Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis. These new findings provide important links between risk factors and the mechanisms of atherogenesis. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to human patients. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors. Moreover, certain treatments that reduce coronary risk also limit inflammation. In the case of lipid lowering with statins, this anti-inflammatory effect does not appear to correlate with reduction in low-density lipoprotein levels. These new insights into inflammation in atherosclerosis not only increase our understanding of this disease but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.

Inflammatory abnormalities are a large group of disorders that underlie a vast variety of human diseases. The immune system is often involved with inflammatory disorders, demonstrated in both allergic reactions and some myopathies, with many immune system disorders resulting in abnormal inflammation. Non-immune diseases with causal origins in inflammatory processes include cancer, atherosclerosis, and ischemic heart disease.

Examples of disorders associated with inflammation include:

- Acne vulgaris

- Asthma

- Autoimmune diseases

- Autoinflammatory diseases

- Celiac disease

- Chronic prostatitis

- Colitis

- Diverticulitis

- Glomerulonephritis

- Hidradenitis suppurativa

- Hypersensitivities

- Inflammatory bowel diseases

- Interstitial cystitis

- Mast Cell Activation Syndrome

- Mastocytosis

- Otitis

- Pelvic inflammatory disease

- Reperfusion injury

- Rheumatic fever

- Rheumatoid arthritis

- Rhinitis

- Sarcoidosis

- Transplant rejection

- Vasculitis

There are seven classes of medications associated with acute pancreatitis: statins, ACE inhibitors, oral contraceptives/hormone replacement therapy (HRT), diuretics, antiretroviral therapy, valproic acid, and oral hypoglycemic agents. Mechanisms of these drugs causing panreatitis are not known exactly; but it is possible that statins has direct toxic effect on the pancreas or through the long term accumulation of toxic metabolites. Meanwhile, ACE inhibitors causes angioedema of the pancreas through the accumulation of bradykinin. Oral contraceptives/HRT causes arterial thrombosis of the pancreas through the accumulation of fat (hypertriglyceridemia). Diuretics such as furosemide has direct toxic effect on the pancreas. Meanwhile, thiazide diuretics causes hypertriglyceridemia and hypercalcemia, where the latter is the risk factor for pancreatic stones. HIV infection itself can cause a person to more likely to get pancreatitis. Meanwhile, antiretroviral drugs may cause metabolic disturbances such as hyperglycemia and hypercholesterolemia, which predisposes to pancreatitis. Valproic acid may have direct toxic effect on the pancreas. There are various oral hypoglycemic agents that contributes to pancreatitis including metformin. But, glucagon-like peptide-1 (GLP-1) is more strongly associated with pancreatits by promoting inflammation.

Atypical antipsychotics such as clozapine, risperidone, and olanzapine can also cause pancreatitis.

A number of infectious agents have been recognized as causes of pancreatitis including:

- Viruses

- Coxsackie virus

- Cytomegalovirus

- Hepatitis B

- Herpes simplex virus

- Mumps

- Varicella-zoster virus

- Bacteria

- Legionella

- Leptospira

- Mycoplasma

- Salmonella

- Fungi

- Aspergillus

- Parasites

- Ascaris

- Cryptosporidium

- Toxoplasma

The annual incidence of chronic pancreatitis is 5 to 12 per 100,000 persons, the prevalence is 50 per 100,000 persons.

In chronic recurrent sialadenitis or chronic sclerosing sialadenitis, acute attacks are managed with conservative therapies such as hydration, analgesics (mainly NSAIDs), sialogogues to stimulate salivary secretion, and regular, gentle gland massage. If infection is present, appropriate cultures should be obtained, followed by empirical antibiotic therapy initially, for example amoxicillin/clavulanate or clindamycin which cover oral flora.

If there are attacks more than approximately 3 times per year or severe attacks, surgical excision of the affected gland should be considered.

Sialadenitis (sialoadenitis) is inflammation of a salivary gland. It may be subdivided temporally into acute, chronic and recurrent forms.

