Inflammation of subcutaneous fat

With panniculitis, inflammation of the subcutaneous fat is observed. It is localized in fatty lobules or interlobular septa and leads to their necrosis and overgrowth with connective tissue. This dermatological disease has a progressive course and leads to the formation of nodes, infiltrates or plaques. And with its visceral form, the fatty tissues of internal tissues and organs are damaged: the pancreas, kidneys, liver, retroperitoneal space and omentum.

In this article, we will acquaint you with the alleged causes, varieties, main manifestations, methods for diagnosing and treating panniculitis. This information will help you make a timely decision about the need for treatment by a specialist, and you will be able to ask him questions that interest you.

Panniculitis is accompanied by increased peroxidation of fats. In half of the cases, an idiopathic form of the disease is observed (or Weber-Christian panniculitis, primary panniculitis) and more often it is detected in women 20-40 years old (usually overweight). In other cases, the disease is secondary and develops against the background of various provoking factors or diseases - immunological disorders, dermatological and systemic ailments, taking certain medications, exposure to cold, etc.

The reasons

This disease was first described in 1925 by Weber, but references to its symptoms are also found in descriptions dated 1892. Despite the development of modern medicine and a large number of studies on the study of panniculitis, scientists have not been able to get an accurate idea of ​​​​the mechanisms of development of this disease.

It is known that the disease is provoked by various bacteria (usually streptococci and staphylococci), which penetrate into the subcutaneous fat through various microtraumas and damage to the skin. In most cases, tissue damage occurs in the leg area, but it can also occur in other parts of the body.

Predisposing factors to its development can be various diseases and conditions:

• skin diseases -, and, athlete's foot, etc .;
• injuries - any, even the most minor, injuries (insect bites, scratches, abrasions, wounds, burns, etc.) increase the risk of infection;
• lymphogenous edema - edematous tissues are prone to cracking, and this fact increases the chance of infection of the subcutaneous fat;
• diseases that cause a weakening of the immune system - cancerous tumors, etc .;
• previous panniculitis;
• intravenous drug use;
• obesity.

Classification

Panniculitis can be:

• primary (or idiopathic, Weber-Christian panniculitis);
• secondary.

Secondary panniculitis can occur in the following forms:

• cold - a local form of damage caused by strong cold exposure and manifested by the appearance of pink dense nodes (after 14-21 days they disappear);
• lupus panniculitis (or lupus) - observed in severe systemic lupus erythematosus and is manifested by a combination of manifestations of two diseases;
• steroid - observed in childhood, develops 1-2 weeks after ingestion of corticosteroid drugs, does not need special treatment and is cured on its own;
• artificial - caused by taking various medicines;
• enzymatic - observed in pancreatitis against the background of an increase in the level of pancreatic enzymes;
• immunological - often accompanies systemic vasculitis, and in children it can be observed with;
• proliferative-cellular - develops against the background of leukemia, histocytosis, lymphoma, etc.;
• eosinophilic - manifests itself as a non-specific reaction in some systemic or skin diseases (skin vasculitis, injection lipophatic granuloma, systemic lymphoma, insect bites, eosinophilic cellulitis);
• crystalline - caused by deposits in the tissues of calcifications and urates in renal failure, or after the administration of Meneridine, Pentazocine;
• associated with a deficiency of an α-protease inhibitor - observed in a hereditary disease that is accompanied by nephritis, hepatitis, hemorrhages and vasculitis.

According to the shape of the changes on the skin formed during panniculitis, the following options are distinguished:

• knotted;
• plaque;
• infiltrative;
• mixed.

The course of panniculitis can be:

• acute inflammatory;
• subacute;
• chronic (or recurrent).

Symptoms

The main manifestations of spontaneous panniculitis include the following symptoms:

• the appearance of nodes located at different depths under the skin;
• redness and swelling in the affected area;
• fever and a feeling of tension and pain in the affected area;
• red dots, rash or blisters on the skin.

More often lesions of the skin appear on the legs. In more rare cases, lesions appear on the arms, face, or torso.

In addition to lesions of the subcutaneous fat with panniculitis, patients often show signs of general malaise that occurs with acute infectious diseases:

• fever;
• weakness;
• discomfort and pain in muscles and joints, etc.

After the disappearance of the nodes on the skin, areas of atrophy are formed, which are rounded foci of sunken skin.

In the visceral form of the disease, all fat cells are affected. With such panniculitis, symptoms of hepatitis, nephritis and pancreatitis develop, and characteristic nodes form in the retroperitoneal space and on the omentum.

Knotty panniculitis

The disease is accompanied by the formation of nodes limited from healthy tissues ranging in size from a few millimeters to 10 or more centimeters (usually from 3-4 mm to 5 cm). The color of the skin above them can vary from bright pink to flesh.

Plaque panniculitis

The disease is accompanied by the fusion of nodes into a densely elastic conglomerate. The color above it can vary from bluish-purple to pink. Sometimes the lesion captures the entire surface of the lower leg, thigh or shoulder. With such a course, compression of the neurovascular bundles occurs, causing severe pain and severe swelling.

