Drug-induced gingival enlargement

Drug-induced gingival enlargement is a side-effect of certain drugs where the gingival tissue is not the intended target organ. The key offending drug classes are anticonvulsants, immunosuppressants, and calcium channel blockers. It is estimated that 50% of adults treated with phenytoin experience gingival enlargement, 30% with cyclosporine, and 20% with nifedipine. This overgrowth impedes proper dental hygiene and, apart from the cosmetic damage, causes painful chewing and eating. The common mechanism of action at the cellular level of all these three categories of dissimilar drugs appears to be inhibition of cation influx, particularly sodium and calcium ions. The modalities of treatment are medical and surgical. Medical management is the first line of therapy and includes discontinuing or changing the medication must be placed under consideration. Surgery is reserved for recurrences or cases that persist despite good medical treatment.

 

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Celiac disease

 

Celiac disease (CD) is an immune-mediated, multisystem disorder that affects genetically

 susceptible individuals who are exposed to gluten-containing grains such as wheat, barley, and rye.

Also known as gluten-sensitive enteropathy, Celiac disease is a condition in which the body responds

 to gluten with an inappropriate immune response causing small intestinal inflammation and damage.

CD can be associated with different autoimmune and idiopathic diseases, including type 1 diabetes

 mellitus, Hashimoto’s thyroiditis, selective IgA deficiency, alopecia areata, Addison’s disease, connective

 tissue diseases (mainly Sjogren’s syndrome), chromosomal diseases (Down, Turner, and William’s

 syndromes), neurological diseases (cerebellar ataxia, peripheral neuropathy, epilepsy with and without

 occipital calcifications), hepatic autoimmune diseases (primary biliary cholangitis, autoimmune hepatitis,

 primary sclerosing cholangitis), and idiopathic dilated cardiomyopathy.

Extraintestinal symptoms are common and may include:

• Anemia due to defective absorption of vitamin B12, folate or iron
• Coagulopathy due to impaired absorption of vitamin K
• Osteoporosis
• Neurological symptoms like muscle weakness, paresthesias, seizures and ataxia

Dermatitis herpetiformis is an extraintestinal manifestation that is pathognomonic for celiac disease.

 Because the rash is an immunologic response to gluten, it is sometimes referred to as celiac disease of the

 skin. This papulovesicular rash is extremely pruritic and found on extensor surfaces, such as the elbows,

 knees, buttocks, and scalp.

The two antibodies measured are anti-tissue transglutaminase antibodies (by enzyme-linked

 immunosorbent assay or ELISA measured numerically) and anti-endomysial antibodies.

Esophagogastroduodenoscopy with small bowel biopsy is recommended to confirm the diagnosis in most

 patients, including those with a negative serologic test for whom clinical suspicion of celiac disease

 persists.

Genetic testing for human leukocyte antigen alleles DQ2 or DQ8 may be performed in select cases.

A gluten-free diet for life is the primary treatment

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Rhabdomyolysis

Creatine kinase (CK) is an intracellular enzyme present in skeletal muscle, myocardium & brain; smaller amounts in visceral tissues. Released after disruption of cell membranes due to hypoxia or other injury.

Sustained increases in these levels can be a sensitive indicator of underlying muscle damage.
CK may increase to as much as 30 times the upper limit within 24 hrs of strenuous physical activity, then slowly decline over next 7 days.
The definitive diagnosis of rhabdomyolysis is reliably made by serologic testing for creatine kinase (CK). Elevated levels of CK are the hallmark of rhabdomyolysis.
CK functions as an energy reservoir for ATP:
Creatine + ATP = creatine kinase + ADP (adenosine diphosphate).
CK has a half-life of 1.5 days; its level elevated in the first 12 hours, peaks during the first 3 days, and normalizes at around 5 days after injury.
CK level five times the upper limit of normal (≈1000 U/L), without apparent cardiac or brain injury, confirms the diagnosis.
Risk of developing AKI is usually low when the CK level is below 10,000 U/L.
AKI at lower levels of CK noted with coexisting conditions, such as sepsis, hypotension, or underlying CKD.
Myoglobin levels rise rapidly (within 3 hours) and peak prior to serum CK levels.
Myoglobin has a short half-life of 2 - 3 hours and is rapidly excreted by the kidneys.
Rapid and unpredictable metabolism makes serum myoglobin a less useful marker of muscle injury than CK, and is rarely used in assessing the risk of AKI.

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