The Xanthogranulomatous Process (XP), also known as Xanthogranulomatous Inflammation is a form of acute and chronic inflammation characterized by an exuberant clustering of foamy macrophages among other inflammatory cells. Localization in the kidney and renal pelvis has been the most frequent and better known occurrence followed by that in the gallbladder but many others have been subsequently recorded. The pathological findings of the process and etiopathogenetic and clinical observations have been reviewed by Cozzutto and Carbone.

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.

The xanthogranulomatous type of inflammation is most-commonly seen in pyelonephritis and cholecystitis, although it has more recently been described in an array of other locations including bronchi, lung, endometrium, vagina, fallopian tubes, ovary, testis, epydidymis, stomach, colon, ileum, pancreas, bone, lymph nodes, bladder, adrenal gland, abdomen and muscle. Telling apart clinically a XP from a tumor condition can be challenging as pointed out by several authors. Cozzutto and Carbone suggested that a wide array of entities characterized by a large content of histiocytes and foamy macrophages could be traced back at least in part to a xanthogranulomatous inflammation. These include such varied disturbances as xanthoma disseminatum, ceroid granuloma of the gallbladder, Whipple's disease, inflammatory pseudotumor of the lung, plasma cell granuloma of the lung, malakoplakia, verruciform xanthoma, foamy histiocytosis of the spleen in thrombocytopenic purpura, isolated xanthoma of the small bowel, xanthofibroma of bone, and gastric xanthelasma.

A pathogenetic model might be suggested as follows:

1. suppuration, hemorrhage and necrosis,

2. granulomatous tissue with granular histiocytes and foamy macrophages,

3. fibrohistiocytoma-like or plasma cell granuloma-like patterns,

4. possible myofibroblast metaplasia.

A reactive fibrohistiocytic lesion simulating fibrous histiocytoma has been reported by Snover et al. Reactive granular cells in sites of trauma have been regarded of histiocytic nature. Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease) might share several aspects of the XP. Likewise there might be some superimpositions between the XP and the plasma cell granuloma/histiocytoma-inflammatory myofibroblastic tumor complex.> The XP might be an important stage of this complex.

A prospective study in 1994 noted that body mass index remains the strongest predictor of symptomatic gallstones among young women. Other risk factors are having over four pregnancies, weight gain, and cigarette smoking. Alcohol was shown to have an inverse relationship between use and gallbladder disease.

There is evidence for a link between inflammation and depression. Inflammatory processes can be triggered by negative cognitions or their consequences, such as stress, violence, or deprivation. Thus, negative cognitions can cause inflammation that can, in turn, lead to depression.

In addition there is increasing evidence that inflammation can cause depression because of the increase of cytokines, setting the brain into a "sickness mode". Classical symptoms of being physically sick like lethargy show a large overlap in behaviors that characterize depression. Levels of cytokines tend to increase sharply during depressive episodes in manics and drop off during remission. Furthermore, it has been shown in clinical trials that anti-inflammatory medicines taken in addition to antidepressants not only significantly improves symptoms but also increases the proportion of subjects positively responding to treatment.

Inflammations that lead to serious depression could be caused by common infections such as those caused by a virus, bacteria or even parasites.

90% of cases are smokers, however only a very small fraction of smokers appear to develop this lesion. It has been speculated that either the direct toxic effect or hormonal changes related to smoking could cause squamous metaplasia of lactiferous ducts. It is not well established whether the lesion regresses after smoking cessation.

Extrapuerperal cases are often associated with hyperprolactinemia or with thyroid problems. Also diabetes mellitus may be a contributing factor in nonpuerperal breast abscess.

Granuloma is an inflammation found in many diseases. It is a collection of immune cells known as histiocytes (macrophages). Granulomas form when the immune system attempts to wall off substances it perceives as foreign but is unable to eliminate. Such substances include infectious organisms including bacteria and fungi, as well as other materials such as keratin and suture fragments.

Crohn's disease is an inflammatory condition of uncertain cause characterized by severe inflammation in the wall of the intestines and other parts of the abdomen. Within the inflammation in the gut wall, granulomas are often found and are a clue to the diagnosis.

Xanthogranulomatous osteomyelitis (XO) is a peculiar aspect of osteomyelitis characterized by prevalent histiocytic infiltrate and foamy macrophage clustering.