Infiltrative panniculitis

The disease is accompanied by the appearance of fluctuations observed with ordinary phlegmon or abscesses, in separate melted conglomerates and nodes. The color of the skin over such lesions can vary from purplish to bright red. After opening the infiltrate, a foamy or oily mass of yellow color is poured out. Ulceration appears in the area of ​​the focus, which suppurates for a long time and does not heal.

Mixed panniculitis

This variant of the disease is rarely observed. Its course is accompanied by the transition of the nodular variant to plaque, and then to infiltrative.

The course of panniculitis

In an acute course, the disease is accompanied by a pronounced deterioration in the general condition. Even against the background of treatment, the patient's health is constantly getting worse, and remissions are rare and do not last long. A year later, the disease leads to death.

The subacute form of panniculitis is accompanied by less severe symptoms, but is also difficult to treat. A more favorable course is observed with a recurrent episode of the disease. In such cases, exacerbations of panniculitis are less severe, usually not accompanied by a violation of general well-being and are replaced by long-term remissions.

The duration of panniculitis can range from 2-3 weeks to several years.

Possible Complications

Panniculitis can be complicated by the following diseases and conditions:

• phlegmon;
• abscess;
• skin necrosis;
• gangrene;
• bacteremia;
• lymphangitis;
• sepsis;
• (with damage to the face).

Diagnostics

To diagnose panniculitis, a dermatologist prescribes the following examinations to the patient;

• blood analysis;
• biochemical analysis;
• Reberg's test;
• blood tests for pancreatic enzymes and liver tests;
• Analysis of urine;
• blood culture for sterility;
• node biopsy;
• bacteriological examination of discharge from the nodes;
• immunological tests: antibodies to ds-DNA, antibodies to SS-A, ANF, complements C3 and C4, etc.;
• Ultrasound of internal organs (to identify nodes).

Diagnosis for panniculitis is aimed not only at its detection, but also at determining the causes of its development (i.e., background diseases). In the future, based on these data, the doctor will be able to draw up a more effective treatment plan.

Differential diagnosis is performed with the following diseases:

• lipoma;
• pathomymia;
• insulin lipodystrophy;
• oleogranuloma;
• skin calcification;
• deep lupus erythematosus;
• actinomycosis;
• sporotrichosis;
• necrosis of the subcutaneous fat of newborns;
• gouty nodes;
• Farber's disease;
• skin sarcoids Darier-Roussy;
• vascular hypodermatitis;
• eosinophilic fasciitis;
• other forms of panniculitis.

Treatment

Treatment of panniculitis should always be comprehensive. The tactics of therapy is always determined by its form and nature of the course.

Patients are prescribed the following drugs:

• vitamins C and E;
• antihistamines;
• broad-spectrum antibacterial drugs;
• hepatoprotectors.

In subacute or acute course, corticosteroids (Prednisolone, etc.) are included in the treatment plan. Initially, a high dosage is prescribed, and after 10-12 days it is gradually reduced. If the disease is severe, then the patient is prescribed cytostatics (Methotrexate, Prospidin, etc.).

With secondary panniculitis, the treatment of a disease that contributes to the development of the disease is mandatory.

Panniculitis (PN) are diseases of a heterogeneous nature, which are characterized by pathological changes in the subcutaneous fat (SAT). Often, these diseases also affect the musculoskeletal system.

What is the problem with diagnostics?

Mon are diverse in their clinical and morphological manifestations, there are a large number of forms of the disease, while there are currently no criteria that would lead to a common denominator for diagnosis. Patients with PN turn to different specialists precisely because of the polymorphism of clinical symptoms. Such situations lead to insufficiently rapid diagnosis, and in connection with this, treatment begins untimely.
Classification attempts

At present, there is no classification that would be the same for all countries of the world. Some authors offer their own vision and order Mon according to etiology and pathomorphological picture. Thus, septal (SPN) and lobular are now distinguished panniculitis(LPN), that is, an inflammatory process located in the connective tissue septa and in the lobules of adipose tissue, respectively. Both variants of the disease can be combined with the phenomena of vasculitis and proceed without it.

Erythema nodosum (UE)

UE is a typical representative of septal panniculitis. The immunoinflammatory process in this pathology is nonspecific. There are many reasons for its appearance:

Distinguish between primary and secondary UE. Primary is most often idiopathic. Clinical symptoms that occur with UE are characterized by the state of the immune system, the etiology of the disease, the localization of the pathological focus, and prevalence.

It is possible to diagnose UE only after a carefully collected anamnesis, patient complaints, on the basis of the clinic and research data, laboratory and instrumental.

Brief description of case study #1

The patient is 31 years old and has a history of chronic tonsillitis from the age of 15 and frequent antibiotics for it. In 2009, painful nodes were discovered after another exacerbation of tonsillitis. The knots were located on the left leg. Treatment with glucocorticosteroid hormone dexamethasone was carried out, after which a positive trend was observed. After 3 years, tonsillitis provoked the appearance of 2 more nodes on the legs. After two months of homeopathic therapy, the nodes regressed. At the end of the year, there was a recurrence of painful formations on the lower leg.

