The characteristic symptom of Degos disease is the development of papules. Initially, individuals may have skin lesions or rashes, but they will proceed to develop distinct bumps, or papules. Papules are circular in shape, have a porcelain-white center and red border. As papules age, the white centers will skin in and only the border will remain raised. Typically, papules range from 0.5 to 1 cm in width. Papules appear on the trunk and upper extremities and are not found on the individual's palms, soles, scalp, or face.

Depending on whether an individual has the benign variant or malignant variant of the disease symptoms will vary. Both the benign and malignant forms have development of the characteristic papules. Individuals with the benign form will have the typical papules persisting anywhere from a few years to throughout their whole lives. In the benign form, no inner organs are affected. If an individual develops the malignant form, it means that not only are the papules present, but inner organs are involved. Most malignant cases involve problems of the gastrointestinal tract leading to small intestine lesions, abdominal pain, diarrhea, and bowel perforation. If the central nervous system is involved, symptoms can include headaches, dizziness, seizures, paralysis of cranial nerves, weakness, stroke, damage to small areas of the brain due to artery blockage (cerebral infarcts, and cerebral hemorrhage). Additional organs commonly impacted include the heart, lungs, and kidneys. Symptoms that may develop from damage to these organs include double vision (diploplia), clouding of lenses of eyes, swelling of the optic disc (papilledema), partial loss of vision, shortness of breath, chest pain, epilepsy,and thickening of pericardium.

Someone with the benign form may suddenly develop symptoms of the malignant form. Symptoms can last anywhere from a few weeks to several years. Onset of symptoms typically begins to manifest between the ages of 20-50. A few cases of this condition in newborns have also been described.

Degos disease, also known as Köhlmeier-Degos disease or malignant atrophic papulosis (MAP), is an extremely rare condition caused by blockage of arteries and veins. Individuals with this condition will develop papules. Those diagnosed with this disease may also develop complications due to impairment of internal organs. The exact underlying mechanism is still unknown, and an effective treatment is still being developed. There are fewer than 50 living patients presently known worldwide, and fewer than 200 reported in medical literature. However, it is important to note that many individuals may go undiagnosed due to rarity of the disease. Most individuals develop symptoms between the ages of 20-50; however, cases outside of this age range have been reported as well.

Kyrle disease symptoms are chronic and have an onset during adulthood between the ages of 30 and 50 years of age. However, there were reported cases of early onset as early as 5 years of age and late onset as late as 75 years of age. The main symptom is the development of small papules into painless lesions that are surrounded by silvery scales. The lesions are painless, however, there is a chance that the patient may experience extreme urges to itch them. In time, these lesions grow up to a radius of 0.75 inch and develop into red-brown nodules with a central plug of keratin. As more lesions develop, they can come together and form larger keratotic plaques. These lesions are usually observed on the lower extremities, however, can also develop on the upper extremities, such as, the arms, the head and the neck. The only parts of the body that Kyrle disease do not form are the palms, soles, and mucous membranes. Lesions may heal spontaneously without treatment, however, new ones will develop in its place.

Other symptoms that may be observed:

- Hyperkeratotic cone-shaped papular plugs

- Hyperkeratotic verrucous plaques

- Diabetes mellitus

- Hepatic insufficiency

- Presence of albumin in the urine

- Excess sugar in the urine

Kyrle disease or hyperkeratosis follicularis et parafollicularis in cutem penetrans is identified as a form of an acquired perforating disease. Other major perforating diseases are elastosis perforans serpiginosa and reactive perforating collagenosis. Recently, however, there is a controversy on categorizing Kyrle disease with perforating dermatosis or a subtype of acquired perforating collagenosis.