Women are almost twice as likely as men to form gallstones especially during the fertile years; the gap narrows after the menopause. The underlying mechanism is female sex hormones; parity, oral contraceptive use and estrogen replacement therapy are established risk factors for cholesterol gallstone formation. Female sex hormones adversely influence hepatic bile secretion and gallbladder function. Estrogens increase cholesterol secretion and diminish bile salt secretion, while progestins act by reducing bile salt secretion and impairing gallbladder emptying leading to stasis. A new 4th generation progestin, drospirenone, used in some oral contraceptives may further heighten the risk of gallstone disease and cholecystectomy; however, the increased risk is quite modest and not likely to be clinically meaningful.

A retrospective (historical) cohort study was performed on a very large data base including 1980 and 1981 Medicaid billing data from the states of Michigan and Minnesota in which 138,943 users of OCs were compared with 341,478 nonusers. Oral contraceptives were shown as risk factors for gallbladder disease, although the risk is of sufficient magnitude to be of potential clinical importance only in young women.

The 1984 Royal College of General Practitioners' Oral Contraception Study suggests that, in the long-term, oral contraceptives are not associated with any increased risk of gallbladder disease, although there is an acceleration of the disease in those women susceptible to it.

Newer research suggests otherwise. A 1993 meta-analysis concludes that oral contraceptive use is associated with a slightly and transiently increased rate of gallbladder disease, but laters confirms that modern low-dose oral contraceptives are safer than older formulas, though an effect cannot be excluded.

A 2001 comparative study of the IMS LifeLink Health Plan Claims Database interpreted that in a large cohort of women using oral contraceptives, there was found a small, statistically significant increase in the risk of gallbladder disease associated with desogestrel, drospirenone and norethisterone compared with levonorgestrel. No statistically significant increase in risk was associated with the other formulations of oral contraceptive (etynodiol diacetate, norgestrel and norgestimate).

Also called Zuska's disease (only nonpuerperal case), subareolar abscess is a subcutaneous abscess of the breast tissue beneath the areola of the nipple. It is a frequently aseptic inflammation and has been associated with squamous metaplasia of lactiferous ducts.

The term is usually understood to include breast abscesses located in the retroareolar region or the periareolar region, but not those located in the periphery of the breast.

Subareolar abscess can develop both during lactation or extrapuerperal, the abscess is often flaring up and down with repeated fistulation.

"Duct ectasia" in the literal sense (literally: duct widening) is a very common and thus rather unspecific finding, increasing with age. However, in the way in which the term is mostly used, duct ectasia is an inflammatory condition of the larger-order lactiferous ducts. It considered likely that the condition is associated with aseptic (chemical) inflammation related to the rupture of ducts or cysts. It is controversial whether duct dilation occurs first and leads to secretory stasis and subsequent periductal inflammation or whether inflammation occurs first and leads to an inflammatory weakening of the duct walls and then stasis. When the inflammation is complicated by necrosis and secondary bacterial infection, breast abscesses may form. Subareolar abscess, also called Zuska's disease (only nonpuerperal case), is a frequently aseptic inflammation and has been associated with squamous metaplasia of the lactiferous ducts.

The duct ectasia—periductal mastitis complex affects two groups of women: young women (in their late teens and early 20s) and perimenopausal women. Women in the younger group mostly have inverted nipples due to squamous metaplasia that lines the ducts more extensively compared to other women and produces keratin plugs which in turn lead to duct obstruction and then duct dilation, secretory stasis, inflammation, infection and abscess. This is not typically the case for women in the older group; in this group, there is likely a multifactorial etiology involving the balance in estrogen, progesterone and prolactin.

Treatment of mastitis and/or abscess in nonlactating women largely the same as that of lactational mastitis, generally involving antibiotics treatment, possibly surgical intervention by means of fine-needle aspiration and/or incision and drainage and/or interventions on the lactiferous ducts (for details, "see also" the articles on treatment of mastitis, of breast abscess and of subareolar abscess). Additionally, an investigation for possible malignancy is needed, normally by means of mammography, and a pathological investigation such as a biopsy may be necessary to exclude malignant mastitis. Although no "causal" relation with breast cancer has been established, there appears to be an increased statistical risk of breast cancer, warranting a long-term surveillance of patients diagnosed with non-puerperal mastitis.

Nonpuerperal breast abscesses have a higher rate of recurrence compared to puerperal breast abscesses. There is a high statistical correlation of nonpuerperal breast abscess with diabetes mellitus (DM). On this basis, it has recently been suggested that diabetes screening should be performed on patients with such abscess.

The exact cause of IOI is unknown, but infectious and immune-mediated mechanisms have been proposed. Several studies have described cases where onset of orbital pseudotumor was seen simultaneously or several weeks after upper respiratory infections. Another study by Wirostko et al. proposes that organisms resembling Mollicutes cause orbital inflammation by destroying the cytoplasmic organelles of parasitized cells.