Upon admission, the general condition is satisfactory, the physique is normosthenic, the body temperature is normal. Other indicators of examination and laboratory tests were also not changed.

On palpation of the formations on the lower leg, pain is noted. Ultrasound of the node revealed an area of ​​some blurring with increased echogenicity and a high content of blood vessels.

The diagnosis made by the doctors sounded like stage 2-3 erythema nodosum and chronic tonsillitis. After treatment with benzylpenicillin, non-steroidal anti-inflammatory drugs, the introduction of a protective regimen and local treatment with sodium clobetasol and heparin ointments, the disease regressed after 21 days. There were no exacerbations of pathology during the year.
Of the causes of the disease in the first place with streptococcal infection 9a, the above case indicates the association of UE (septal panniculitis) with streptococcal infection, in particular, with tonsillitis) is sarcoidosis.

Case Brief #2

A 25-year-old patient was admitted to the hospital with complaints of painful nodules on the legs and arms, pain in many joints (ankle, wrist), swelling in them, fever up to 39C, excessive sweating.

She fell ill on December 7, 2013, when arthritis of the ankle joint appeared for the first time. After 2 days, nodes appeared on the legs, which were sharply painful. A few days later, a large number of the same formations appeared with symptoms of general intoxication (fever, sweating).

After examination by the therapist, a diagnosis of probable reactive arthritis was made. Dexamethasone was used for treatment. The effect turned out to be positive. However, relapses continued.

According to laboratory data, inflammatory changes were determined in the blood. Chest CT showed enlarged lymph nodes and there were signs of chronic. On ultrasound of the node, its structure was lumpy, some areas were non-echoic and rich in vessels.

After consultation with a pulmonologist, sarcoidosis of the intrathoracic lymph nodes was exposed. The final diagnosis looked like Löfgren's syndrome, sarcoidosis of the lymph nodes of the chest at stage 1, secondary UE, polyarthritis, febrile syndrome.

The patient was treated with dexamethasone with cyclophosphamide parenterally. Then methylprednisolone was prescribed orally. Cyclophosphamide was also administered weekly, accompanied by a non-steroidal anti-inflammatory drug. The therapy led to a positive dynamics of the disease and at the moment the patient is under the supervision of doctors.

Differential diagnosis of UE

There are many diseases, the clinical picture of which is similar to the symptoms of UE, so it is necessary to conduct a thorough differential diagnosis. If differential diagnosis is carried out incorrectly or out of time, inadequate therapy is prescribed, which leads to a prolongation of the disease and the appearance of various complications and a deterioration in the quality of human life.

Example of a clinical case No. 3

A 36-year-old patient came to the hospital for medical help at the beginning of 2014 in connection with complaints of painful induration of her lower leg. The patient believes that the disease first appeared in 2012 after (SARS). Then there was a painful induration on the lower leg. The doctors diagnosed thrombophlebitis. He was treated with vascular drugs, physiotherapy was prescribed. The patient completed the treatment with positive dynamics. In April 2013, the painful induration reappeared. Laboratory studies were carried out, which did not reveal inflammatory changes. Ultrasound of the veins revealed insufficiency of the perforating veins of the leg. The patient was referred for a consultation at the NIIR them. V.A. Nasonova, where during the examination a seal was found on the lower leg. The data of laboratory and instrumental studies are within the normal range. On ultrasound of the internal organs, some diffuse changes in the pancreas and liver. On the ultrasound of the node, microvascularization, clumpy structure and thickening of the pancreas.
After all examinations and consultations, a diagnosis of lobular panniculitis, chronic course, lipodermatosclerosis. Varicose veins. Chronic venous insufficiency class IV.

Treated with hydroxychloroquine due to low disease activity. A month later, the dynamics of the disease is positive.

Discussion of specific cases

We have presented to your attention 3 different cases of differential diagnosis, which are currently very common.

In the first patient after streptococcal infection on the background of antibiotics and anti-inflammatory drugs, the disease regressed. Moreover, we note the color dynamics of formations on the skin: a pale red color at the beginning to a yellow-green color at the end of the disease, the so-called bruise flowering symptom.

For UE, this dynamics is very typical, and even in the later stages of the disease it can be determined. The nodules themselves disappear without a trace after 3-5 weeks. Skin atrophy and scarring are not observed.
Simultaneously with skin manifestations, articular syndrome also manifests. There are pains and swelling in the joints in half of the patients with UE. The most common lesion of the ankle joints. Regression of arthritis is observed within six months. Such patients do not develop heart disease, as in rheumatic fever, even though joint pain appears after a primary streptococcal infection.

If patients with UE have valvular pathology of the heart, it does not worsen. In this regard, we can say that UE is not a reflection of the activity of the rheumatic process.