Kyrle disease was first described by Josef Kyrle in 1916 when a diabetic woman presented generalized hyperkeratotic nodules. The disease is distinguished by large papules with central keratin plus on the skin, usually on the legs of the patient and is often in conjunction with hepatic, renal or diabetic disorders. It can affect both females and males with a 6:1 ratio. The papules usually show up on the patient with an average age of 30 years. Kyrle disease is a rare disease unless there is a high count of patients with chronic renal failure. The disease seems to be more prevalent in African Americans, which can be correlated to the high incidence of diabetes mellitus and renal failure in the population.

Although the dermatological changes are the most obvious symptoms of Urbach–Wiethe disease, many patients also have neurological symptoms. About 50–75% of the diagnosed cases of Urbach–Wiethe disease also show bilateral symmetrical calcifications on the medial temporal lobes. These calcifications often affect the amygdala and the periamygdaloid gyri. The amygdala is thought to be involved in processing biologically relevant stimuli and in emotional long term memory, particularly those associated with fear, and both PET and MRI scans have shown a correlation between amygdala activation and episodic memory for strongly emotional stimuli. Therefore, Urbach–Wiethe disease patients with calcifications and lesions in these regions may suffer impairments in these systems. These calcifications are the result of a buildup of calcium deposits in the blood vessels within this brain region. Over time, these vessels harden and the tissue they are a part of dies, causing lesions. The amount of calcification is often related to disease duration. The true prevalence of these calcifications is difficult to accurately state as not all patients undergo brain imaging. Some patients also exhibit epilepsy and neuropsychiatric abnormalities. Epilepsy symptoms could begin with light anxiety attacks and it can be controlled with "Epilum" (Epilepsy Medicine) Other patients present with symptoms similar to schizophrenia while some suffer from mood, anxiety, and psychotic disorders.

Although symptoms can vary greatly between affected individuals, even those within the same family, symptoms normally begin in infancy and are typically a result of thickening skin and mucous membranes. The first symptom is often a weak cry or a hoarse voice due to a thickening of the vocal cords. The hoarse voice can be one of the most striking clinical manifestations of the disease. Lesions and scars also appear on the skin, usually the face and the distal parts of the limbs. This is often the result of poor wound healing and the scarring continues to increase as the patient ages, leaving the skin with a waxy appearance. Skin may be easily damaged as a result of only a minor trauma or injury, leaving many blisters and additional scars. The skin is also usually very dry and wrinkly. White or yellow infiltrates form on the lips, buccal mucosa, tonsils, uvula, epiglottis and frenulum of the tongue. This can lead to upper respiratory tract infection and sometimes requires tracheostomy to relieve the symptom. Too much thickening of the frenulum can restrict tongue movement and may result in speech impediments. Beading of the papules around the eyelids is a very common symptom and is often used as part of a diagnosis of the disease. Some other dermatological symptoms that are sometimes seen but less common include hair loss, parotitis and other dental abnormalities, corneal ulceration, and focal degeneration of the macula.

The most common presentation of Milroy Disease is bilateral lower extremity lymphedema, and may also be accompanied by hydrocele.

Vulvar Paget disease presents as a variety of clinical lesions that may occur over a protracted course. Initially it is velvety, soft, and red or bright pink with scattered white islands of hyperkeratosis. (a strawberry and cream appearance) The lesions become erythematous, plaque like, and desquamating especially when located in dry areas. Rarely the appearance is ulcerated. The borders appear irregular, slightly elevated, and sharply demarcated. The visible borders of vulvar Paget disease are often misleading as Paget cells may spread along the basal layers of normal appearing skin with multicentric foci. Involvement may be extensive including the perianal region, genitocrural, and inguinal folds. Clinical examination should determine the presence of periurethral and perianal lesions. In these cases an involvement of the skin by a noncutaneous internal neoplasm may occur.

Symptoms are not specific; most patients report itching, burning, and soreness. A small subset of patients may be asymptomatic. Presence of vulvar pain, bleeding, and tumor formation are reported to be more common in patients affected by invasive disease.Signs and symptoms are skin lesions, often mistaken as eczema, that may be itchy or painful.

