Porphyria cutanea tarda has a prevalence estimated at approximately 1 in 10,000. An estimated 80% of porphyria cutanea tarda cases are sporadic. The exact frequency is not clear because many people with the condition never experience symptoms and those that do are often misdiagnosed with anything ranging from idiopathic photodermatitis and seasonal allergies to hives.

While inherited deficiencies in uroporphyrinogen decarboxylase often lead to the development of PCT, there are a number of risk factors that can both cause and exacerbate the symptoms of this disease. One of the most common risk factors observed is infection with the Hepatitis C virus. One review of a collection of PCT studies noted Hepatitis C infection in 50% of documented cases of PCT. Additional risk factors include alcohol abuse, excess iron (from iron supplements as well as cooking on cast iron skillets), and exposure to chlorinated cyclic hydrocarbons and Agent Orange.

It can be a paraneoplastic phenomenon.

Acute porphyria can be triggered by a number of drugs, most of which are believed to trigger it by interacting with enzymes in the liver which are made with heme. Such drugs include:

- Sulfonamides, including sulfadiazine, sulfasalazine and trimethoprim/sulfamethoxazole.

- Sulfonylureas like glibenclamide, gliclazide and glimepiride, although glipizide is thought to be safe.

- Barbiturates including thiopental, phenobarbital, primidone, etc.

- Systemic treatment with antifungals including fluconazole, griseofulvin, ketoconazole and voriconazole. (Topical use of these agents is thought to be safe due to minimal systemic absorption.)

- Some anesthetics like ketamine and etomidate.

- Certain antibiotics like rifapentine, rifampicin, rifabutine, isoniazid, nitrofurantoin and, possibly, metronidazole.

- Ergot derivatives including dihydroergotamine, ergometrine, ergotamine, methysergide, etc.

- Certain antiretroviral medications (e.g. indinavir, nevirapine, ritonavir, saquinavir, etc.)

- Progesterones

- Some anticonvulsants including: carbamazepine, ethosuximide, phenytoin, topiramate, valproate.

- Some painkillers like dextropropoxyphene, ketorolac, metamizole, pentazocine

- Some cancer treatments like bexarotene, busulfan, chlorambucil, estramustine, etoposide, flutamide, idarubicin, ifosfamide, irinotecan, ixabepilone, letrozole, lomustine, megestrol, mitomycin, mitoxantrone, paclitaxel, procarbazine, tamoxifen, topotecan

- Some antidepressants like imipramine, phenelzine, trazodone

- Some antipsychotics like risperidone, ziprasidone

- Some retinoids used for skin conditions like acitretin and isotretinoin

- Miscellaneous others including: cocaine, methyldopa, fenfluramine, disulfiram, orphenadrine, pentoxifylline, sodium aurothiomalate, etc.

Some liver diseases may cause porphyria even in the absence of genetic predisposition. These include hemochromatosis and hepatitis C. Treatment of iron overload may be required.

Patients with the acute porphyrias (AIP, HCP, VP) are at increased risk over their life for hepatocellular carcinoma (primary liver cancer) and may require monitoring. Other typical risk factors for liver cancer need not be present.

Sun avoidance, avoidance of tanning booths, and usage of broad spectrum sunscreen that blocks both UVA and UVB.

Identification and avoidance of the offending drug.

Pseudoporphyria can be induced by a wide range of medications, excessive UV-A exposure, and hemodialysis. One frequently reported drug is naproxen. A frequent source of UV-A exposure is tanning booths.

As recognition of pseudoporphyria increases and the number of new medications expands, the list of etiologic agents associated with pseudoporphyria will most likely continue to grow. Agents associated with pseudoporphyria are as follows:

- Propionic acid derivatives (NSAIDs) - naproxen, diflunisal, ketoprofen, oxaprozin, mefenamic acid, rofecoxib

- Ketone NSAID-nabumetone

- Antibiotics - nalidixic acid, tetracycline, oxytetracycline, ampicillin-sulbactam, cefepime, fluoroquinolones (M Poh, personal communication, June 1999)

- Antifungals - voriconazole

- Diuretics - furosemide, chlorthalidone, butamide, triamterene/hydrochlorothiazide

- Antiarrhythmics - amiodarone

- Chemotherapy - 5-fluorouracil

- Immunosuppressants - cyclosporine

- Sulfones - dapsone

- Vitamins - brewers' yeast, pyridoxine

- Vitamin A derivatives - etretinate, isotretinoin

- Muscle relaxants - carisoprodol/aspirin

- Nonsteroidal antiandrogens - flutamide

- Other - hemodialysis, excessive UV-A, cola, oral contraceptive pills (levonorgestrel and ethinylestradiol), narrowband UV-B phototherapy (rarely)