The epidemiology of Idiopathic sclerosing mesenteritis disease is extremely rare and has only been diagnosed in about an estimated 300 patients worldwide to date (as of 2014), it is probably under diagnosed.

It can occur in children.

Evidence does not support a role for specific foods including spicy foods and coffee in the development of peptic ulcers. People are usually advised to avoid foods that bother them.

Although there can be various causes of dog pancreatitis, such as drugs, fatty diet, trauma, etc., the pathophysiology is very complex. Pancreatitis can be idiopathic; no real causation factor can be found. Obese animals as well as animals fed a diet high in fat may be more prone to developing acute and chronic pancreatitis. Certain breeds of dogs are considered predisposed to developing pancreatitis including miniature schnauzers, Cocker Spaniels, and some terrier breeds. Miniature Schnauzers as a breed tend toward developing hyperlipidemia, an excess of circulating fats in the blood. The breed which appears to be at risk for the acute form of pancreatitis is the Yorkshire Terrier, while Labrador Retrievers and miniature Poodles seem to have a decreased risk for the acute form of the disease. It is suggested that genetics may play a part in the risk factor. Dogs suffering from diabetes mellitus, Cushing's disease (hyperadrenocorticism), hypothyroidism and epilepsy are at increased risk for pancreatitis. Diabetes and hypothyroidism are also associated with hyperlipidemia. Those with other types of gastrointestinal conditions and dogs who have had previous pancreatitis attacks are also at increased risk for the disorder.

Rectitis is an inflammation of the inner rectum. It mainly affects the rectal mucous membrane. The condition can be acute or it may be a chronic condition. Rectitis may be caused due to conditions such as ulcerative colitis or Chron's disease.

Among the causes of chronic pancreatitis are the following:

The relationship between etiologic factors, genetic predisposition, and the pace of disease progression requires further clarification, though recent research indicates smoking may be a high-risk factor to develop chronic pancreatitis. In a small group of patients chronic pancreatitis has been shown to be hereditary. Almost all patients with cystic fibrosis have established chronic pancreatitis, usually from birth. Cystic fibrosis gene mutations have also been identified in patients with chronic pancreatitis but in whom there were no other manifestations of cystic fibrosis. Obstruction of the pancreatic duct because of either a benign or malignant process may result in chronic pancreatitis.

Surgery-associated ischemia may contribute inflammation at the anal transitional zone.

Patients whose cuffitis is refractory to mesalamine and/or corticosteroids should be evaluated for other disease in the cuff area, such as fistula or anastomotic leaks. Cuffitis that is refractory to medication can also be a sign of Crohn's disease of the pouch.

Chronic cuffitis can also contribute to the development of anastomotic stricture.

Cuffitis that is refractory, Crohn's-related, or is associated with surgical complications can contribute to pouch failure.

Gastritis may also develop after major surgery or traumatic injury ("Cushing ulcer"), burns ("Curling ulcer"), or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the banding or reconstruction of the digestive tract.

"Acute bacterial parotitis:"

is most often caused by a bacterial infection of Staphylococcus aureus but may be caused by any commensal bacteria.

"Parotitis as Extrapulmonary Tuberculosis:"

The mycobacterium that cause tuberculosis can also cause parotid infection. Those infected tend to have enlarged, nontender, but moderately painful glands. The diagnosis is made by typical chest radiograph findings, cultures, or histologic diagnosis after the gland has been removed. When diagnosed and treated with antitubercular medications, the gland may return to normal in 1–3 months.

"Acute viral parotitis (mumps):"

The most common viral cause of parotitis is mumps. Routine vaccinations have dropped the incidence of mumps to a very low level. Mumps resolves on its own in about ten days.

"HIV parotitis:" Generalized lymphadenopathy has long been associated with HIV, but the localized enlargement of the parotid gland is less well known.

