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 upon exposure to gluten-containing grains such as wheat, barley, and rye. Also known as gluten-sensitive enteropathy, CD is characterized by an inappropriate immune response to gluten, leading to inflammation and damage of the small intestinal mucosa.

CD is associated with various autoimmune and idiopathic conditions, including:

• Type 1 diabetes mellitus

• Hashimoto’s thyroiditis

• Selective IgA deficiency

• Alopecia areata

• Addison’s disease

• Connective tissue diseases (primarily Sjögren’s syndrome)

• Chromosomal disorders (e.g., Down syndrome, Turner syndrome, and Williams syndrome)

• Neurological disorders (e.g., cerebellar ataxia, peripheral neuropathy, epilepsy with or without occipital calcifications)

• Hepatic autoimmune diseases (e.g., primary biliary cholangitis, autoimmune hepatitis, and primary sclerosing cholangitis)

• Idiopathic dilated cardiomyopathy

Extraintestinal manifestations are common and may include:

• Anemia due to impaired absorption of vitamin B12, folate, or iron

• Coagulopathy due to vitamin K deficiency

• Osteoporosis

• Neurological symptoms such as muscle weakness, paresthesias, seizures, and ataxia

Dermatitis herpetiformis is a pathognomonic extraintestinal manifestation of CD. This papulovesicular, extremely pruritic rash appears on extensor surfaces including the elbows, knees, buttocks, and scalp. It represents an immunologic skin response to gluten and is often referred to as celiac disease of the skin.

Diagnosis involves serologic testing and histologic confirmation:

• Serologic tests include anti–tissue transglutaminase (tTG) antibodies (measured quantitatively by enzyme-linked immunosorbent assay, ELISA) and anti-endomysial antibodies.

• Esophagogastroduodenoscopy (EGD) with small bowel biopsy remains the gold standard for diagnosis, particularly in patients with negative serology but strong clinical suspicion.

• Genetic testing for HLA-DQ2 or HLA-DQ8 alleles may be considered in selected cases, especially when the diagnosis remains uncertain.

Management consists of strict lifelong adherence to a gluten-free diet, which is the cornerstone of treatment and typically results in clinical and histological improvement.

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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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