Hereditary coproporphyria (HCP) is a disorder of heme biosynthesis, classified as an acute hepatic porphyria. HCP is caused by a deficiency of the enzyme coproporphyrinogen oxidase, coded for by the "CPOX" gene, and is inherited in an autosomal dominant fashion, although homozygous individuals have been identified. Unlike acute intermittent porphyria, individuals with HCP can present with cutaneous findings similar to those found in porphyria cutanea tarda in addition to the acute attacks of abdominal pain, vomiting and neurological dysfunction characteristic of acute porphyrias. Like other porphyrias, attacks of HCP can be induced by certain drugs, environmental stressors or diet changes. Biochemical and molecular testing can be used to narrow down the diagnosis of a porphyria and identify the specific genetic defect. Overall, porphyrias are rare diseases. The combined incidence for all forms of the disease has been estimated at 1:20,000. The exact incidence of HCP is difficult to determine, due to its reduced penetrance.

Hepatoerythropoietic porphyria is a very rare form of hepatic porphyria caused by a disorder in both genes which code Uroporphyrinogen III decarboxylase (UROD).

It has a similar presentation to porphyria cutanea tarda (PCT), but with earlier onset. In classifications which define PCT type 1 as "sporadic" and PCT type 2 as "familial", hepatoerythropoietic porphyria is more similar to type 2.

There is no cure for HCP caused by the deficient activity of coproporphyrinogen oxidase. Treatment of the acute symptoms of HCP is the same as for other acute porphyrias. Intravenous hemin (as heme arginate or hematin) is the recommended therapy for acute attacks. Acute attacks can be severe enough to cause death if not treated quickly and correctly. Hospitalization is typically required for administration of hemin, and appropriate drug selection is key to avoid exacerbating symptoms with drugs that interact poorly with porphyrias. Proper drug selection is most difficult when it comes to treatment of the seizures that can accompany HCP, as most anti-seizure medications can make the symptoms worse. Gabapentin and levetiracetam are two anti-seizure drugs that are thought to be safe.

In patients where management of symptoms is difficult even with hemin, liver transplant is an option before the symptoms have progressed to advanced paralysis. Combined liver and kidney transplants are sometimes undertaken in patients with renal failure.

Long term treatment of acute porphyrias is centered on the avoidance of acute attacks by eliminating precipitating factors, such as drugs, dietary changes, and infections. Females often have attacks coincident with their menstrual cycle, which can be managed effectively with hormonal birth control. Because of the reduced penetrance of HCP, family members of a patient may carry the same mutation without ever presenting with symptoms. Molecular analysis of "CPOX" is the best way to identify these patients, as they will not express a biochemical phenotype on laboratory testing unless they are symptomatic. Identification of asymptomatic patients allows them to adjust their lifestyle to avoid common triggering factors.

It is possible to acquire this disease later in life.

Causes include ingesting expired tetracyclines (where tetracycline changes to form epitetracycline and anhydrotetracycline which damage proximal tubule), and as a side effect of tenofovir in cases of pre-existing renal impairment. In the HIV population, Fanconi syndrome can develop secondary to the use of an antiretroviral regimen containing tenofovir and didanosine.

Lead poisoning also leads to Fanconi syndrome.

Multiple myeloma or monoclonal gammopathy of undetermined significance can also cause the condition.

Additionally, Fanconi Syndrome can develop as a secondary or tertiary effect of certain autoimmune disorders.

Cystinosis is the most common cause of Fanconi syndrome in children.

Other recognised causes are Wilson's disease (a genetically inherited condition of copper metabolism), Lowe syndrome, tyrosinemia (type I), galactosemia, glycogen storage diseases, and hereditary fructose intolerance.

Two forms, Dent's disease and Lowe syndrome, are X linked.

A recently described form of this disease is due to a mutation in the peroxisomal protein EHHADH. This mutation misdirects the EHHADH to the mitochondria. This interfers with respiratory complex I and with beta oxidation of fatty acids. The end result is a decrease in the ability of the mitochondria to produce ATP.

Tetter refers to any skin condition characterized by reddish vesicular eruptions and intense itching. Common diseases called tetter include:

- Eczema and Duhring's disease

- Herpes

- Porphyria cutanea tarda (PCT)

- Psoriasis

- Ringworm and jock itch

According to one hypothesis, "POIS is caused by Type-I and Type-IV allergy to the males' own semen". Specifically,

POIS could also be caused by an auto-immune reaction not to semen itself, but to another substance that is released during ejaculation, such as to cytokines.

The allergy hypothesis has been disputed. According to one study, "IgE-mediated semen allergy in men may not be the potential mechanism of POIS".

The cause of POIS is unknown. Some doctors hypothesize that POIS is caused by an auto-immune reaction. Other doctors suspect a hormone imbalance as the cause. While other causes have been proposed as well, none of the proposed causes seem to fully explain the disease.