Galli–Galli disease is a rare inherited condition that has close resemblance clinically to Dowling-Degos' disease, but is histologically distinct, characterized by skin lesions that are 1- to 2-mm slightly keratotic red to dark brown papules which are focally confluent in a reticulate pattern. The disease is also characterized by slowly progressive and disfiguring reticulate hyperpigmentation of the flexures, clinically and histopathologically diagnostic for Dowling-Degos disease but also associated with suprabasal, nondyskeratotic acantholysis.

Milroy's disease (MD) is a familial disease characterized by lymphedema, commonly in the legs, caused by congenital abnormalities in the lymphatic system. Disruption of the normal drainage of lymph leads to fluid accumulation and hypertrophy of soft tissues. It is also known as Milroy disease, Nonne-Milroy-Meige syndrome and hereditary lymphedema.

It was named by Sir William Osler for William Milroy, a Canadian physician, who described a case in 1892, though it was first described by Rudolf Virchow in 1863.

Grover's disease often starts quite suddenly. There are intensely itchy spots on the central back, mid chest and occasionally elsewhere. Frequently, it follows sweating or some unexpected heat stress.

The itchy eruption lasts an average of 10–12 months. It is characterized by papules and papulovesicles with excoriations occurring on the chest, back, lower sternum, arms, and thighs. The papules are most commonly found on the mid chest.

Sometimes the features of Grover's are found in people who do not itch or have a conspicuous rash. Most of the people with Grover's who visit a dermatologist, however, itch a lot.

The histiocytosis of Rosai–Dorfman disease can occur in lymph nodes, causing lymphadenopathy, or can occur outside lymph nodes in extranodal disease.

Arthralgia is seen in up to half of people, and is usually a non-erosive poly or oligoarthritis primarily of the large joints of the lower extremities.

Kidney complications are a common and serious effect of the disease; kidney insufficiency and kidney failure may worsen throughout life. The presence of protein in the urine (which causes foamy urine) is often the first sign of kidney involvement. End-stage kidney failure in those with Fabry disease typically occurs in the third decade of life, and is a common cause of death due to the disease.

Lung involvement is typically in the form of hemoptysis, pleuritis, cough, or fever, and in severe cases can be life-threatening if the outlet pulmonary artery develops an aneurysm which ruptures causing severe vascular collapse and death from bleeding in the lungs. Nodules, consolidations, cavities and ground glass lesions are common in patients with pulmonary involvement. Pulmonary artery thrombosis may occur.

Angiokeratomas (tiny, painless papules that can appear on any region of the body, but are predominant on the thighs, around the belly button, buttocks, lower abdomen, and groin) are common.

Anhidrosis (lack of sweating) is a common symptom, and less commonly hyperhidrosis (excessive sweating).

Additionally, patients can exhibit Raynaud's disease-like symptoms with neuropathy (in particular, burning extremity pain).

Ocular involvement may be present showing cornea verticillata (also known as vortex keratopathy), i.e. clouding of the corneas. Keratopathy may be the presenting feature in asymptomatic patients, and must be differentiated from other causes of vortex keratopathy (e.g. drug deposition in the cornea). This clouding does not affect vision.

Other ocular findings can include conjunctival and retinal vascular abnormalities and anterior/posterior spoke-like cataract. Visual reduction from these manifestations is uncommon.

VHL disease can be subdivided according to the clinical manifestations, although these groups often correlate with certain types of mutations present in the VHL gene.

Vascular disease is a class of diseases of the blood vessels – the arteries and veins of the circulatory system of the body. It is a subgroup of cardiovascular disease. Disorders in this vast network of blood vessels, can cause a range of health problems which can be severe or prove fatal.

Rosai–Dorfman disease, originally known as sinus histiocytosis with massive lymphadenopathy, is a rare disorder of unknown cause that is characterized by abundant histiocytes in the lymph nodes or other locations throughout the body.