Orbital pseudotumor has also been observed in association with Crohn’s disease, systemic lupus erythematosus, rheumatoid arthritis, diabetes mellitus, myasthenia gravis, and ankylosing spondylitis all of which strengthen the basis of IOI being an immune-mediated disease. Response to corticosteroid treatment and immunosuppressive agents also support this idea.

Trauma has also been seen to precede some cases of orbital pseudotumor. However, one study by Mottow-Lippe, Jakobiec, and Smith suggests that the release of circulating antigens caused by local vascular permeability triggers an inflammatory cascade in the affected tissues.

Although these mechanisms have been postulated as possible causes of IOI, their exact nature and relationships to the condition still remain unclear.

IOI or orbital pseudotumor is the second most common cause of exophthalmos following Grave’s orbitopathy and the third most common orbital disorder following thyroid orbitopathy and lymphoproliferative disease accounting for 5–17.6% of orbital disorders, There is no age, sex, or race predilection, but it is most frequently seen in middle-aged individuals. Pediatric cases account for about 17% of all cases of IOI.

Adenitis is a general term for an inflammation of a gland. Often it is used to refer to lymphadenitis which is the inflammation of a lymph node.

The term nonpuerperal mastitis describes inflammatory lesions of the breast (mastitis) that occur unrelated to pregnancy and breastfeeding.

It is sometimes equated with duct ectasia, but other forms can be described.

There are roughly 12–13 cases annually per 10,000 population in women receiving outpatient treatment and 3–4 cases requiring admission. In men, 2–3 cases per 10,000 are treated as outpatients and 1– cases/10,000 require admission. Young women are most often affected, probably reflecting sexual activity in that age group. Infants and the elderly are also at increased risk, reflecting anatomical changes and hormonal status. Xanthogranulomatous pyelonephritis is most common in middle-aged women. It can present somewhat differently in children, in whom it may be mistaken for Wilms' tumor.

As of 2011 five cases had been reported, involving rib, tibial epiphysis, ulna, distal tibia and femur. Young individuals are prevalently affected but one case involved a 50-year-old woman. Pain, swelling of possibly long duration, fever and increased ESR are some of the main clinical findings. X-ray examination shows lytic foci with sclerotic margins. A neoplastic process can be suspected.

Cholecystitis occurs when the gallbladder becomes inflamed. Gallstones are the most common cause of gallbladder inflammation but it can also occur due to blockage from a tumor or scarring of the bile duct. The greatest risk factor for cholecystitis is gallstones. Risk factors for gallstones include female sex, increasing age, pregnancy, oral contraceptives, obesity, diabetes mellitus, ethnicity (Native North American), rapid weight loss.

Cholecystitis accounts for 3–10% of cases of abdominal pain worldwide. Cholecystitis caused an estimated 651,829 emergency department visits and 389,180 hospital admissions in the US in 2012. The 2012 US mortality rate was 0.7 per 100,000 people. The frequency of cholecysitis is highest in people age 50–69 years old.

"Lymph adenitis" or "lymph node adenitis" is caused by infection in lymph nodes. The infected lymph nodes typically become enlarged, warm and tender. A swelling of lymph nodes due to growth of lymph cells is called lymphadenopathy. Types include:

- Neck

- Cervical adenitis is an inflammation of a lymph node in the neck.

- Tuberculous adenitis (scrofula) is a tuberculous infection of the skin of the neck caused by "Mycobacterium tuberculosis". Non-tuberculous adenitis can also be caused by "Mycobacterium scrofulaceum" or "Mycobacterium avium".

- Abdomen

- Mesenteric adenitis is an inflammation of the mesenteric lymph nodes in the abdomen. It can be caused by the bacterium "Yersinia enterocolitica". If it occurs in the right lower quadrant, it can be mistaken for acute appendicitis, often preceded by a sore throat.

Oophoritis is an inflammation of the ovaries.

It is often seen in combination with salpingitis (inflammation of the fallopian tubes). It may develop in response to infection.

DPB is idiopathic, which means an exact physiological, environmental, or pathogenic cause of the disease is unknown. However, several factors are suspected to be involved with its pathogenesis (the way in which the disease works).

The major histocompatibility complex (MHC) is a large genomic region found in most vertebrates that is associated with the immune system. It is located on chromosome 6 in humans. A subset of MHC in humans is human leukocyte antigen (HLA), which controls the antigen-presenting system, as part of adaptive immunity against pathogens such as bacteria and viruses. When human cells are infected by a pathogen, some of them can present parts of the pathogen's proteins on their surfaces; this is called "antigen presentation". The infected cells then become targets for types of cytotoxic T-cells, which kill the infected cells so they can be removed from the body.