Cognitive behavioral therapy is the mainstay of treatment. At other times counseling, anti-anxiety and antidepressant medications have been shown to be of use.

Erectile dysfunction from vascular disease is usually seen only amongst elderly individuals who have atherosclerosis. Vascular disease is common in individuals who have diabetes, peripheral vascular disease, hypertension and those who smoke. Any time blood flow to the penis is impaired, erectile dysfunction is the end result.

Hormone deficiency is a relatively rare cause of erectile dysfunction. In individuals with testicular failure like in Klinefelter syndrome, or those who have had radiation therapy, chemotherapy or childhood exposure to mumps virus, the testes may fail and not produce testosterone. Other hormonal causes of erectile failure include brain tumors, hyperthyroidism, hypothyroidism or disorders of the adrenal gland.

Structural abnormalities of the penis like Peyronie's disease can make sexual intercourse difficult. The disease is characterized by thick fibrous bands in the penis which leads to a deformed-looking penis.

Drugs are also a cause of erectile dysfunction. Individuals who take drugs to lower blood pressure, uses antipsychotics, antidepressants, sedatives, narcotics, antacids or alcohol can have problems with sexual function and loss of libido.

Priapism is a painful erection that occurs for several hours and occurs in the absence of sexual stimulation. This condition develops when blood gets trapped in the penis and is unable to drain out. If the condition is not promptly treated, it can lead to severe scarring and permanent loss of erectile function. The disorder occurs in young men and children. Individuals with sickle-cell disease and those who abuse certain medications can often develop this disorder.

Some doctors believe dhat syndrome to be either a culture-bound presentation of clinical depression, as a somatized set of symptoms, or a result of Western doctors' misinterpretation of patients' descriptions of their condition.

It is very common in Nepali culture as well. Most of them come with the complaints of "drops" and become extremely anxious about it and see it as loss of "male power". It is often related with obsessive ruminations and somatoform symptoms. Others see it as a distinct clinical entity which is less culture-bound than these critics assert, and describe it as one form of a syndrome of "semen-loss anxiety" which also occurs in other Eastern cultures as jiryan and shen-k'uei, as well as in Western cultures.

Chlamydia infection might also be related to it because of similar symptoms in case of infection of the urethra (urethritis), which is usually symptomatic, causing a white discharge from the penis with or without pain on urinating (dysuria).

The ischemic (ischaemic) cascade is a series of biochemical reactions that are initiated in the brain and other aerobic tissues after seconds to minutes of ischemia (inadequate blood supply). This is typically secondary to stroke, injury, or cardiac arrest due to heart attack. Most ischemic neurons that die do so due to the activation of chemicals produced during and after ischemia. The ischemic cascade usually goes on for two to three hours but can last for days, even after normal blood flow returns.

A cascade is a series of events in which one event triggers the next, in a linear fashion. Thus "ischemic cascade" is actually a misnomer, since the events are not always linear: in some cases they are circular, and sometimes one event can cause or be caused by multiple events. In addition, cells receiving different amounts of blood may go through different chemical processes. Despite these facts, the ischemic cascade can be generally characterized as follows:

1. Lack of oxygen causes the neuron's normal process for making ATP for energy to fail.

2. The cell switches to anaerobic metabolism, producing lactic acid.

3. ATP-reliant ion transport pumps fail, causing the cell to become depolarized, allowing ions, including calcium (Ca), to flow into the cell.

4. The ion pumps can no longer transport calcium out of the cell, and intracellular calcium levels get too high.

5. The presence of calcium triggers the release of the excitatory amino acid neurotransmitter glutamate.

6. Glutamate stimulates AMPA receptors and Ca-permeable NMDA receptors, which open to allow more calcium into cells.

7. Excess calcium entry overexcites cells and causes the generation of harmful chemicals like free radicals, reactive oxygen species and calcium-dependent enzymes such as calpain, endonucleases, ATPases, and phospholipases in a process called excitotoxicity. Calcium can also cause the release of more glutamate.

8. As the cell's membrane is broken down by phospholipases, it becomes more permeable, and more ions and harmful chemicals flow into the cell.

9. Mitochondria break down, releasing toxins and apoptotic factors into the cell.

10. The caspase-dependent apoptosis cascade is initiated, causing cells to "commit suicide."

11. If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around it. Toxins poison nearby neurons, and glutamate can overexcite them.

12. If and when the brain is reperfused, a number of factors lead to reperfusion injury.

13. An inflammatory response is mounted, and phagocytic cells engulf damaged but still viable tissue.

14. Harmful chemicals damage the blood–brain barrier.

15. Cerebral edema (swelling of the brain) occurs due to leakage of large molecules like albumins from blood vessels through the damaged blood brain barrier. These large molecules pull water into the brain tissue after them by osmosis. This "vasogenic edema" causes compression of and damage to brain tissue (Freye 2011; Acquired Mitochondropathy-A New Paradigm in Western Medicine Explaining Chronic Diseases).

