Situation: A 34-year-old woman has had chronic diarrhea with pale, bulky, foul-smelling stools that float, a 6-kg weight loss over 6 months, and iron-deficiency anemia. Celiac disease is suspected. She reports easy bruising and bleeding gums. Results are shown with normal ranges in parentheses. International normalized ratio (INR): 1.9 (0.8–1.2) Platelet count: 260,000/mm³ (150,000–400,000) Serum calcium: 8.2 mg/dL (8.6–10.2) Which cause of her bruising do these findings MOST support?

Vitamin K is fat-soluble, so fat malabsorption reduces its absorption, lowers vitamin K–dependent clotting factors, and prolongs the INR. The normal platelet count and the high INR together point to vitamin K deficiency; the low calcium reflects vitamin D and calcium malabsorption.

Why the bruising occurs

Celiac disease damages the small-bowel mucosa, which impairs the absorption of dietary fat. Because vitamin K is a fat-soluble vitamin, fat malabsorption reduces its uptake. Vitamin K is required for the hepatic γ-carboxylation of clotting factors II, VII, IX, and X ^[1]. Without adequate vitamin K, these factors remain undercarboxylated and functionally inactive, which prolongs the prothrombin time and elevates the INR. The patient’s INR of 1.9 with a normal platelet count of 260,000/mm³ is the classic pattern of a coagulation-factor defect rather than a platelet or vascular problem.

The combination of a prolonged INR and a normal platelet count points to vitamin K deficiency from fat malabsorption. Platelets are not involved in this pathway, so the normal count does not rule out a bleeding tendency; it helps rule out thrombocytopenia as the cause.

Why the other findings fit the same mechanism

The low serum calcium of 8.2 mg/dL also reflects malabsorption. Vitamin D is another fat-soluble vitamin, and its deficiency reduces intestinal calcium absorption. In addition, vitamin K deficiency can impair bone mineralization over time ^[1][2]. Therefore, the low calcium is a parallel consequence of fat malabsorption, not the cause of the bruising.

Key point! Calcium participates in the clotting cascade as a cofactor, but hypocalcemia at this mild level does not prolong the INR or cause easy bruising. The INR elevation is specifically explained by reduced vitamin K–dependent clotting factors.

Differential reasoning for the options

Option	Why it does not fit
1. Low serum calcium slowing the clotting cascade	Calcium is a cofactor, but the INR is prolonged by deficient clotting factors, not by mild hypocalcemia. The calcium level reflects vitamin D malabsorption.
2. Poor absorption of a fat-soluble clotting vitamin	Vitamin K is fat-soluble and required for factors II, VII, IX, and X. Malabsorption lowers these factors and raises the INR [1][2].
3. Platelet loss linked to iron-deficiency anemia	The platelet count is normal, so thrombocytopenia is not present. Iron deficiency does not directly cause bruising through platelet loss.
4. Vitamin C deficiency weakening capillary walls	Vitamin C deficiency causes perifollicular hemorrhage and poor wound healing, but it does not elevate the INR. The INR abnormality points to a coagulation-factor defect.

Clinical significance in malabsorptive disorders

Chronic gastrointestinal diseases that impair nutrient absorption can produce vitamin K deficiency and bleeding complications ^[1][2]. In celiac disease, the proximal small intestine is the main site of injury. Vitamin K is absorbed in the small intestine, and when mucosal integrity is lost, oral vitamin K may be only partially effective . In severe cases, parenteral vitamin K may be required because enteral absorption remains unreliable until the mucosa heals .

A high INR with a normal platelet count in a patient with steatorrhea should prompt assessment for vitamin K deficiency. The bleeding manifestations—easy bruising and bleeding gums—are consistent with impaired secondary hemostasis. Watch out! Do not attribute bruising to iron-deficiency anemia alone; iron deficiency affects red cell production, not clotting factor synthesis.