UE and sarcoidosis

Against the background of sarcoidosis, UE has features of the course and manifestations:

• swelling of the legs, which often precedes UE;
• severe pain in the joints;
• there are a lot of elements of skin seals and they are extremely common, while each element is capable of merging with another similar node;
• localization of nodes mainly in the area of ​​​​the legs;
• the dimensions of the elements are large, more than 2 cm in diameter;
• in laboratory tests, there may be an increase in the titer of antibodies to antistreptolysin-O and to Yersinia;
• Respiratory tract involvement with symptoms such as shortness of breath, chest pain, cough.

UE (septal panniculitis), hilar lymphadenopathy, fever, and joint involvement suggest Löfgren's syndrome. Despite this, enlarged lymph nodes can be

Mesenteric is a very rare pathological condition in which chronic inflammation of the subcutaneous fatty tissue of the intestinal mesentery, omentum, preperitoneal and retroperitoneal space occurs. It is nonspecific, that is, it is impossible to identify the microorganism that would cause this inflammation.

basic information

Symptoms for this condition can vary, but the most common are abdominal pain of unknown origin, weight loss, fever, bowel dysfunction, and small masses that are palpable.

At the initial stage of the disease, some patients may have no symptoms at all. Computed tomography and magnetic tomography play an important role in the diagnosis.

The main symptoms will depend on which factor prevails the most - fatty, inflammatory or fibrotic. The use of surgical methods is often considered useless, so the main treatment is conservative, that is, the use of only drugs, physiotherapy and other methods.

The main problem is the differential diagnosis, because it is not so easy to identify mesenteric panniculitis. The symptoms of this pathology often resemble diseases of the stomach and intestines, therefore, it is often possible to make the correct diagnosis only after numerous diagnostic studies.

The reasons

Unfortunately, the cause of panniculitis remains unknown. It is still not clear why seals appear in the subcutaneous fat, which can be easily felt on palpation.

In addition to subcutaneous fat, internal organs are also affected - the liver, kidneys, pancreas, and intestines. There is an assumption that provoking factors can be considered:

1. Mycoses.
2. Dermatitis.
3. Eczema.
4. Shingles.
5. Injuries.
6. Lymphatic edema.
7. AIDS.
8. Leukemia.
9. Diabetes.
10. Oncology.
11. intravenous drug use.
12. Obesity.

How does it manifest

Symptoms of the disease do not always appear and they can be barely noticeable. Most often, pathology is diagnosed in men or in children. In women, panniculitis practically does not occur.

It is impossible to identify the disease only by existing complaints, since there are simply no specific manifestations, and the patient practically does not have complaints. Sometimes there may be fever or abdominal pain, which is not specific and can be diffused throughout the abdomen. It is not possible to specify the exact location of pain in the patient.

There may be nausea or vomiting, some malaise. Even with treatment in an acute course, the patient's condition does not improve. Most often, recovery occurs spontaneously, without medical intervention, but there is a high risk of relapse.

Complications

Even when contacting a medical institution, there is a huge risk of developing a variety of complications. It could be:

1. Phlegmon.
2. Abscess.
3. Skin necrosis.
4. Gangrene.
5. The appearance of bacteria in the blood.
6. Lymphangitis.
7. Sepsis.
8. , which is mainly observed when neoplasms appear in the face.

How to get rid

Treatment of mesenteric panniculitis is carried out only complex. It should be carried out by the surgeon together with the therapist. It is also necessary to find out the cause of the pathology, otherwise any therapy will be useless.

Patients with this diagnosis are assigned:

1. Vitamins, especially ascorbic acid and those that belong to group B.
2. Antihistamines.
3. Broad spectrum antibiotics.
4. Hepatoprotectors.

If the disease occurs with many symptoms and in an acute form, treatment with corticosteroids is mandatory, but only a doctor can prescribe it. High dosages are used only in the first week, and then they begin to be reduced. In severe cases, cytostatics can be used.

For a faster recovery, physiotherapy methods such as phonophoresis using hydrocortisone, ultrasound, UHF, ozocerite applications, magnetotherapy and laser therapy can be used.

Pinniculitis is a dangerous disease that requires mandatory medical intervention. But only a specialist can prescribe this or that medicine and draw up a treatment plan. With independent attempts to get rid of the disease, a variety of complications develop very quickly.