Genetic predisposition for DPB susceptibility has been localized to two HLA haplotypes (a nucleotide or gene sequence difference between paired chromosomes, that is more likely to occur among a common ethnicity or trait) common to people of East Asian descent. HLA-B54 is associated with DPB in the Japanese, while HLA-A11 is associated with the disease in Koreans. Several genes within this region of class I HLA are believed to be responsible for DPB, by allowing increased susceptibility to the disease. The common genetic background and similarities in the HLA profile of affected Japanese and Korean individuals were considered in the search for a DPB gene. It was suggested that a mutation of a suspected disease-susceptibility gene located somewhere between HLA-B and HLA-A had occurred on an ancestral chromosome carrying both HLA-B54 and HLA-A11. Further, it is possible that a number of genetic recombination events around the disease locus (location on a chromosome) could have resulted in the disease being associated with HLA-B54 in the Japanese and HLA-A11 in Koreans. After further study, it was concluded that a DPB susceptibility gene is located near the HLA-B locus at chromosome 6p21.3. Within this area, the search for a genetic cause of the disease has continued.

Because many genes belonging to HLA remain unidentified, positional cloning (a method used to identify a specific gene, when only its location on a chromosome is known) has been used to determine that a mucin-like gene is associated with DPB. In addition, diseases caused by identified HLA genes in the DPB-susceptibility region have been investigated. One of these, bare lymphocyte syndrome I (BLS I), exhibits a number of similarities with DPB in those affected, including chronic sinusitis, bronchiolar inflammation and nodules, and the presence of "H. influenzae". Also like DPB, BLS I responds favorably to erythromycin therapy by showing a resolution of symptoms. The similarities between these two diseases, the corresponding success with the same mode of treatment, and the fact that the gene responsible for BLS I is located within the DPB-causing area of HLA narrows the establishment of a gene responsible for DPB. Environmental factors such as inhaling toxic fumes and cigarette smoking are not believed to play a role in DPB, and unknown environmental and other non-genetic causes—such as unidentified bacteria or viruses—have not been ruled out.

Cystic fibrosis (CF), a progressive multi-system lung disease, has been considered in the search for a genetic cause of DPB. This is for a number of reasons. CF, like DPB, causes severe lung inflammation, abundant mucus production, infection, and shows a genetic predominance among Caucasians of one geographic group to the rarity of others; whereas DPB dominates among East Asians, CF mainly affects individuals of European descent. While no gene has been implicated as the cause of DPB, mutation in a specific gene—much more likely to occur in Europeans—causes CF. This mutation in the CF-causing gene is not a factor in DPB, but a unique polymorphism (variation) in this gene is known to occur in many Asians not necessarily affected by either disease. It is being investigated whether this gene in any state of mutation could contribute to DPB.

Most cases of "community-acquired" pyelonephritis are due to bowel organisms that enter the urinary tract. Common organisms are "E. coli" (70–80%) and "Enterococcus faecalis". Hospital-acquired infections may be due to coliform bacteria and enterococci, as well as other organisms uncommon in the community (e.g., "Pseudomonas aeruginosa" and various species of "Klebsiella"). Most cases of pyelonephritis start off as lower urinary tract infections, mainly cystitis and prostatitis. "E. coli" can invade the superficial umbrella cells of the bladder to form intracellular bacterial communities (IBCs), which can mature into biofilms. These biofilm-producing "E. coli" are resistant to antibiotic therapy and immune system responses, and present a possible explanation for recurrent urinary tract infections, including pyelonephritis. Risk is increased in the following situations:

- Mechanical: any structural abnormalities in the urinary tract, vesicoureteral reflux (urine from the bladder flowing back into the ureter), kidney stones, urinary tract catheterization, ureteral stents or drainage procedures (e.g., nephrostomy), pregnancy, neurogenic bladder (e.g., due to spinal cord damage, spina bifida or multiple sclerosis) and prostate disease (e.g., benign prostatic hyperplasia) in men

- Constitutional: diabetes mellitus, immunocompromised states

- Behavioral: change in sexual partner within the last year, spermicide use

- Positive family history (close family members with frequent urinary tract infections)

Parametritis is an inflammation of the parametrium (connective tissue adjacent to the uterus).

It is considered a form of pelvic inflammatory disease.

Parametritis is inflammation of the ligaments around the uterus. Parametritis is different from perimetritis which is inflammation of the serosa surrounding the uterus.