Vitamin C

Vitaminum C

For medical students2 min readUpdated 2026-10-10

Vitamin C (Vitaminum C) is one of the most significant micronutrients, the profound deficiency of which leads to a severe pathology known in clinical practice as scurvy. In the study of the pathophysiology of vitamin deficiencies, acquired biotin deficiency is traditionally discussed alongside vitamin C deficiency. Both conditions demonstrate how severely dietary and iatrogenic factors can disrupt homeostasis, causing systemic disorders ranging from dermatological issues to severe bone and hematopoietic system changes.

ScurvyThe extreme degree of vitamin C deficiency, manifesting as hematomas and bone lesions.

Sharp rosarySpecific rib thickenings in scurvy that visually resemble rachitic rosary.

AntibioticsProlonged use suppresses intestinal microflora, causing acquired biotin deficiency.

AvidinA raw egg white protein that binds biotin and leads to seborrhea and alopecia.

Introduction to Vitamin C Deficiency (Scurvy)

Inadequate intake of Vitaminum C triggers a cascade of pathological reactions that ultimately form the full clinical picture of scurvy. This condition is characterized by systemic involvement of various organs and tissues. In the early stages of vitamin C deficiency, general, nonspecific symptoms come to the forefront and significantly reduce the patient's quality of life.

Such baseline clinical manifestations include:

Marked irritability, indicating nervous system involvement in the pathological process.
Dyspnea, which may bother the patient even at relative rest or with minor physical exertion.
Anorexia, manifesting as a persistent decrease or complete lack of appetite.
Low-grade fever (subfebrile temperature), indicating a systemic response to the developing deficiency.

Specific Bone and Hemorrhagic Manifestations of Scurvy

As vitamin C deficiency progresses, more severe and specific symptoms develop, affecting the vascular bed and musculoskeletal system. These signs are critical for diagnosis.

Hemorrhagic syndrome: due to impaired vascular permeability, patients develop extensive hematomas. According to clinical data, hemorrhages localize predominantly intramuscularly and subperiosteally (known as subperiosteal hematomas).
Bone deformations: marked and extremely painful enlargement of the epiphyses of long bones is observed.
Chest changes: specific thickenings form on the ribs, termed "rosary". Visually, they closely resemble analogous formations occurring in rickets, but in scurvy, these costal "beads" have a significantly sharper shape.

Etiology of Acquired Biotin Deficiency

Biotin deficiency is studied in close connection with the topic of vitamin insufficiency. Unlike many other conditions, biotin deficiency is strictly acquired. Pathological physiology identifies two main causes (etiology) for the development of this disease:

Dietary cause: associated with nutritional habits, specifically the consumption of excessively large amounts of raw egg white. Raw egg white contains a specific glycoprotein, avidin. Upon entering the digestive tract, avidin tightly binds biotin to form an insoluble complex, making vitamin absorption into the bloodstream impossible.
Iatrogenic cause: caused by the prolonged use of certain groups of drugs, primarily sulfonamides and antibiotics. These medications strongly suppress the growth and reproduction of normal intestinal microflora. Since intestinal bacteria normally synthesize a significant portion of the body's required biotin, their death naturally leads to vitamin deficiency.

Systemic Clinical Manifestations of Biotin Deficiency

The clinical picture of acquired biotin deficiency is extremely diverse and affects several major body systems simultaneously. The symptom complex includes the following groups of disorders:

Dermatological manifestations: patients develop severe dermatitis accompanied by excessive sebaceous gland secretion, leading to seborrhea. Additionally, active hair loss (alopecia) and pathological brittleness of the nail plates are observed.
Muscular manifestations: intensive muscle pain, referred to as myalgia, is a characteristic symptom.
Hematological manifestations: various types of anemia are registered in the blood system, indicating impaired hematopoiesis.
Neurological manifestations: the central nervous system suffers, clinically expressed as the development of profound clinical depression.

Mnemonic

To remember the general symptoms of scurvy, use the mnemonic I-DAF: Irritability, Dyspnea, Anorexia, Fever (low-grade). For bone manifestations: "Sharp rosary on painful epiphyses."

Frequently asked questions

In the synthesis of which main structural tissue protein does vitamin C participate?

Vitamin C participates in the synthesis of collagen, which is the main structural protein of tissues.

During its synthesis, ascorbic acid acts as a cofactor for the enzymes prolyl 4-hydroxylase and lysyl hydroxylase. It ensures the hydroxylation of proline and lysine residues in procollagen by maintaining the iron atom in the enzyme's active center in the reduced form (Fe²⁺). The formation of hydroxyproline is necessary to form hydrogen bonds that stabilize the triple helix of the tropocollagen molecule.

Biochemically, biotin serves as a coenzyme for which class of enzymes?

Biotin is a coenzyme for enzymes of the ligase class (specifically carboxylases).

It participates in carboxylation and transcarboxylation reactions as part of the following enzymes:

Pyruvate carboxylase
Acetyl-CoA carboxylase
Propionyl-CoA carboxylase

The coenzyme form of biotin is N⁵-carboxylbiotin, and its function is tissue uptake of carbon dioxide (adding CO₂ to the substrate).

How to differentiate costal "rosary" in scurvy from those in rickets?

In vitamin C deficiency (scurvy), the rib thickenings have a significantly sharper shape compared to the classic, smoother rachitic "rosary".

Where do hematomas predominantly localize in vitamin C deficiency?

According to the clinical picture, hemorrhages in scurvy most frequently form intramuscularly and beneath the periosteum (subperiosteal hematomas).

Why can raw egg consumption provoke vitamin deficiency?

Raw egg white contains a specific glycoprotein called avidin. In the gastrointestinal tract, it tightly binds biotin, rendering it unavailable for absorption and assimilation by the body.

What is the mechanism of biotin deficiency development during antibiotic therapy?

Prolonged administration of antibiotics and sulfonamides suppresses normal intestinal microflora. Since these bacteria synthesize biotin, their death causes acquired vitamin deficiency.

Go deeper

Pathogenesis of subperiosteal and intramuscular hematoma formation in scurvy.
Mechanisms of anorexia and low-grade fever development in vitamin C deficiency.
Biochemical interaction of glycoprotein avidin and biotin in the intestine.
Types of anemia developing in biotin deficiency and their hematological picture.
Differential diagnosis of dermatitis, seborrhea, and alopecia in vitamin deficiency.