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The frequency of PN in different regions of the world varies widely and depends on the prevalence of a particular disease, which is the etiological factor of the pathology in question in this particular area.
There is currently no unified concept of the etiology and pathogenesis of PN. Infections (viral, bacterial), trauma, hormonal and immune disorders, medications, pancreatic diseases, malignant neoplasms, etc. can play a certain role in the development of PN. At the heart of the pathogenesis of PN are violations of the processes of lipid peroxidation. At the same time, highly active intermediate oxidation products accumulate in organs and tissues. The latter inhibit the activity of a number of enzymes and disrupt the permeability of cell membranes, leading to degeneration of cell structures and cytolysis. .
The term "panniculitis" was first proposed by J. Salin in 1911. However, somewhat earlier, in 1892, V. Pfeifer first described the "syndrome of focal dystrophy" of panniculitis with localization of nodes on the cheeks, mammary glands, upper and lower extremities, which was accompanied by progressive weakness. In 1894, M. Rotmann observed similar changes in the lower extremities and chest without damage to the internal organs. Later, similar formations of G. Hen-schen and A.I. Apricots were designated by the term "oleogranuloma". Later A.I. Abri-ko-sov developed a classification of oleogranulomas, which almost completely coincides with the Pn classifications that appeared later.
It should be noted that there is no single generally accepted classification of Mon today. A number of authors proposed to group Mon depending on the etiology and histomorphological picture. In particular, septal (SPn) and lobular (LPn) Pn are distinguished. In SPN, inflammatory changes are predominantly localized in the connective tissue septa (septa) between the fat lobules. LPN is characterized mainly by the defeat of the fat lobules themselves. Both types of PN can occur with or without vasculitis.
The main clinical sign of PN is, as a rule, multiple nodes with predominant localization on the lower and upper extremities, less often on the chest, abdomen, and hands. The nodes have different colors (from flesh to bluish-pink) and sizes (from 5-10 mm to 5-7 cm in diameter), sometimes merge with the formation of conglomerates and extensive plaques with uneven contours and a bumpy surface. Usually, the nodes resolve within a few weeks, leaving "saucer-shaped" retractions of the skin due to atrophy of the pancreas (Fig. 1), in which calcifications can be deposited. Sometimes the node is opened with the release of an oil-nis-to-foamy mass and the formation of poorly healing ulcers and atrophic scars.
These symptoms are more characteristic of LPN. With SPN, the process is usually limited (3-5 nodes).
Most of the messages are devoted to skin forms of Mon. Only in recent decades have there been works that describe changes in adipose tissue in the internal organs, morphologically similar to those in the pancreas. With a systemic variant of the disease, the fatty tissue of the retroperitoneal region and omentum (mesenteric panniculitis) is involved in the pathological process, hepatosplenomegaly, pancreatitis, nephropathy is detected, sometimes in the absence of skin symptoms. In some cases, the development of PN is preceded by fever (up to 41 ° C), weakness, nausea, vomiting, loss of appetite, polyarthralgia, arthritis and myalgia.
Changes in laboratory parameters in PN are nonspecific, reflecting the presence and severity of the inflammatory process. Therefore, they (with the exception of α 1 -antitrypsin, amylase and lipase) make it possible to judge only the activity of the disease, and not the nosological affiliation.
Of great importance for the verification of PN is the histomorphological picture, characterized by necrosis of adipocytes, infiltration of the pancreas by inflammatory cells, and fat-filled macrophages (“foam cells”).
Success in diagnosing PN, first of all, depends on a carefully collected anamnesis indicating information about previous diseases, medications taken, background pathology, as well as on an adequate assessment of clinical symptoms and identification of typical morphological changes. Perhaps an atypical course of the disease with mild skin symptoms and the absence of characteristic morphological features. In such cases, a definite diagnosis is established after several months and even years.
The classic representative of ES is erythema nodosum (UE) - a non-specific immune-inflammatory syndrome that occurs as a result of various causes (infections, sarcoidosis, autoimmune diseases, medication, inflammatory bowel disease, pregnancy, malignant neoplasms, etc.). UE is more common in women at any age. It manifests itself as a skin lesion in the form of sharply painful soft single (up to 5) erythematous nodes with a diameter of 1-5 cm, localized on the shins, in the area of ​​the knee and ankle joints (Fig. 2). Skin rashes may be accompanied by fever, chills, malaise, polyarthralgia and myalgia. Characteristic for UE is the color dynamics of skin lesions from pale red to yellow-green (“bruising bloom”), depending on the stage of the process. In UE, the nodules completely regress without ulceration, atrophy, or scarring.
Lipodermatosclerosis - degenerative-dystrophic changes in the pancreas that occur in middle-aged women against the background of chronic venous insufficiency. Manifested by seals on the skin of the lower third of the lower leg (s), more often in the area of ​​the medial malleolus, followed by induration, hyperpigmentation (Fig. 3) and atrophy of the pancreas. In the future, in the absence of treatment of venous pathology, the formation of trophic ulcers is possible.
Eosinophilic fasciitis (Schulman's syndrome) belongs to the scleroderma group of diseases. For example, in 1/3 of cases, there is a connection between its development and previous physical activity or injury. In contrast to systemic scleroderma, tissue induration begins in the forearms and/or lower legs with a possible spread to the proximal limbs and trunk. Fingers and face remain intact. Skin lesions of the "orange peel" type, flexion contractures, eosinophilia, hypergammaglobulinemia, and elevated ESR are characteristic. Carpal tunnel syndrome and aplastic anemia may develop. In a histomorphological study, the most pronounced changes are found in the subcutaneous and intermuscular fascia. Pathological signs in skeletal muscles and skin are weak or absent.