The annual prevalence in the general population of chronic pelvic pain syndrome is 0.5%. 38% of primary care providers, when presented with a vignette of a man with CPPS, indicate that they have never seen such a patient. However, the overall prevalence of symptoms suggestive of CP/CPPS is 6.3%. The role of the prostate was questioned in the cause of CP/CPPS when both men and women in the general population were tested using the (1) National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) —with the female homolog of each male anatomical term use on questionnaires for female participants— (2) the International Prostate Symptom Score (IPSS), and (3) additional questions on pelvic pain. The prevalence of symptoms suggestive of CPPS in this selected population was 5.7% in women and 2.7% in men, placing in doubt the role of the prostate gland. New evidence suggests that the prevalence of CP/CPPS is much higher in teenage males than once suspected.

In recent years the prognosis for CP/CPPS has improved with the advent of multimodal treatment, phytotherapy, protocols aimed at quieting the pelvic nerves through myofascial trigger point release and anxiety control, and chronic pain therapy.

These are also collectively known as chronic punctate parotitis or chronic autoimmune parotitis.

"Sjögren's syndrome:"

Chronic inflammation of the salivary glands may also be an autoimmune disease known as Sjögren's syndrome. The disease most commonly appears in people aged 40–60 years, but it may affect small children. In Sjögren syndrome, the prevalence of parotitis in women versus men is approximately 9:1. The involved parotid gland is enlarged and tender at times. The cause is unknown. The syndrome is often characterized by excessive dryness in the eyes, mouth, nose, vagina, and skin.

"Lymphoepithelial lesion of Godwin:"

Most frequently associated with a circumscribed tumor with the histologic features of Sjögren syndrome. This designation has also fallen out of favour.

Uveitis may be an immune response to fight an infection inside the eye. While representing the minority of patients with uveitis, such possible infections include:

- brucellosis

- leptospirosis

- Lyme disease

- presumed ocular histoplasmosis syndrome

- syphilis

- toxocariasis

- toxoplasmic chorioretinitis

- tuberculosis

- Zika fever

Sinusitis is a common condition, with between 24 and 31 million cases occurring in the United States annually. Chronic sinusitis affects approximately 12.5% of people.

The Mayo Clinic in Rochester reported a large study of 92 patients, with widely ranging severity of their symptoms. The majority were male, with an average age of 65 years. They commonly had abdominal pain (70%), diarrhea (25%) and weight loss (23%). Depending on the stage of the scarring and fibrosis, several different treatments, including surgery for bowel obstruction, or drugs were used to halt the progression of the disease.

In that case series, 56% of patients received only pharmacological therapy, most often receiving tamoxifen with a reducing dose of reducing prednisone, or also had colchicine, azathioprine or thalidomide.

Their findings suggest that sclerosing mesenteritis can be debilitating although relatively benign. Symptomatic patients benefited from medical therapy, usually tamoxifen and prednisone, but further follow-up information would strengthen these results.

Systemic disorders that can be associated with uveitis include:

- ankylosing spondylitis

- Behçet's disease

- chronic granulomatous disease

- enthesitis

- inflammatory bowel disease

- juvenile rheumatoid arthritis

- Kawasaki's disease

- multiple sclerosis

- polyarteritis nodosa

- psoriatic arthritis

- reactive arthritis

- sarcoidosis

- systemic lupus erythematosus

- Vogt–Koyanagi–Harada disease

- Whipple's disease

Since 1992, chronic gastritis lesions are classified according to the Sydney system.

It has been hypothesized that biofilm bacterial infections may account for many cases of antibiotic-refractory chronic sinusitis. Biofilms are complex aggregates of extracellular matrix and inter-dependent microorganisms from multiple species, many of which may be difficult or impossible to isolate using standard clinical laboratory techniques. Bacteria found in biofilms have their antibiotic resistance increased up to 1000 times when compared to free-living bacteria of the same species. A recent study found that biofilms were present on the mucosa of 75% of people undergoing surgery for chronic sinusitis.

Cuffitis is inflammation at the anal transition zone or “cuff” created as a result of ileal pouch-anal anastomosis (IPAA). It is considered a variant form of ulcerative colitis that occurs in the rectal cuff. Cuffitis is a common complication of IPAA, particularly when a stapled anastomosis without mucosectomy procedure has been used.