Pelvic floor dysfunction can be an underlying cause of sexual dysfunction in both women and men, and is treatable by physical therapy.

The fact that the ischemic cascade involves a number of steps has led doctors to suspect that neuroprotectants such as calcium channel blockers or glutamate antagonists could be produced to interrupt the cascade at a single one of the steps, blocking the downstream effects. Though initial trials for such neuroprotective drugs led many to be hopeful, until recently, human clinical trials with neuroprotectants such as NMDA receptor antagonists were unsuccessful.

On October 7, 2003, a U.S. patent number 6630507 entitled "Cannabinoids as Antioxidants and Neuroprotectants" was awarded to the United States Department of Health and Human Services, based on research carried out at the National Institute of Mental Health (NIMH), and the National Institute of Neurological Disorders and Stroke (NINDS). This patent claims that cannabinoids are "useful in the treatment and prophylaxis of wide variety of oxidation associated diseases such as ischemia, inflammatory ... and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma..."

On November 17, 2011, in accordance with 35 U.S.C. 209(c)(1) and 37 CFR part 404.7(a)(1)(i), the National Institutes of Health, Department of Health and Human Services, published in the Federal Register, that it is contemplating the grant of an exclusive patent license to practice the invention embodied in U.S. Patent 6,630,507, entitled “Cannabinoids as antioxidants and neuroprotectants” and PCT Application Serial No. PCT/US99/08769 and foreign equivalents thereof, entitled “Cannabinoids as antioxidants and neuroprotectants” [HHS Ref. No. E-287-1997/2] to KannaLife Sciences Inc., which has offices in New York, U.S. This patent and its foreign counterparts have been assigned to the Government of the United States of America. The prospective exclusive license territory may be worldwide, and the field of use may be limited to: The development and sale of cannabinoid(s) and cannabidiol(s) based therapeutics as antioxidants and neuroprotectants for use and delivery in humans, for the treatment of hepatic encephalopathy, as claimed in the Licensed Patent Rights.

The exact cause of cyclothymia is unknown. It is known that major depression, bipolar disorder, and cyclothymia often occur together within families. There may be a genetic component to cyclothymia: In one study, it was found that an individual is 2–3 times more likely to have the disorder if an identical twin is affected.

It is also believed that a person suffering with PTSD may experience similar shifts in mood based on how many flashbacks they've been dealing with.

Cyclothymia (), also called cyclothymic disorder, is a type of chronic mood disorder widely considered to be a more chronic but milder or subthreshold form of bipolar disorder. Cyclothymia is characterized by numerous mood swings, with periods of hypomanic symptoms that do not meet criteria for a manic episode, alternating with periods of mild or moderate symptoms of depression that do not meet criteria for a major depressive episode.

An individual with cyclothymia may feel stable at a baseline level but experience a noticeable shift to an emotional high during subthreshold hypomanic episodes of elation or euphoria, with symptoms similar to those of mania but less severe, and often cycle to emotional lows with moderate depressive symptoms. To meet the diagnostic criteria for cyclothymia, a person must experience this alternating pattern of emotional highs and lows for a period of at least two years with no more than two consecutive symptom-free months. For children and adolescents, the duration must be at least one year.

The diagnosis of cyclothymia is rare compared to other mood disorders. Diagnosis of cyclothymia entails the absence of any major depressive episode, manic episode or mixed episode, which would qualify the individual for diagnosis of other mood disorders. When a major episode manifests after an initial diagnosis of cyclothymia, the individual may qualify for a diagnosis of bipolar I or bipolar II disorder. Although estimates vary greatly, 15–50% of cases of cyclothymia later advance to the diagnostic criteria for bipolar I and/or bipolar II disorder (with cyclothymic features). Although the emotional highs and lows of cyclothymia are less extreme than those of bipolar disorder and generally do not cause the same conditions, the symptomatology, longitudinal course, family history and treatment response of cyclothymia are consistent with bipolar spectrum.

Lifetime prevalence of cyclothymic disorder is 0.4–1%. Frequency appears similar in men and women, though women more often seek treatment. People with cyclothymia during periodic hypomania (euphoria) tend to feel an inflated self-worth, self-confidence and elation, often with rapid speech, racing thoughts, not much need to sleep, increased aggression and impulsive behavior, showing little regard for consequences of decisions—but may sometimes be somewhat, fully or hyper-productive for a period of several days at a time.

Mortality of IIA is high, unruptured IIA are associated with a mortality reaching 30%, while ruptured IIA has a mortality of up to 80%. IIAs caused by fungal infections have a worse prognosis than those caused by bacterial infection.

IIAs are uncommon, accounting for 2.6% to 6% of all intracranial aneurysms in autopsy studies.