Eosinophilia-myalgia syndrome (EMS) is a disease that occurs with a primary lesion of the skin and hematopoietic system, as well as internal organs. At the turn of the 1980-90s. There were more than 1600 patients with SME in the USA. As it turned out, many cases of the disease were due to the use of L-tryptophan in connection with anxiety and depression. It is more common in women (up to 80%), characterized by an acute onset with the development of fever, weakness, intense myalgia of a generalized nature, unproductive cough and severe eosinophilia (more than 1000/mm3). Acute symptoms are quickly relieved by glucocorticoids. In the case of a chronic process, skin lesions are observed according to the type of indurative edema with hyperpigmentation. Proximal, less often generalized muscle weakness progresses, often in combination with convulsions and neuropathy. There is damage to the lungs with the development of respiratory failure in a restrictive type. Perhaps the simultaneous appearance of cardiac pathology (conduction disorders, myocarditis, endocarditis, dilated cardiomyopathy), eosinophilic gastroenteritis, hepatomegaly. In 20% of cases, arthritis is observed, in 35-52% - arthralgia, in some patients flexion contractures are formed with predominant fasciitis phenomena.
Superficial migratory thrombophlebitis (Fig. 4) is most often observed in patients with venous insufficiency. Superficial thrombophlebitis in combination with organ thrombosis occurs in Behcet's disease, as well as in paraneoplastic syndrome (Trousseau's syndrome), caused by cancer of the pancreas, stomach, lungs, prostate, intestines and bladder. The disease is characterized by numerous, often linearly arranged seals on the lower (rarely upper) limbs. The localization of seals is determined by the affected areas of the venous bed. Ulcer formation is not observed.
Cutaneous polyarteritis nodosa is a benign form of polyarteritis, characterized by a polymorphic rash and occurring, as a rule, without signs of systemic pathology. The disease is manifested by reticular or racemous livedo in combination with skin nodular and nodular infiltrates, mobile and painful on palpation. The skin above them is red or purple, less often the usual color. Infiltrates are up to several centimeters in diameter, persist for up to 2-3 weeks, do not tend to suppurate, but in their center the formation of hemorrhagic necrosis is possible. The predominant localization is the lower limbs (the area of ​​the calf muscles, feet, ankle joints) (Fig. 5). Most patients have general disorders (weakness, malaise, migraine headache, paroxysmal pain in the abdomen, sometimes fever), increased sensitivity of the legs to cooling, paresthesia in the feet. Histological examination of lesions reveals necrotizing angiitis in the deep vasculature of the skin.
The most prominent representative of LDL is idiopathic lobular panniculitis (ILPn) or Weber-Christian disease. The main clinical manifestations are soft, moderately painful nodes, reaching a diameter of ≥ 2 cm, located in the pancreas of the lower and upper extremities, less often in the buttocks, abdomen, chest and face. Depending on the shape of the node, ILPN is divided into nodular, plaque and infiltrative. With the nodular variant, the seals are isolated from each other, do not merge, and are clearly delimited from the surrounding tissue. Depending on the depth of occurrence, their color varies from the color of normal skin to bright pink, and the diameter ranges from a few millimeters to 5 cm or more. The plaque variety is the result of the fusion of individual nodes into a densely elastic, tuberous conglomerate, the skin color above it varies from pink to bluish-purple. Sometimes seals extend to the entire surface of the lower leg, thigh, shoulders, etc., which often leads to swelling and severe pain due to compression of the neurovascular bundles. The infiltrative form is characterized by the occurrence of fluctuations in the zone of individual nodes or conglomerates of bright red or purple color. The opening of the focus occurs with the release of a yellow oily mass and the formation of poorly healing ulcers (Fig. 6). Patients with this clinical form of SP are often diagnosed with an "abscess" or "phlegmon", although purulent contents are not obtained when the lesions are opened.
In some patients, a gradual occurrence of all of the above varieties (mixed form) is possible.
Rashes are often accompanied by fever, weakness, nausea, vomiting, severe myalgia, polyatralgia, and arthritis.
Cytophagic histiocytic Mon, as a rule, turns into systemic histiocytosis with pancytopenia, impaired liver function, and bleeding tendency. Characterized by the development of recurrent red skin nodules, hepatosplenomegaly, serous effusion, ecchymosis, lymphadenopathy, ulceration in the oral cavity. As the disease progresses, anemia, leukopenia, coagulation disorders (thrombocytopenia, hypofibrinogenemia, decreased levels of factor VIII, etc.) develop. Often ends in death.
Cold panniculitis often develops in children and adolescents, less often in adults, especially women. In the latter case, Mon occurs after hypothermia when riding horses, motorcycles, etc. Lesions appear on the thighs, buttocks, lower abdomen. The skin becomes edematous, cold to the touch, acquires a purple-cyanotic color. Subcutaneous nodes appear here, which exist for 2-3 weeks, regress without a trace or leave behind foci of superficial skin atrophy.
Oil granuloma (oleogranuloma) is a peculiar type of PN that occurs after injections into the pancreas of various substances (povidone, pentazocine, vitamin K, paraffin, silicone, synthetic microspheres) for therapeutic or cosmetic purposes. After a few months or years, dense nodes (plaques) form in the pancreas, usually soldered to the surrounding tissues, in rare cases ulcers form. Perhaps the extensive spread of lesions to other parts of the body, the appearance of arthralgia, Raynaud's phenomenon and signs of Sjögren's syndrome. Histological examination of biopsy specimens reveals the characteristic formation of multiple oil cysts of various sizes and shapes (Swiss cheese symptom).