Signs and symptoms associated with VHL disease include headaches, problems with balance and walking, dizziness, weakness of the limbs, vision problems, and high blood pressure. Conditions associated with VHL disease include angiomatosis, hemangioblastomas, pheochromocytoma, renal cell carcinoma, pancreatic cysts (pancreatic serous cystadenoma), endolymphatic sac tumor, and bilateral papillary cystadenomas of the epididymis (men) or broad ligament of the uterus (women). Angiomatosis occurs in 37.2% of patients presenting with VHL disease and usually occurs in the retina. As a result, loss of vision is very common. However, other organs can be affected: strokes, heart attacks, and cardiovascular disease are common additional symptoms. Approximately 40% of VHL disease presents with CNS hemangioblastomas and they are present in around 60-80%. Spinal hemangioblastomas are found in 13-59% of VHL disease and are specific because 80% are found in VHL disease. Although all of these tumours are common in VHL disease, around half of cases present with only one tumour type.

Grover's disease (GD) is a polymorphic, pruritic, papulovesicular dermatosis characterized histologically by acantholysis with or without dyskeratosis. Once confirmed, most cases of Grover's disease last six to twelve months, which is why it was originally called "transient". However it may last much longer. Nevertheless, it is not to be confused with relapsing linear acantholytic dermatosis.

Clear cell acanthoma (also known as "Acanthome cellules claires of Degos and Civatte," "Degos acanthoma," and "Pale cell acanthoma") is a benign clinical and histological lesion initially described as neoplastic, which some authors now regard as a reactive dermatosis. It usually presents as a moist solitary firm, brown-red, well-circumscribed, 5 mm to 2 cm nodule or plaque on the lower extremities of middle-aged to elderly individuals The lesion has a crusted, scaly peripheral collarette and vascular puncta on the surface. It is characterized by slow growth, and may persist for years. The clinical differential diagnosis includes: dermatofibroma, inflamed seborrheic keratosis, pyogenic granuloma, basal cell carcinoma, squamous cell carcinoma, verruca vulgaris, psoriatic plaque, and melanoma.

Four cardinal symptoms have sometimes been used as diagnostic criteria:

1. painful, fatty lipomas (benign fatty tumors) across anatomy

2. obesity, frequently in menopausal age

3. weakness and fatigue

4. emotional instability, depression, epilepsy, confusion, and dementia.

There are also potential signs of the disease which are identified as the following:

However, as it is unclear which symptoms are cardinal and which symptoms are minor signs in Dercum's disease, it is unclear which should be used as diagnostic criteria. Researchers have proposed a 'minimal definition' based on symptoms most often part of Dercum's disease: 1) Generalized overweight or obesity. 2) Chronic pain in the adipose tissue. The associated symptoms in Dercum's disease include obesity, fatty deposits, easy bruisability, sleep disturbances, impaired memory, depression, difficulty concentrating, anxiety, rapid heartbeat, shortness of breath, diabetes, bloating, constipation, fatigue, weakness and joint and muscle aches. Regarding the associated symptoms in Dercum's disease, only case reports have been published. No study involving medical examinations has been performed in a large group of patients.

There are several types of vascular disease, (which is a subgroup of cardiovascular disease), the signs and symptoms depend on which type, among them are:

- Erythromelalgia - a rare peripheral vascular disease where syndromes includes burning pain, increased temperature, erythema and swelling, of mainly the hands and feet are affected.

- Peripheral artery disease – happens when atheromatous plaques build up in the arteries that supply blood to the arms and legs, plaque causes the arteries to narrow or become blocked.

- Renal artery stenosis - is the narrowing of renal arteries that carry blood to the kidneys from the aorta.

- Buerger's disease – is due to small blood vessels that inflame and swell, vessels then narrow or are blocked by blood clots.

- Raynaud's disease – a rare peripheral vascular disorder of constriction of the peripheral blood vessels, in the fingers and toes when the person is cold.

- Disseminated intravascular coagulation – a widespread activation of clotting in the smaller blood vessels.

- Cerebrovascular disease–a group of vascular diseases that affect brain function.