

Deficient
(high risk)

Low
(medium risk)

Acceptable
(low risk)

Serum ascorbic acid (mg/100 ml)

< 0.2

0.2 - 0.29

> 0.3

Leukocyte ascorbic acid* (nmol/108 cells)

< 57

57 - 114

> 114

Whole blood ascorbic acid (mg/100 ml)

< 0.3

0.3 - 0.49

> 0.5

Source: Sauberlich et al.,1974.
* Data kindly updated by H.E.Sauberlich (1999)

Table 6. Provisional criteria for severity of public health problem of vitamin C deficiency

 

Severity of public health problem

Indicator

Mild

Moderate

Severe

Clinical signs:

³1 clinical case; <1% of population in age group concerned

1-4% of population in age group concerned

³5% of population in age group concerned

Serum ascorbic acid

     

<0.2 mg/100ml

10-29 %

30-49 %

³50 %

<0.3 mg/100ml

30-49 %

50-69 %

³70 %

Derived from: Sauberlich et al., 1974, Desenclos JC et al., 1989.
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