Pancreatic PN develops with an inflammatory or tumor lesion of the pancreas due to an increase in the serum concentration of pancreatic enzymes (lipase, amylase) and, as a result, pancreatic necrosis. In this case, painful inflammatory nodes are formed, localized in the pancreas in various parts of the body. In general, the clinical picture resembles that of Weber-Christian disease (Fig. 7). Often develops polyarthritis and polyserositis. The diagnosis is established on the basis of histological data (foci of fat necrosis) and an increase in the level of pancreatic enzymes in the blood and urine.
Lupus-Mon ​​differs from most other varieties of Mon in the predominant localization of seals on the face and shoulders. The skin over the lesions is not changed or may be hyperemic, poikilodermic, or have signs of discoid lupus erythematosus. The nodes are clearly defined, from one to several centimeters in size, painless, hard, and can remain unchanged for several years (Fig. 8). With regression of the nodes, atrophy or scarring is sometimes observed. To verify the diagnosis, it is necessary to conduct a comprehensive immunological examination (determination of complement C3 and C4, antinuclear factor, antibodies to double-stranded DNA, cryoprecipitins, immunoglobulins, antibodies to cardiolipins).
Skin lesions in sarcoidosis are characterized by nodes, plaques, maculopapular changes, lupus pernio (lupus pernio), cicatricial sarcoidosis. Changes are painless symmetrical raised red lumps or nodes on the trunk, buttocks, limbs and face. Elevated, dense patches of skin, purplish-bluish on the periphery and paler, atrophic in the center, are never accompanied by pain or itching and do not ulcerate (Fig. 9). Plaques are usually one of the systemic manifestations of chronic sarcoidosis, are associated with splenomegaly, lung involvement, peripheral lymph nodes, arthritis, or arthralgia, persist for a long time and require treatment. A typical morphological sign of sarcoidosis occurring with skin lesions is the presence of an unchanged or atrophic epidermis with the presence of a “naked” (i.e., without an inflammatory zone) epithelioid cell granuloma, and a different number of giant cells of the Pirogov-Langhans type and the type of foreign bodies. There are no signs of caseosis in the center of the granuloma. These features make it possible to make a differential diagnosis of skin sarcoidosis with Mon and lupus erythematosus.
PN caused by a deficiency of α1-antitrypsin, which is an inhibitor of α-protease, occurs more often in patients homozygous for the defective PiZZ allele. The disease develops at any age. The nodes are localized on the trunk and proximal parts of the limbs, often open with the release of an oily mass and the formation of ulcers. Other skin lesions include vasculitis, angioedema, necrosis, and hemorrhage. Systemic manifestations associated with α1-antitrypsin deficiency include emphysema, hepatitis, cirrhosis, pancreatitis, and membranous proliferative nephritis.
Indurative tuberculosis, or Bazin's erythema, is localized mainly on the posterior surface of the legs (calf region). It often develops in young women suffering from one of the forms of organ tuberculosis. The formation of slowly developing, slightly painful (even on palpation) nodes of a bluish-red color (Fig. 10) that is not sharply delimited from the unchanged surrounding skin is characteristic. The latter often ulcerate over time, leaving behind foci of cicatricial atrophy. Histological examination reveals a typical tuberculoid infiltrate with foci of necrosis in the center.
In conclusion, it should be emphasized that the variety of forms and variants of the course of PN requires a thorough survey and a comprehensive clinical, laboratory and instrumental examination of the patient in order to verify the diagnosis. 3. Poorten M.C., Thiers B.H. panniculitis. Dermatol. Clin., 2002, 20 (3), 421-33
4. Verbenko E.V. Spontaneous panniculitis. In book. Skin and venereal diseases: a guide for doctors. Ed. Skripkina Yu.K. M., Medicine, 1995, vol. 2, 399-410.
5. Cascajo C, Borghi S, Weyers W. Panniculitis: definition of terms and diagnostic strategy. Am. J. Dermatol., 2000,22,530-49
6. Issa I, Baydoun H. Mesenteric panniculitis: various presentations and treatment regimens. World J Gastroenterol. 2009;15(30):3827-30.
7. Daghfous A, Bedioui H, Baraket O et al. Mesenteric panniculitis simulating malignancy. Tunis Med. 2010.3.1023-27.
8. Requena L, Yus E.S. Erythema nodosum. Dermatol.Clin. 2008.26(4),425-38.
9. Shen L.Y., Edmonson M.B., Williams G.P. et al. Lipoatrophic panniculitis: case report and review of the literature. Arch. Dermatol., 2010,146(8),77-81.
10. Guseva N.G. Systemic scleroderma. In: Rheumatology: National Guide. Ed. E.L. Nasonova, V.A. Nasonova. M., Geotar-Media, 2008: 447-466.
11. Nasonov E.L., Shtutman V.Z., Guseva N.G. Eosinophilia-myalgia syndrome in rheumatology. Wedge. honey. 1994; 2:17-24.
12. Goloeva R.G., Alekberova Z.S., Mach E.S. et al. Vascular manifestations of Behçet's disease. Scientific and practical rheumatology, 2010,2,51-7.
13. Thayalasekaran S, Liddicoat H, Wood E. Thrombophlebitis migrans in a man with pancreatic adenocarcinoma: a case report. Cases J. 2009 ;2:6610.
14. Morgan AJ, Schwartz RA. Cutaneous polyarteritis nodosa: a comprehensive review. Int J Dermatol. 2010;49(7):750-6.
15. Narvaez J, Bianchi MM, Santo P. et al. Pancreatitis, panniculitis, and polyarthritis. Semin Arthritis Rheum. 2010;39(5):417-23.
16. Chee C. Panniculitis in a patient presenting with a pancreatic tumor and polyarthritis: a case report. J Med Case Reports. 2009;3:7331.
17. Park HS, Choi JW, Kim BK, Cho KH. Lupus erythematosus panniculitis: clinicopathological, immunophenotypic, and molecular studies. Am J Dermatopathol. 2010; 32(1):24-30.
18. Sarcoidosis: Uch.-method. allowance. Ed. Vizel A.A., Amirov N.B. Kazan, 2010, 36-38.
19. Valverde R, Rosales B, Ortiz de Frutos FJ et al. Alpha-1-antitrypsin deficiency panniculitis. Dermatol Clin. 2008;26(4):447-51.
20. Daher Ede F, Silva Junior GB, Pinheiro HC, et al Erythema induratum of Bazin and renal tuberculosis: report of an association. Rev Inst Med Trop Sao Paulo. 2004;46(5):295-8.

Inflammation of the subcutaneous adipose tissue (SAT) is called panniculitis (translated from Latin, the ending "IT" means inflammation). At the moment, there is no single classification of panniculitis, but they are combined according to etiological indications and microscopic studies.

Types of inflammation of the subcutaneous adipose tissue

1. Panniculitis associated with changes in connective tissue partitions, directly between areas of subcutaneous adipose tissue, under the influence of an inflammatory process. This inflammation is called septal inflammation of the subcutaneous adipose tissue (from Latin septum, - septum).

2. Panniculitis associated with inflammatory changes in the subcutaneous tissue lobules. And in this case, it will be lobular panniculitis (from lat. Lobules - slice).

under the microscope

Microscopic examination in the subcutaneous adipose tissue can reveal increasing nodes, which in the future is not difficult to notice with the naked eye. Such nodes actively grow and reach sizes of 1 - 6 cm in diameter. They can be painless, and the manifestation of pain in the lesion is also possible. As a rule, such inflamed nodes in the pancreas are located mainly under the skin in various parts of the body (often have a symmetrical arrangement), in the mammary gland, lower leg, thigh, and the buttocks may also be affected.

Cause

The cause of this disease is a violation of metabolism, in particular, fat metabolism. In places where panniculitis appears, general signs of inflammation appear: redness, swelling, soreness (but not always), fever, directly at the site of inflammation (local hyperthermia).

Symptoms

The inflammatory process will also affect the general condition of the patient, i.e. signs of intoxication (feeling unwell, fever, loss of appetite, nausea and vomiting, muscle pain are possible). There may be cases of the appearance in one focus of several inflammatory nodes, while the formation of adhesions between them is possible. The resolution of such nodes occurs depending on the body's immune system, as well as the ability of subcutaneous adipose tissue and skin to regenerate (replacement of damaged areas with new tissue). Quite often, over many years, there are periods of exacerbation of the disease and remission (attenuation). You can do competent dressings at home as prescribed by a doctor to maintain regeneration processes. These can be ointments with solcoseryl or others recommended by the doctor for you.

Outcome and aftermath

Outcomes of panniculitis: in the first case, healing occurs within a few weeks without the formation of skin defects, in the second case, healing can take up to a year. In the latter case, retraction of the skin in the area of ​​​​inflammation and tissue atrophy can be observed. Another option for the outcome is to open the node, highlighting specific content. As a rule, processes of necrosis and ulcer formation are observed. Since not only the epidermis is damaged, but the dermis, in this case, a scar on the skin will necessarily form. The surgeon needs to carry out the correct primary surgical treatment and, if possible, apply a cosmetic suture in order to reduce the scar.

Risk of calcification

It is also impossible to exclude the case of deposition of calcium in the inflamed nodes, and in such cases it will be called calcification. This disease is dangerous primarily because nodes can form in various places, including in internal organs (for example, the fatty capsule of the kidney). This can adversely affect the function of a particular organ. With laboratory research methods, in the general blood test, there will be an increase in the ESR index, the indices of lymphocytes and leukocytes will be reduced.

For treatment, antibacterial (broad-spectrum antibiotics) and vitamin therapy, glucocorticoids, topical application of ointment to the affected areas are prescribed.